ATAR Notes: Forum
Uni Stuff => Universities - Victoria => University of Melbourne => Topic started by: ferrsal on April 02, 2015, 10:07:56 am
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Does anyone know what lectures will be covered in the mid semester test?
Also, thought I'd create this topic for any further queries/discussions regarding this subject :D
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They'll prob let us know later but I'd guess weeks 1-5.
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In lecture 14, im a bit confused about slide 14. Is the diagram shown the corticobulbar tract? Why is the reticulospinal tract shown there?
Does this mean that the primary motor cortex is connected to the descending projections from the brainstem to spinal cord (e.g. reticulospinal tract, colliculospinal tract). I thought the brainstem and cortex axons were separate :-\
Thanks in advance if anyone can help me out
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Re Lecture 14 slide 14. I take it that the diagram to which you are referring is the one concerning motor and non-motor loops of the basal ganglia.
In the above case, the four sections of the diagram just refer to different functions of the basal ganglia. In most instances, the basal ganglia are thought to modulate voluntary movement, hence the motor loops. The following is from Purves: the pre-frontal loop may regulate the initiation and termination of cognitive processes such as planning, working memory, and attention. Likewise, the limbic loop may regulate emotional and motivated behaviour, as well as the transitions from one mood state to another.
Either way, these loops, be they motor or non-motor, all relate back to some form of motor associated modulation.
If, however, you are referring to Lecture 13 slide 14, then I'll presume you you are talking about the indirect pathway from the motor cortex to the spinal cord.
The reticulospinal tract starts in the reticular formation in the pons and medulla (activation and suppression of movement).
In relation to the feed-forward mechanism mentioned in the lecture (pulling on the bar, but gastrocnemius EMG activity measured before biceps EMG activity):
- It is anticipated that posture will somehow change (i.e., pulling on the bar).
- Pre-frontal and motor cortex neurons "activate" the reticular formation (note that only some neurons from these cortices are activated in this way; this is important because most motor neurons do not run in the corticobulbar tract - most run in the corticospinal tract instead).
- Via the reticulospinal tract the relevant parts of the spinal cord become "activated" and their associated motor neurons also become "activated."
From Purves (may be of more clarity): Neurons in the motor cortex that supply the lateral part of the ventral horn to initiate movements of the distal limbs also terminate on neurons in the reticular formation to mediate postural adjustments that support the movement. The reticulospinal pathway terminates in the more medial parts of the ventral horn, where lower motor neurons that innervate axial and proximal muscles are located. Thus, the motor cortex can influence the activity of spinal cord neurons via both direct and indirect routes.
So, to answer your question, yes the brainstem nuclei and motor cortex are largely separate, especially for most voluntary motor control, but in some instances, such as the feed-forward mechanism described above, the corticobulbar does link the motor cortex to the spinal cord via the brainstem.
Lastly, hopefully what I've written makes sense - let me know if it doesn't. And I hope my lecturing numbering is right, otherwise...
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Omg thanks so much for always helping me out and the clear explanations! One more question, given that the corticobulbar sometimes links the motor cortex to the spinal cord via the reticulospinal tract, is this also true regarding the vestibulospinal and colliculospinal tracts?
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While it was not explicitly discussed in the lecture, nor in the lecture notes, I found the following in Purves, but it is a little ambiguous in that it won't give you the exact answer you're looking for.
The reticular formation and the vestibular nuclei (upper motor neurons in the brainstem) are responsible for postural regulation:
- Reticular formation is important for feed-forward control of posture.
- Vestibular nuclei that project to the spinal cord are important for feedback postural mechanisms.
Brainstem pathways can independently organise gross motor control. Direct projections from the motor cortex to local circuit neurons in the brainstem and spinal cord are important for movements of the face and the distal parts of the limbs.
As for the colliculospinal tract (dorsal midbrain):
Superior colliculus upper motor neurons (not sure if all do this or just some) innervate circuits in the reticular formation that supply medial parts of the cervical spinal cord. Functionally, this pathway helps control axial musculature in the neck (generation of orienting movements of the head).
In the lecture, Peter spoke of "hearing a sound and orienting towards its location." So, my best guess would be that there would have to be some sort of higher input, but whether it would be higher motor input is not clear from what I have read.
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Awesome, thanks so much again!
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No problem
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To people who did the subject in recent years, were there diagrams or graphs on the mid semester test?
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I'm assuming that you PoNs guys have done your midsem at this point? If so, how many marks was it out of?
In the NEUR30002 fraternity here the first midsem was out of 32 marks (originally 34) and the upcoming 2nd one out of 37; both are worth 25%, not far from your 30%, which is the most insane midsem mark allocation/assessment I've seen in these 3 years. Even just considering this first one, people who barely pass will be holding onto the potential for a final H1 grade by the skin of their teeth.
Luckily I did well here, but I'm not sure if I would be so lucky for next round and there are also people who are unhappy with their scores this time around.
I was talking to an alumni friend who did NEUR30002 a couple of years ago and she was surprised, so it seems like this was a fairly recent development.
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It's actually the NEUR30002 mid sem results that we just got! Our PoNs mid sem is this tuesday. But yeah, massive weighting that can really make or break your chances of doing well.
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On the plus side for neurophysiology.. if you do well on the mid sems you can really lower that bar for an h1... potentially a 60 something % on the exam will put you over the line if you did well enough on the msts. This set up really favours people who work consistently and rips people who don't... and why don't they just break up the 30% principles mid sem like in neurophysiology?
anywho, lecture 5.3.. if dopamine is so pro-movement , why does it inhibit the cortex in the indirect pathway? I suppose the indirect path is meant to contrast the selected movement so i guess that doesn't stand here??
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Slide 12 of lecture 5.3 sums up why there are inhibitory and excitatory outputs of the substantia nigra pars compacta.
Direct pathway: excitatory dopaminergic (D1) output effectively selects desired movements.
Indirect pathway: inhibitory dopaminergic (D2) output effectively deselects/dampens unwanted movements.
Together, there is a level of contrast sensitivity.
Also, note that different dopaminergic receptors are in play here [from NEUR30002 Lecture 4.3: Dopamine recetpors are GPCR. D1 family: excitatory (D1, D5); D2 family: inhibitory (D2, D3, D4)].
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Does anyone know the difference between "range" and "sensitivity and dynamic range" in those tables that were featured in the somatosensory and hearing lectures? Even with his explanations and google, they seem like the exact same thing to me
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It's more or less the same thing. Take EM radiation for example: our eyes can perceive 400-700 nm (i.e., range), which could be perceived from a single photon or from a ray of sunlight (i.e., dynamic range and sensitivity).
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Did anyone read the textbook references for slides 26-29 of lecture 2.3 (ran out of time in lecture). if so plz spoonfeed me info :P :P :P
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I was in two minds about posting this, because it really is spoon feeding...
Slide 26: different types of mechanoreceptors have distinct cortical mappings.
Slide 27: illustrative of cortical plasticity, whereby if a digit is amputated, its cortical representation is redistributed to the remaining digits.
Slide 28: ethological considerations of cortical plasticity in lactating rat v. non-locating rat.
Slide 29: cortical representation of digits before and after repetitive behavioural task.
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For the first question, I think it was ventricles, but who knows? The first lecture says that Galen studied ventricles and the spinal cord and the brain, so surely he would have seen the difference in the colour of the tissue types.
For the stimulation of the globus pallidus external segment and subthalamic nuclei question, what are the two resulting effects on the frontal cortex?
Obviously these are normally involved in deselecting unwanted movements. But what happens next?
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I got ventricles too but you never know... useless question.
Can't really remember the globus pallidus question but wasn't it just following the diagram as though you're stimulating each of them?
I definitely got the dopamine question wrong too, and many others are under question lol.
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Yeah it was, but my brain just melted on that question.
EDIT: I think increasing the stimulation of GPe leads to increased motor activity, and increasing the stimulation of subthalamic nuclei leads to decreased motor activity, which is not the answer I wrote in the test unfortunately. Does anyone know if that is right?
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Yep I just checked the diagram and that looks right. Can't remember if that's the answer I selected though
Quick sidenote, lecture 10 of neurophys, slide 25.. He starts talking about peptide neurotransmitters in relation to metabotropic receptors. Is this talking about peptide neurotransmitters BINDING to the metabotropic receptors? Is that what all the things in slide 26 also do? (Neuromodulators, Co-transmitters, etc)? :/
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I think I panicked and changed basically every answer I got right to the incorrect choice (e.g. the diuresis control one, ventricles) AHAHA GOODBYE 30%
I'm going to have to knuckle down for the final exam :')
Did anyone actually think the test was easy (I have yet to talk to someone who did)? Maybe they'll give us all pity marks.
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Nah, it was definitely the hardest mid sem i've had. What was the answer to the diuresis and natriuresis one??
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I'm confused, how can a metabotropic receptor release neurotransmitters? Didn't he mean that these Co-transmitters are usually released by a pre-synaptic cell and then bind to a GPCR?
Am I right when I say that in slide 26, neurotransmitters, neuromodulators and co-transmitters are all substances released that BIND to metabotropic receptors? But Autoreceptors and Non-synaptic receptors are actual TYPES of metabotropic receptors?
P.S. Sorry for going off-topic here!
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I'm confused, how can a metabotropic receptor release neurotransmitters? Didn't he mean that these Co-transmitters are usually released by a pre-synaptic cell and then bind to a GPCR?
Sorry, what I wrote before was wrong - what I meant to say was that the presynaptic cell (not the metabotropic receptor) can release peptide and small-molecule NTM. It is very common for an axon terminal to have two NTM types: small-molecules and peptides that are released in different vesicles.
Am I right when I say that in slide 26, neurotransmitters, neuromodulators and co-transmitters are all substances released that BIND to metabotropic receptors? But Autoreceptors and Non-synaptic receptors are actual TYPES of metabotropic receptors?
Yes, that makes sense (much more sense than whatever I wrote in that other post).
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Awesome, thanks for clarifying!
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Hopefully the following clarifies the confusion from a previous post (that I have since deleted because it was plain wrong):
NTM, neuromodulators, and co-transmitters all bind to metabotropic receptors to modulate something (that something could be membrane potential, and the NTM release could hyperpolarise (i.e., modulate) it so that it will not reach threshold as readily; equally, co-transmitters are released from a presynaptic cell to modulate the activity of a postsynaptic cell).
Many transmitter classes (GABA, GLU, ACh, etc.) also have metabotropic receptors. For instance, ACh has both nicotinic (ionotropic) and muscarinic (metabotropic) receptors.
Metabotropic receptors alter neuronal activity via intermediate steps between receptor and ion channels.
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Yeah it was, but my brain just melted on that question.
EDIT: I think increasing the stimulation of GPe leads to increased motor activity, and increasing the stimulation of subthalamic nuclei leads to decreased motor activity, which is not the answer I wrote in the test unfortunately. Does anyone know if that is right?
Yeah, 15 C. The 'normal' role of GP(ex) is to inhibit motor cortex activity. If you suddenly positively stimulate it, the opposite will happen (increase motor activity). No need to follow through the whole pattern!
The answer to diuresis one (last fill in blank) was sympathetic.
I also put ventricles.
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I had sympathetic and changed it to PSNS for literally no reason :'( that test was hard I DON'T NEED TO LOSE EVEN MORE MARKS
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What was the diuresis question again? Can't remember that one.
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Hahaha at least you didn't put ENS like I did.
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What was with the mechanoreceptor question?
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Multichoice? I had ruffini's
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Thought it said small RF?
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If it's the question I think you're referring to, then it was the one about grabbing something. In that case, Ruffini receptors would be detecting skin stretch.
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Yep, that was Ruffini's. As far as I remember it wasn't on the slides but the lecturer mentioned it. I think with Peter Kitchener it's necessary to write down pretty much every detail he speaks... that's definitely something I learnt from this MST
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do you think they're gonna take questions out of this mst? mann, so stressing about results, given its 30%
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do you think they're gonna take questions out of this mst? mann, so stressing about results, given its 30%
As for question 1 (Galen and what he could see) - no. Don't know about any others though.
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Yep, that was Ruffini's. As far as I remember it wasn't on the slides but the lecturer mentioned it. I think with Peter Kitchener it's necessary to write down pretty much every detail he speaks... that's definitely something I learnt from this MST
I would have thought it'd be something with a small receptive field :') he said fine manipulation of the small object rather than object movement so I thought the exact position might be easier to detect with smaller receptive fields? like maybe Merkel receptors? SO WHY IS IT RUFFINI PETER WHY :'(
I swear studying for this MST didn't help at all, understanding the lectures at home did NOT translate into getting the right answers for these questions :x
time to memorise Purves for the final because I feel like I got ~50% after reading what people thought the answers were :'( THIS WAS SUPPOSED TO BE A NICE STRAIGHTFORWARD ELECTIVE AND NOW I'M STRUGGLING TO GET AN 80
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Actually this mst had a real gamsat feeling to it...
the pathway thing anyway..
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Me reading the subject reviews like "this is easiest level 3 subject i've taken"
(https://40.media.tumblr.com/333417d34b9d2ebc18ee0866a3b25691/tumblr_nncs6bvGEB1shji13o1_500.png)
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I would have thought it'd be something with a small receptive field :') he said fine manipulation of the small object rather than object movement so I thought the exact position might be easier to detect with smaller receptive fields? like maybe Merkel receptors? SO WHY IS IT RUFFINI PETER WHY :'(
That's interesting you say that because if small receptive fields were tacit in the question but not explicitly stated (can't remember it's wording at all), then what fine manipulation is interpreted to mean might differ from person to person. Just considering the semantics of the question, if it did say fine manipulation of a small object, well that's not exactly the same as stating "small receptive fields." Anyway, it is what it is I guess...
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That's interesting you say that because if small receptive fields were tacit in the question but not explicitly stated (can't remember it's wording at all), then what fine manipulation is interpreted to mean might differ from person to person. Just considering the semantics of the question, if it did say fine manipulation of a small object, well that's not exactly the same as stating "small receptive fields." Anyway, it is what it is I guess...
I feel like a few of the questions were like that. Galen's one threw me off for e.g. because I read it as a theoretical question rather than based off the lectures, it was worded in an open sort of way. But yes, it is what it is :'D TOTALLY AGREE WITH FERRSAL, Y'ALL LIARS
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I would have thought it'd be something with a small receptive field :') he said fine manipulation of the small object rather than object movement so I thought the exact position might be easier to detect with smaller receptive fields? like maybe Merkel receptors? SO WHY IS IT RUFFINI PETER WHY :'(
I swear studying for this MST didn't help at all, understanding the lectures at home did NOT translate into getting the right answers for these questions :x
time to memorise Purves for the final because I feel like I got ~50% after reading what people thought the answers were :'( THIS WAS SUPPOSED TO BE A NICE STRAIGHTFORWARD ELECTIVE AND NOW I'M STRUGGLING TO GET AN 80
I put down Merkel as well haha, thought it had to be small receptive field. But I wasn't sure if Merkel or Pacinian because wouldn't it be dependent on how much pressure you would be applying? i dunno it threw me off lol
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I put Merkel too. Sigh.
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what did you guys put for in for that question that asks you what would happen if you were to selectively activate the D2 receptor drug?
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what did you guys put for in for that question that asks you what would happen if you were to selectively activate the D2 receptor drug?
No movement I think (similar to PD).
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I said more movement because Peter said in the lecture that dopamine is "ALWAYS pro-movement", like he emphasised that point when referring to action on D2 receptors in the indirect pathway. But apparently it just deselects unnecessary movements. I feel like he should take that one off the quiz @_@
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I remember him saying that as well, but if you follow the pathway you get inhibition right?
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Google says D2 agonists are used for treatment of Parkinson's disease so I assume they would be pro movement which then doesn't make sense if it's inhibitory in the pathway
*sigh*
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Google says D2 agonists are used for treatment of Parkinson's disease so I assume they would be pro movement which then doesn't make sense if it's inhibitory in the pathway
*sigh*
Wow... not confusing at all LOL
I thought D2 was inhibitory. The only reason I think they would be used is to reduce the dyskinesia (the unwanted tremors) associated with L-DOPA?
Because as melonbar said above if you followed that pathway, I think the only answer would have been inhibition of movement.
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I said inhibition too, but apparently it was more movement :'(
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I said inhibition too, but apparently it was more movement :'(
Don't even know what to think anymore.
Slide 11 in Lecture 12 (Neurophys) says that D2R inhibits unwanted movement.
Online it says both so fuarkk.. so confusing..
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Wat... how does indirect pathway inhibit movement then?
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I found this on the internet
"Dopamine therefore increases the excitatory effect of the direct pathway (via D1 causing movement) and reduces the inhibitory effect of the indirect pathway (via D2 preventing full inhibition of movement)."
This makes sense in terms of D2 being inhibitory but at the same time being pro-movement. However, they never mentioned anything like this in the lecture even though it clarifies a lot of things. (????)
So in the case of that question, stimulating D2 receptors will lead to a greater inhibition of the indirect pathway and therefore ultimately increasing movement.
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I found this on the internet
"Dopamine therefore increases the excitatory effect of the direct pathway (via D1 causing movement) and reduces the inhibitory effect of the indirect pathway (via D2 preventing full inhibition of movement)."
This is what I had from my notes, he had said it in the lecture. So in that MST question, I think the answer was more movement
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ah I must have missed that. that makes sense then!
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D2 being inhibitory but at the same time being pro-movement.
(http://m0.joe.ie/wp-content/uploads/2015/04/22120955/ce9c949d6c73dbfb889f6036bac022dd.gif)
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How's NEUR30003 been treating you guys so far ?
Any advice/tips/recommendations etc...
Curious to know as I plan on taking the subject next year.
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How's NEUR30003 been treating you guys so far ?
Any advice/tips/recommendations etc...
Curious to know as I plan on taking the subject next year.
I think that neuroscience is a subject that will appeal to some people but not others. As the title suggests, it covers the principles, so expect to cover a range of topics in varying levels of detail, some of which you may love, and others that won’t enjoy as much. As far as tips go, just work hard like you would in any other subject.
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They do realize that these multiple choice tests dont have to be marked manually, right.....? lol
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Quite ridiculous how long it has actually been.
I know I did shit, but I just want to get a mark back for motivation to study for the final exam.... :(
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peter made an announcement saying there was an 'issue' which should be resolved tonight
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They're up.............
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They're up.............
Yup, got rekt
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lol. no choice but to kill the exam now....
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lol. no choice but to kill the exam now....
HAHA dude i know that feeling, need like 90% or something for h1 HAHAHAHAFML
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They do realize that these multiple choice tests dont have to be marked manually, right.....? lol
When ever you rub out an answer and change it to another answer, they have to by hand, whiteout the rubbed out shaded box, because the machine gets confused because of this, thinking that you have shaded in two answers. so it's not as easy as just putting answer sheet and getting a result from it.
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When ever you rub out an answer and change it to another answer, they have to by hand, whiteout the rubbed out shaded box, because the machine gets confused because of this, thinking that you have shaded in two answers. so it's not as easy as just putting answer sheet and getting a result from it.
That's quite understandable but the fact that we had to wait a significantly long time for results to be released is a little frustrating to say the least. Out of the subjects I've done, I don't think I've had to wait this long.
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^ the problem wasn't machine based but admin based. We got the average and statistics of performance approximately a week before the release of the results due to some staff leave of absence.
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They're up.............
That's odd I don't see mine :/
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That's odd I don't see mine :/
Go to My Grades and click the All subjects tab. It is hiddened somewhere in that list of all your subject assessment scores.
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Go to My Grades and click the All subjects tab. It is hiddened somewhere in that list of all your subject assessment scores.
Yeah I tried that too, nothing in Principles of Neuroscience :/ Maybe they are not all put up instantly
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Did peter say there won't be exam questions on lecture 7.2 (big neuroscience) ?
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Did peter say there won't be exam questions on lecture 7.2 (big neuroscience) ?
Big neuroscience will not be examined directly. You should just understand what was discussed, but you do not need to learn all of the details. At least that's what I was told.
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Have they said anything about MST feedback? I need to know where I went wrong!
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Wanted to get this thread up again since the exam is coming up soon.
Had a few questions:
1) Does LTP (especially late phase - like we covered in neurophys where there is formation of new active zones) mean that the particular memory is in long term memory?
2) For the purposes of NEUR30003, do we assume that dopamine =/= reward but is instead the anticipation of the reward?
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Wanted to get this thread up again since the exam is coming up soon.
Had a few questions:
1) Does LTP (especially late phase - like we covered in neurophys where there is formation of new active zones) mean that the particular memory is in long term memory?
2) For the purposes of NEUR30003, do we assume that dopamine =/= reward but is instead the anticipation of the reward?
1. LTP = potentiation (strengthening of synapses). Early phase is phosphorylation (of AMPA and PSD95), but this is only transient. Late phase is structural, so formation of new active zones as you have said. Since the latter is a structural change (i.e., more permanent), and involves protein synthesis (via CREB), it contributes to long-term memory. LTP alone is not long-term memory as far as I can tell: say that you have potentiation of synapses but for only a short period of time, then you would expect the early phase of LTP, but not the late phase. Going by my reasoning, that would not constitute a long-term memory.
2. VTA dopaminergic neurons encode the "accuracy to which a reward can be predicted." Or something along those lines. Just go with whatever the lecturer said since it is a different subject.
(http://i.imgur.com/YPPVgKY.png)
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1. LTP = potentiation (strengthening of synapses). Early phase is phosphorylation (of AMPA and PSD95), but this is only transient. Late phase is structural, so formation of new active zones as you have said. Since the latter is a structural change (i.e., more permanent), and involves protein synthesis (via CREB), it contributes to long-term memory. LTP alone is not long-term memory as far as I can tell: say that you have potentiation of synapses but for only a short period of time, then you would expect the early phase of LTP, but not the late phase. Going by my reasoning, that would not constitute a long-term memory.
2. VTA dopaminergic neurons encode the "accuracy to which a reward can be predicted." Or something along those lines. Just go with whatever the lecturer said since it is a different subject.
(http://i.imgur.com/YPPVgKY.png)
Thanks mate for the reply.
With regards to CREB - do we need to know how it is phosphorylated (like what causes its phosphorylation?)
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With regards to CREB - phosphorylated by protein kinase A.
I don't think it's that important to know btw. (Just my opinion)
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Thanks mate for the reply.
With regards to CREB - do we need to know how it is phosphorylated (like what causes its phosphorylation?)
I wish, because I actually know that from one of my pharm subjects. But since the slides are fairly straightforward, I would not expect anything beyond 'long-term memory requires protein synthesis and is mediated by CREB'.
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Thanks for the reply guys. I knew it was PKA but I didn't know what was upstream (what events came about - I assumed it was a GPCR linked to Gs but for neurophys the GPCR was mGluR1 linked to Gq (PLC)) :P
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Hey guys, lecture 24 regarding changes in addicted individuals, what is the difference between "basal glutamate" and "stimulated (phasic) glutamate"? Why does one increase and the other decrease?
Also what does "hypofrontal" mean? Everything on my slide is annotated from listening to the lecture but I'm still confused lol
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Could someone plss explain the C14 hippocampus stem cell thing? Lecture 2.2 (fuck)
Link to actual paper if needed: http://www.sciencedirect.com/science/article/pii/S0092867413005333
Is it because the graph is going down, its indicating that the hippocampal neurons that incorporated the 14C from the bombs are dying (and being replaced/turned over? -> evidence that theres generation of new hippocampal cells?)
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Could someone plss explain the C14 hippocampus stem cell thing?
Bomb testing: C14 increase in neurons.
Cessation of bomb testing: C14 decreases.
The neurons are turning over, hence there is regeneration in the brain. The C14 comes from the environment, so eating a plant that incorporates atmospheric C14 into its fruit would lead to the presence of C14 in neurons. Once there is less C14 in the environment, eating fruit (arbitrary) won't have the same incorporation of C14. The whole C14 thing is just a proxy for measuring neuron turnover in humans because you can't just go and do mass spec. on people brains. Human ethics committee wouldn't give the approval!
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Right, so if there was no turnover, then the 14C levels would be constant after the bombs?
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Right, so if there was no turnover, then the 14C levels would be constant after the bombs?
Everyone born before the bombs were dropped would have C12 assuming no turnover (C14 would not be incorporated into their neurons since the neurons are not having to regenerate). So, only people conceived/in utero around that time would have C14, which would be constant minus any loss of neurons during development/ageing.
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Everyone born before the bombs were dropped would have C12 assuming no turnover (C14 would not be incorporated into their neurons since the neurons are not having to regenerate). So, only people conceived/in utero around that time would have C14, which would be constant minus any loss of neurons during development/ageing.
Oh right, thanks man. I thought 14C can invade adult neurons as well.
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Anyone know whether LTP is invovled in Implicit memory?
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Hey guys, lecture 24 regarding changes in addicted individuals, what is the difference between "basal glutamate" and "stimulated (phasic) glutamate"? Why does one increase and the other decrease?
Also what does "hypofrontal" mean? Everything on my slide is annotated from listening to the lecture but I'm still confused lol
So the net effect on an addicted individual is a reduced level of basal (ongoing) glutamatergic and dopaminergic inputs, and increased phasic Glut and Da, phasic meaning only when stimulated, so here being during drug consumption.
The reduced basal input implicates a reduction in sensitivity to normal frontal inputs (the case of hypofrontal behaviour) and so essentially their motivation for normal behaviour is diminished while the drug behaviour is reinforced. The increased phasic inputs (particularly Glutamate) underlie the increased excitability with drug behaviour because the glutamate activates second messenger pathways. This wasn't elaborated further but I think it's enough to get you to see the big picture on how drugs have their effects in maintaining addictive behaviour.
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Anyone know whether LTP is invovled in Implicit memory?
I don't remember this being in the lectures, but I don't see why procedural memories wouldn't be using LTP too :S
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I don't remember this being in the lectures, but I don't see why procedural memories wouldn't be using LTP too :S
Thanks for the reply!!
Super worried about the exam - the last few lectures on PFC + consciousness + language were so conceptual and everything (I only know the very basics... :( )
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I really hope this exam is easy... I've got thorough notes for the whole course but absolutely *none* of it is sticking and I can't remember a single thing unless I've looked at it in the last 3 or 4 minutes. Good luck tomorrow, everyone!
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I wish your dorsolateral PFC the best of luck tomorrow. Please exercise the use of your ventral medial PFC when exiting the exam and not scream of its easiness when other people fail. Kind regards, PONS.
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Resigned to an all nighter (still up to week 8...smh). GL everyone
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I wish your dorsolateral PFC the best of luck tomorrow. Please exercise the use of your ventral medial PFC when exiting the exam and not scream of its easiness when other people fail. Kind regards, PONS.
Haha - I'm glad you're making PoNs jokes! I'm certainly not in the mood. To all the late night PoNs battlers out there, I wish you all the best!
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Spent way too long on the first half of the course, definitely suffered a little there... I don't think I even want to know what the answers are.
Hope everyone went well! Very glad that's over, I'm never looking at brains again.
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That was harder than gamsat
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Hope everyone went well! Very glad that's over, I'm never looking at brains again.
I found neurophys to be the better of the two first sem neuro subjects. I feel like some of the stuff we had to learn in PoNs seemed so far removed from science that it wasn't even science! Hopefully next semester there's more of an emphasis on science and no more abstract stuff!
(http://i.imgur.com/yUI6PLi.png)
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I thought it was a fair exam. Found the most difficult question to be the statements for language (pretty sure I got 0-1/3) and the pain question took me a while.
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I thought it was a fair exam. Found the most difficult question to be the statements for language (pretty sure I got 0-1/3) and the pain question took me a while.
Yeah, I thought it was pretty fair too. As for those language questions, they weren't exactly what I had in mind for a neuroscience test! The third one seemed a little ambiguous because it didn't really fit in with the postulates of either theory, but at the same time, it didn't exactly preclude itself from either theory. At least that's how I saw it.
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Yeah, I thought it was pretty fair too. As for those language questions, they weren't exactly what I had in mind for a neuroscience test! The third one seemed a little ambiguous because it didn't really fit in with the postulates of either theory, but at the same time, it didn't exactly preclude itself from either theory. At least that's how I saw it.
Totally agree about the third language one. The first two qs were ok if you listened to his lecture though.
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Yep, definitely preferred the neurophys exam over this. Had a few hiccups with this one, especially with the brain imaging techniques which I think I got all wrong lol
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Yep, definitely preferred the neurophys exam over this. Had a few hiccups with this one, especially with the brain imaging techniques which I think I got all wrong lol
There was only like 1-2 questions iirc?
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After looking through my notes, I realized that every pair of question that I had a fifty-fifty of getting right I got wrong (e.g. alpha and gamma waves, ventral and dorsal stream). But I probably got a decent score, I personally thought it was much easier than the MST, but this is probably because I changed my study strategy after that.
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What was the imaging? MRI for MS is all I can remember.
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What was the imaging? MRI for MS is all I can remember.
2-3 MC questions i think, something about the one with the best temporal resolution? Can't remember the other one. Probably easy questions with obvious answers but I hate those topics so much I just avoided them completely
Is anyone else mad how much of the first half of the course they left out? Like I know we already got tested on that but the exam is worth 70% like..... mix it up lol
Anyway all we can do now is hope for the best :)
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What was the imaging? MRI for MS is all I can remember.
omg Peter sucks I put MRI but changed it impulsively to CAT because it was pluralised and didn't fit grammatically JUST LIKE HOW HE HAS ERRORS ALL OVER HIS SLIDES and I was stupid enough to pick grammar over the correct answer
:'( :'( :'( :'( :'( :'( :'( :'( :'( :'(
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What was the imaging? MRI for MS is all I can remember.
I put in MEG for best temporal resolution (because there wasn't an EEG option, otherwise I would be confused).
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I put in MEG for best temporal resolution (because there wasn't an EEG option, otherwise I would be confused).
MEG was the option in the list, but it has temporal resolution that is more or less equivalent to EEG. They both work in similar ways. The other three options were fMRI, CAT (I think?), and PET, all of which have very poor temporal resolution.
omg Peter sucks I put MRI but changed it impulsively to CAT because it was pluralised and didn't fit grammatically JUST LIKE HOW HE HAS ERRORS ALL OVER HIS SLIDES and I was stupid enough to pick grammar over the correct answer
:'( :'( :'( :'( :'( :'( :'( :'( :'( :'(
Yeah, there were so many grammatical and orthographical errors in the test. I was really surprised that they didn't pick those up.
What was the imaging? MRI for MS is all I can remember.
Yeah, MRI for MS, the MEG / temporal resolution question, and maybe you can include the clinical diagnostic technique for PD since it's kind of related (not imaging per se though).
Is anyone else mad how much of the first half of the course they left out? Like I know we already got tested on that but the exam is worth 70% like..... mix it up lol
And, yes, it was a little surprising that so little of the course was on the test. Peter did say, however, that he would be emphasising the second half of the course...
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Tbh I was expecting 25% 1st half, 75% 2nd half which would've made the assessment around 50%-50%.
But yeh, heaps fo spelling mistakes (i.e. motoneuron? LOL)
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Daingit, my GPA will get pummeled. ^ 'motoneuron' is actually a word (well he wrote it on his lecture slides) but its one of those freaky ones that should not exist
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For the last question (Q40.) of section B, where it asked for the critical period for the development of stereopsis in humans, the question said that the critical period for humans is 30x greater than that for cats. The answers were either in x? days?, 3? months, 3 years, or 9 years.
What did everyone go with?
I thought of lecture 2.1 (below), but lecture 10.2 will give you a different answer.
(http://i.imgur.com/JnAC57o.png)
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For the last question (Q40.) of section B, where it asked for the critical period for the development of stereopsis in humans, the question said that the critical period for humans is 30x greater than that for cats. The answers were either in x? days?, 3? months, 3 years, or 9 years.
What did everyone go with?
I thought of lecture 2.1 (below), but lecture 10.2 will give you a different answer.
(http://i.imgur.com/JnAC57o.png)
I went with 3 years (1month X30 --> 30 months ~3 years) - but it was a Kitchener question though (not from Colin Andeson so I picked that instaed of the 10.)
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I went with 3 years (1month X30 --> 30 months ~3 years) - but it was a Kitchener question though (not from Colin Andeson so I picked that instaed of the 10.)
I get that it's Peter's question, but when we're presented with figures that don't match, then how is that fair?
EDIT: Also, where did you get the one month value from for kittens? Lecture 10.2 slides show that monocular deprivation takes 6 days at the most critical period, or 2.5 months from birth.
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I get that it's Peter's question, but when we're presented with figures that don't match, then how is that fair?
EDIT: Also, where did you get the one month value from for kittens? Lecture 10.2 slides show that monocular deprivation takes 6 days at the most critical period, or 2.5 months from birth.
UGH not another wrong question :'( picked 3 years as well, though 2.5 x 9 is 6.5 years, not 9. Dafuq
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UGH not another wrong question :'( picked 3 years as well, though 2.5 x 9 is 6.5 years, not 9. Dafuq
Yeah I know... I see this quite often with tests and alike at uni. Nobody bothers to check if all of the questions can be answered in a reasonable manner. You always get these questions that were either never taught ("mentioned in passing, set for reading" as people would probably claim :P) or lack clear cut answers.
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I picked 9 years (same slide usage as nino).
Anyone else pick up that Statement 2 of Language said Wernickes area was located in PARIETAL Cortex....
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Anyone else pick up that Statement 2 of Language said Wernickes area was located in PARIETAL Cortex....
What?!?! Haha, now that is ridiculous!
Was this from that series of three questions that you mentioned before?
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Yes. Statement 2 was about Broca's and Wernicke's area. However, the stem of the question said "assume the statement was true" so I think its a typo, - not testing whether you know the location of Wernickes.
What about critical period for abuse in childhood? pre school, teenager, etc?
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I get that it's Peter's question, but when we're presented with figures that don't match, then how is that fair?
EDIT: Also, where did you get the one month value from for kittens? Lecture 10.2 slides show that monocular deprivation takes 6 days at the most critical period, or 2.5 months from birth.
Hmmm... that's interesting.
Well let's say it was 6 days for cats - then 30X 6 days ==> 180 days ~6 months? That wasn't a choice :/
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Yes. Statement 2 was about Broca's and Wernicke's area. However, the stem of the question said "assume the statement was true" so I think its a typo, - not testing whether you know the location of Wernickes. I guess thats akin to the good old "choose the best answer."
What about critical period for abuse in childhood? pre school, teenager, etc?
Do you remember what the whole question was for the "critical period for abuse in childhood?" I put pre-school (social cognition develops at around three years), but think option A was earlier in life, which might be a better response depending on what the question was.
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It's either 'first year of life' or 'pre school'. I chose pre school.
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Yes. Statement 2 was about Broca's and Wernicke's area. However, the stem of the question said "assume the statement was true" so I think its a typo, - not testing whether you know the location of Wernickes.
What about critical period for abuse in childhood? pre school, teenager, etc?
I chose the earliest possible option (which I don't remember what it was). During the exam I remembered the 'Child of Rage' video Peter had in his slides, in which abuse to a girl in the first few years of her life completely changed her early infancy behavior.
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Do you remember what the whole question was for the "critical period for abuse in childhood?" I put pre-school (social cognition develops at around three years), but think option A was earlier in life, which might be a better response depending on what the question was.
I'm fairly sure that was the 1st year of life tbh.
I got the other one wrong - the self referential one
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I chose the earliest possible option (which I don't remember what it was). During the exam I remembered the 'Child of Rage' video Peter had in his slides, in which abuse to a girl in the first few years of her life completely changed her early infancy behavior.
this seems key to answering the question (aka, how much is 'few years'). it's a vague question and we shall never know!
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On hindsight, I would argue that the '(...)or even seen' in the sentence 'The “critical period” for normal adult social behaviours is not when these behaviours are taught or modeled or even seen' strengthens the first option. But I'm honestly not sure.
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What?!?! Haha, now that is ridiculous!
Was this from that series of three questions that you mentioned before?
Wernicke's area IS near the parietal cortex... Not a massive transgression. But it said to assume it was true anyway, so moot point. I'm going to stop looking at the thread now - I don't want to know just how many questions I got wrong (given I ruined the neurofilament tau and MRI MS ones despite KNOWING THE ANSWERS 100%, I don't think I've done too flash). Regarding the social behaviour q, I picked 1st yr of life but don't remember him giving any precise time. I really hope they do quality control for this exam :S so many iffy interpretation-based questions, and some of them relied on grammatical/orthographical errors which is a bit unfair.
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I was wondering if anyone still have downloaded lecture recordings of NEUR30003?? I'm sitting a supplementary exam for it sometime in the next few weeks. thanks :)
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I was wondering if anyone still have downloaded lecture recordings of NEUR30003?? I'm sitting a supplementary exam for it sometime in the next few weeks. thanks :)
?? i thought you could just log on the LMS to download them?
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?? i thought you could just log on the LMS to download them?
The changes to the LMS for the past few days have meant the link to the lecture recordings is gone for all subjects :(
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The changes to the LMS for the past few days have meant the link to the lecture recordings is gone for all subjects :(
Sorry to hear that man >_<
Have you got none of the lectures?
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I downloaded every lecture from lecture 1 to lecture 20, unfortunately I didn't do that for lecture 21 onwards....
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Yup I've got them, could give them to you on a USB if you're in the city tomorrow
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Yup I've got them, could give them to you on a USB if you're in the city tomorrow
that would be awesome! unfortunately, I can't private message you on atarnotes. I'll be in the ERC at uni tommorow at around 1-2, if it wouldn't be too much of a hassle for you.
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I'm doing painting techniques and I have a break from 12:30-1:30 so I can tram up and give it to you then :)
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Yup I've got them, could give them to you on a USB if you're in the city tomorrow
Would you be able to upload them on a dropbox, if that'll make things easier. I only need lectures 23-35. if not that's fine, i can see you tommorow
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Won't be able to upload sorry, internet is not at that level haha
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No worries, I'll see you tommorow in the ERC ground level, sometime between 12.30 to 1.30.
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I'll be there around 1 as I'll be heading there from the VCA :P And I'll message you via this thread tomorrow haha
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yepp, sure, thanks again :)
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I'll be at the far back when you walk through the door of the ERC ground level