Principles of Neuroscience

[MelonBar]

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 

[nino quincampoix]

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.

[nino quincampoix]

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?

[ferrsal]

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.

[nino quincampoix]

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?

[ferrsal]

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)? :/

[LeviLamp]

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.

[MelonBar]

Nah, it was definitely the hardest mid sem i've had. What was the answer to the diuresis and natriuresis one??

[ferrsal]

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!

[nino quincampoix]

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).

[ferrsal]

Awesome, thanks for clarifying!

[nino quincampoix]

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.

[REBORN]

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.

[LeviLamp]

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

[nino quincampoix]

What was the diuresis question again? Can't remember that one.