Principles of Neuroscience

[MelonBar]

Have they said anything about MST feedback? I need to know where I went wrong!

[ChickenCh0wM1en]

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?

[nino quincampoix]

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.

[ChickenCh0wM1en]

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.

(Image removed from quote.)

Thanks mate for the reply.

With regards to CREB - do we need to know how it is phosphorylated (like what causes its phosphorylation?)

[nino quincampoix]

With regards to CREB - phosphorylated by protein kinase A.

I don't think it's that important to know btw. (Just my opinion)

[fireyeah]

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'.

[ChickenCh0wM1en]

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))

[ferrsal]

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

[MelonBar]

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?)

[nino quincampoix]

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!

[MelonBar]

Right, so if there was no turnover, then the 14C levels would be constant after the bombs?

[nino quincampoix]

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.

[MelonBar]

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.

[ChickenCh0wM1en]

Anyone know whether LTP is invovled in Implicit memory?

[emiinaaa]

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.