why study neurology?

Brian zhil at online.no
Sun Jan 13 11:40:19 EST 2002

"mat" <mats_trash at hotmail.com> skrev i melding
news:43525ce3.0201130825.6cd8975e at posting.google.com...
> Though admittedly not an expert of any kind in this area (or any
> other!) I would be weary of saying that Synpatic Plasticity = Memory
> and even more weary of saying that CREB encodes memories.  You can
> only begin to talk about higher functions such as memory at a circuit
> or systems level.  Though of course CREB is important in memory as
> Kandel showed in Aplysia, in humans the situation is far more complex
> than just that.  I would not think that a synapse can be regarded as
> encoding a bit of information similar to a transistor in a CPU.  That
> is taking a far to simplistic view of neurones.

We're aware of that.
And that's why I said further experiments are needed to determine what is what.

> Its the same kind of problem as when people say 'serotonin receptors
> are responsible for mood/depressive state' because SSRIs help in
> depression.  It is not the receptor proteins themsevles, but the part
> they play in the brain's systems that is important.
> By the way there are numerous other mechanisms of synaptic plasticity.
>  Some require protein synthesis e.g. CREB, while others don't.
> NMDA-receptor mediated potentiation is just one example.

N-methyl-D-aspartate is a neuro-transmitter.
It's just one in a huge 'family' of transmitters, ionotropic (direct) or metabotropic
(indirect) - the last through a second-messenger.
We're not saying that CREB-1 (not no.2, that is deconstruction) will enhance memory, but
if it can expand it.
To enhance memory, we'd have to do something with the synaptic functions, and possibly
functions in the soma and the hillock.
Thus the talk of plasticity.
Plasticity is not a sign of the memory-'piece' (which can be everything), but rather how
easily it is to transform.
Is the plasticity a sign of intelligence ??
And if it is, then how will a decrease in CREB-2 decrease the overall plasticity ?
Will an artificial increase in CREB-1 production inhibit the plasticity of the neuron
(as an comparison of the synapse) ?
Tough questions, but then, that's the reason I study.


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