>> 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.
NMDA is not a neurotransmitter. Excitatory amino acid (glutamate,
aspartate and a few other minor AAs) receptors are classified on the
basis of the first ligands discovered that activated them. These were
NMDA and AMPA for the ionotropic receptors, but these are not
physiological ligands. Same as muscarine and nicotine are not the
physiological agonists of the acetylcholine receptors. Ionotropic and
metabotropic does not refer to the transmitter. Receptors define the
intracellular effects. Glutamate can activate both types of
transmitter, NMDA and AMPA are ionotropic glutamate receptors, whereas
there are eight metabotropic receptors currently known that activate
G-proteins on binding glutamate.
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.
CREB is a transcription factor and so works in the nucleus, so if you
are studying that then of course its working in the soma. I'm not
sure what you are defining plasticity as here. Do you mean the actual
change in spatial orientation of a neurone's synapses i.e. growing new
ones and degrading old, or just the change in strength of a synpatic