"mat" <mats_trash at hotmail.com> skrev i melding
news:43525ce3.0201140651.63c9ac60 at posting.google.com...
> > N-methyl-D-aspartate is a neuro-transmitter.
> > It's just one in a huge 'family' of transmitters, ionotropic (direct) or
> > (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.
AMPA,kainate and NMDA; named after the _synthetic_ agonists that activate them....
> 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.
Thanks for your corrections.
I should have known this as I studied it just yesterday :(
Well, time to reread chapter 12 in Principles.
> 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
> > 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
> > 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
> > (as an comparison of the synapse) ?
> > Tough questions, but then, that's the reason I study.
> > Brian
>> 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.
Plasticity - the easiness of change, to transform the function of a synapse.
IE sya that a synapse is enhanced by first deconstructing it (with CREB-2 through
transcription of new protein), and then regrown with CREB-1.
> 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
The first one, degeneration and growth.
If a new synapse is grown from the soma, then that represents a new opportunity, a new
shot at establishing a memory; which can be everything.
Plasticity is not as I see it an enhancement of a synaptic connection.
Why not use the word 'enhancement' ('enhanced axo-dendritic synapse')?