why study neurology?
mats_trash at hotmail.com
Mon Jan 14 16:54:43 EST 2002
"Brian" <zhil at online.no> wrote in message news:<VbG08.1720$8e6.42584 at news4.ulv.nextra.no>...
> "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
> > connection?
> 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')?
New synapses would very unlikely be grown from the soma, you'd first
have to grow another axon etc. New synapses can be formed by the
numerous final divisions of the axonal branches, but these are long
term changes. Changing the efficency of a synapse by long/short term
depression/potentiation is a form of plasticity, and certainly very
important in memory formation as shown by hippocampal studies and
knockout mice lacking important proteins for LTP and LTD. Cells
exhibiting plasticity of the form you describe were recently
photographed doing so in a paper in the journal Cell, probably worth a
look (Principles of Neural Science is only an intro!). But again I
would be weary of the direct associations you make. It is by no means
certain that the cognitive functions into which we have divided our
minds map isomorphically to singular neural processes, in fact I would
tentatively suggest that it is highly unlikely.
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