Neuron function question

David Todtman dtodtmanREMOVETHHIS at
Fri Oct 24 22:06:55 EST 2003

Thank you too for your reply.  It fills in even more details for me.
"NMF" <neil.fournier at> wrote in message
news:ujhmb.10880$VQ3.561883 at
> You stated:
> "Am I correct to understand that the metabotropic process does not
> cause the action potential?  My question here is about the other end of
> cell:  I gather that ionotropic action causes the vesicles to migrate to
> cell wall to release neurotransmitters.  So, I think this means that
> metabotropic action does not directly cause the vesicular process.  It
> (metabo.) may come into play with regard to modulating the production of
> neurotransmitters within the cell (which then are deposited into the
> vesicles awaiting release).  Eh?"
> I believe most aspects of your previous msg was answered for the most
> However, this statement that you stated above is not correct.  Ionotropic
> receptors are essentially directly ligand(or transmitter)-gated channels.
> Binding of the particular transmitter elicits in the conformational
> structure of the ion channel allowing it to either open (or sometimes
> in response to a signal.  The ligand, itself, when directly binding to the
> appropriate receptor will cause/elicit the conformational changes in
> strcuture and allow for the resulting flow of current.   An example of
> receptors are non-NMDA receptors (like the AMPA) or the NMDA receptor;
> GABA type B Cl- gated channels.  Stimulation of their respective receptors
> will cause a direct opening of the ion channel.  Moreover, metabotropic
> receptors, gates ion channels only indirectly.  The receptor and effector
> functions of gating are carried out by separate molecules.   A significant
> level of time is required in order for the channels to open. So in one
> condition (i.e. ionotropic) open of the channel is relatively fast along
> levels of 1-2 microsec, whereas, in the opposite condition would require a
> longer period of time (hundreds of milliseconds to seconds).
> Action potentials are mediate by something completely different than from
> what takes place by the action of ionotropic and metabotropic.  Granted
> opening and closing of either ionotropic or metabotropic receptors can
> to adding sufficient depolarization (or hyperpolarization) current at the
> level of the axonal hillock, but the action of metabotropic or ionotropic
> will not influence vesicle recruitment.  Vesicles are found at the axonal
> terminal ends (boutons).  The actions of these receptors can effect
> intracellular biochemical signal transductions within the cell.  For
> example, the action of metabotropic receptors can lead to activation or
> suppression of specific genes, cause structural changes at the dendritic
> spines themselves, Or even change the density (upregulation or
> downregulation) of ion channel expression.  Certain signalling factors
> be responsible for this.  For example, metabotropic glutamate receptor
> signalling could lead to changes in calpain-fodrin interaction which can
> lead to structural changes that cause the un-occluding of the (previously
> hidden) receptor systems.  This has been considered to be the correlate
> the cellular basis of learning or memory (i.e. long-term potentation
> proposed by Donald Hebb).
>  Just remember the vesicle process (in example transmitter release) is
> through a completely different mechanism than ionotropic or metabotropic
> receptor action.  The vesicles are released due to the entrance of Ca++
> through voltage-gated calcium channels at the terminal end of the axon,
> which causes the moblization of vesicles and their fusing with the
> membrane and subsequent release of transmitter.  Also metabotropic
> are not found at the terminal end of axons but are generally localized
> within certain spatial regions of the dendritic arborization (for the most
> part, however, there are often localization of these receptors around the
> soma).
> You also mentioned about 1st messengers, 2nd messengers etc.  Although
> sometimes people don't
> use these delineation, however, 1st messengers (transmitter/ligand
> interaction), 2nd messengers (G-protein coupled receptors or TrK
> and often 3rd messengers are considered (e.g. CREB; MAPK) b/c these
> rely from the plasm membrane to the nucleus in order to elicit changes in
> transcription factors and/or gene regulation.

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