Neil,
Thank you too for your reply. It fills in even more details for me.
Ciao,
David
"NMF" <neil.fournier at sympatico.ca> wrote in message
news:ujhmb.10880$VQ3.561883 at news20.bellglobal.com...
> You stated:
> "Am I correct to understand that the metabotropic process does not
directly
> cause the action potential? My question here is about the other end of
the
> cell: I gather that ionotropic action causes the vesicles to migrate to
the
> 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
part.
> 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
close)
> in response to a signal. The ligand, itself, when directly binding to the
> appropriate receptor will cause/elicit the conformational changes in
channel
> strcuture and allow for the resulting flow of current. An example of
these
> receptors are non-NMDA receptors (like the AMPA) or the NMDA receptor;
and,
> 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
the
> 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
lead
> 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
will
> 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
for
> 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
terminal
> membrane and subsequent release of transmitter. Also metabotropic
receptors
> 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
receptors),
> and often 3rd messengers are considered (e.g. CREB; MAPK) b/c these
signals
> rely from the plasm membrane to the nucleus in order to elicit changes in
> transcription factors and/or gene regulation.
>> NMF
>>>
