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Neuron function question

NMF neil.fournier at sympatico.ca
Fri Oct 24 16:51:26 EST 2003

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

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.


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