IUBio

minature inhibitor postsynaptic currents

Matt Jones jonesmat at physiology.wisc.edu
Tue Sep 21 12:53:37 EST 2004


r norman <rsn_ at _comcast.net> wrote in message news:<3gikk0tgq5t0cmhssqpl25du52a7pf01q2 at 4ax.com>...
> On Fri, 17 Sep 2004 01:38:13 GMT, BilZ0r
> <BilZ0r at TAKETHISOUThotmail.com> wrote:
> 
> >r norman <rsn_ at _comcast.net> wrote in 
> >news:44bkk0dri5sa7othkk641e3eldm1md6b8l at 4ax.com:
> >
> >>>Oh... I thought spontaneous potentials were the result of sponateous 
> >>>firing of a neuron, as against evoked firing.
> >> 
> >> No, it is the spontaneous release of a vesicle, as against release
> >> evoked by presynaptic depolarization and consequent Ca++ events.
> >
> >Then what do you call potentials induced by spontaneously firing neurons?
> 
> Action potentials?
> 
> The issue here is synaptic events.  Once an action potential is
> triggered and travels down the axon, the presynaptic terminal can't
> tell whether the AP was "evoked" by some other cell's synaptic input
> or an experimenter's stimulus or whether it was "spontaneous".  So if
> you are talking about post-synaptic events, which you are when you
> talk of psp's or psc's, that distinction doesn't matter.
> 
> If you are recording action potentials in axons, then you might be
> interested in the difference between spontaneous and evoked
> potentials.  But when you use the term "spontaneous potential" you
> must carefully provide an antecedent to indicate just what kind of
> potential you mean. Spontaneous minis always means vesicle release not
> evoked by a presynaptic action potential.
> 
> You have to be careful, here.  Many cells function quite nicely
> without action potentials at all.  Graded potentials in the
> presynaptic terminal modulate transmitter release.  In those cells,
> the notion of "spontaneous" release is somewhat questionable.  The
> frequency of these release events depends upon, and therefore is in a
> sense evoked by, changes in potential.


Hi guys,

If I may, please let me chime in with some currently accepted
nomenclature.

Although Richard is correct that Katz originally referred to
"spontaneous miniature potentials", the words "spontaneous" and
"miniature" have taken on different shades of meaning now.

Just as he said, "miniature" always refers to the (presumed) release
of a single vesicle, and its postsynaptic response. This does happen
spontaneously. However, one can also evoke miniature (single vesicle)
events by a variety of means. For example, one can lower calcium so
much that the spike-dependent release probablity becomes extremely
low. In this case action potentials almost always result in complete
failure, but when they don't, only one vesicle will probably ever be
released at a time. Thus this would be evoked release, but still
produce miniature (single vesicle) responses. Fatt & Katz,  Boyd &
Martin, and Isaacson & Walmsley have all used this "evoked miniature"
technique to study quantal release mechanisms. Alternatively, one can
apply hyperosmotic solutions or certain toxins (alpha-latrotoxin ofr
example - see Auger & Marty) that cause the dribbling out of single
vesicles. Again, these are miniatures, but they're also evoked. In
general, the main experimental requirement for getting miniatures is
that you have TTX present in the bath to block multivesicular release
driven by spikes. The exception is the low-Ca evoked mini experiment
described above.

Nowadays, the term "spontaneous" is most often used to talk about just
plain old spontaneous events that can either be miniatures, or driven
by spontaneous spiking. If you just sit in a slice and watch events go
by, many of them are spike-driven, and many are minis. Thus, if
recording without TTX or any other special means of isolating
spike-driven from miniature events, one usually calls these
"spontaneous". If you make an amplitude histogram of "spontaneous"
events, you often see two peaks, one corresponding to the minis and
one corresponding to the spike-driven ones.

Miniature events generally have their frequency but not amplitude
altered by things that affect presynaptic release (including
extracellular calcium in some cases, because some single vesicle
events may be triggered by non-spike driven calcium fluctuations in
the bouton), and have their amplitude but not frequency altered by
things that affect the postsynaptic receptors.

The miniature amplitude and shape distributions show a lot of
variability. Empirically, they are very rarely gaussian (people argue
about why this is the case - a lot of people think it's because of
spatial variation and therefore differential filtering of minis coming
from different locations), and often have a pretty wide spread. This
spread is part of what makes classical quantal analysis so damn
difficult except at special synapses like the neuromuscular junction
or calyceal synapses in the auditory system, where spatial problems
are less severe.

Cheers,

Matt



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