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LTP and post-tetanic potentiation

Grushnik james.teo at chch.ox.ac.uk
Tue Apr 6 08:32:25 EST 1999


On 6 Apr 1999 02:26:03 GMT, flefever at ix.netcom.com(F. Frank LeFever)
wrote:

>My understanding is that LTP as usually studied IS "post-tetanic"
>potentiation, because the usual procedure has been to use high rates of
>suprathreshold stimulation, driving the neurons--i.e. into tetanus.

That's not what I meant. The tetanus used to induce it is regularly
100Mhz of theta burst firing (Bliss & Lomo 1973, Bliss & Collingridge
1993), but the difference between LTP and PTP is that LTP is probably
not an artefact of the method, as it occurs minutes AFTER the tetanus
and lasts alot longer (hours, days?). PTP on the other hand occurs
immediately after stimulation and only lasts at most a minute.

>More recently, some have adopted a procedure using stimulation
>parameters more like those occurring naturally, called "prime burst
>potentiation" sometimes (or sometimes simply "LTP", but with
>specification that the stimuli are not tetanic).  It has been argued
>that LTP accomplished this way is vulnerable to manipulations of
>conditions that tetanic LTP is not (e.g. altered cortisol levels??),
>and thus more physiologically relevant.

Yes, I heard about those. PTP in this case was not observed, but LTP,
STP and LTD was. I don't understand why LTP in this case would be more
vulnerable to manipulations. If I am correct this prime burst
potentiation is still quite unphysiological.

>I don't know exact details of what Sturla refers to, but this may be
>relevant: NO normally amplifies/perpetuates/spatially distributes
>effects of NMDA activation, including enhanced LTP; but excessive or
>untimely NO will block LTP.  (see, for example, Izumi & Zorumski,
>Neuroreport 1993, 4, 1131-1134; I had the pleasure of discussing this
>with Izumi when he stopped by my poster at Society for Neuroscience,
>1996)

Cool! What was your poster on?

I am uncertain of the full implications of this, but the other
retrograde signal to be considered is arachidonic acid. For a starts,
that inhibits uptake of glutamate into glial cells (and also to an
extent neurones) by acting the Na-Glu pump (Barbour et al 1989,
Volterra et al 1992). Could *this* be the source of the potentiation
detected?

Grushnik
------------------------------------------------------------------
References:
Barbour et al(1989) Nature, vol 342, pages 918-920

Bliss & Collingridge (1993) Nature, vol 361, pages 31-39

Bliss & Lomo (1973) Journal of Neurophysiology, vol 232, pages 331-356

Volterra A et al (1992)  Journal of Neurochemistry, vol 59(2), pages
600-602



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