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LTP and post-tetanic potentiation

F. Frank LeFever flefever at ix.netcom.com
Tue Apr 6 21:28:31 EST 1999


re question near the bottom: poster was a rather speculative attempt to
account for phenomena of "mental fatigue" and "lapses" after mild head
trauma (postconcussion syndrome). 

 Building on a previous attempt to account for chronic symptoms after
mild head injury in terms of neuroimmune processes (IL-1 and brain mast
cells among the players), this focused on accelerated deterioration of
performance with sustained mental effort, increased variability of
performance, and with complaints of memory problems often out of
proportion to memory deficits on formal test (I infer episodic lapses).

I cited two possibilities for upregulated NO production: influence of
IL-1 on mast cells, and greater survival of NOS containing neurons
relative to others after trauma (or other brain insults).

re mast cells: they are especially concentrated in the thalamus, a good
site for interruption of various activites, including attention.

I argued that in contrast to massive, tonic NO overproduction (as in
sepsis,  or as has been suggested for cerebral malaria), the phenomena
I was considering might better fit a model in which phasic but (very
short-term) cumulative overproduction might interrupt NMDA--->LTP
activity.

Izumi was a bit taken aback by my unusual format (boxes and arrows,
rather than coolumns, paragraphs, etc.) but after I talked him through
it and he reflected on it a while, I was immensely relieved to hear him
say that I had a good argument.

I had not (and still have not very well) considered the possible role
of glial proliferation and increased glutamate uptake...

F. Frank LeFever, Ph.D.
New York Neuropsychology Group






In <370a08ca.3760457 at news.ox.ac.uk> james.teo at chch.ox.ac.uk (Grushnik)
writes: 
>
>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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