X-Message-Number: 26366
From: "Basie" <>
Subject: GABAA action 
Date: Tue, 21 Jun 2005 21:10:59 -0400

I came across this interesting presentation.

Start of quote:

Oral 2. Use-dependent shift from inhibitory to excitatory GABAA action in 
interneurons induces beta-gamma oscillations in the hippocampus
K.L ms  and T.Taira

Department of Biosciences, and Institute of Biotechnology, University of 
Helsinki, FIN-00014.

Background: Glutamatergic excitation has a critical role in the generation 
and maintenance of fast network oscillations in the hippocampus. In addition 
to glutamatergic input, excitatory drive to hippocampal neurons can also be 
provided by synaptic activation of GABAA receptors (GABAARs). However, the 
physiological relevance and the generation mechanisms of this "paradoxical" 
GABAA action in different cell types are largely unknown.

Results: We now show that in the absence of glutamatergic transmission a 
fast switch from inhibitory to excitatory GABAA action induces bursts of 
synchronous beta (15-30 Hz) and low gamma frequency (30-40 Hz) oscillations 
in the CA3 interneuronal network. The GABAAR-mediated postsynaptic 
potentials (PSPs) in the interneurons were typically hyperpolarizing, but by 
an increase in the GABAAR-mediated conductance the PSPs became depolarizing 
and excitatory. During mutual excitation of interneurons, GABAAR-mediated 
currents displayed beta-gamma oscillations. A shift of GABAAR-mediated PSPs 
to depolarizing by the GABAAR permeant weak acid anion formate (20-30 mM) or 
by up-modulation of the GABAA conductance with pentobarbital (100  M) 
provoked interneuronal population bursting. The synchronous beta-gamma 
rhytmicity, however, was dependent on electrotonic coupling, since it was 
abolished by gap-junction blockers, although the population discharges were 
preserved.

Conclusions: We conclude that the use-dependent switch from inhibitory to 
excitatory GABAA action provides a mechanism for the generation of 
synchronous b-g bursts in the interneuron network. Further, it provides an 
alternative mechanism for short-term plasticity in excitatory synapses in 
interneurons.

End of quote.

Basie

http://www.agingtheory.com/pages/1/index.htm

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