Meeting details menu

Meeting Authors
Meeting Abstracts
Keynote lectures
Oral communications
Poster presentations
Special symposia
Other

Acta Physiologica Congress

Back

Acta Physiologica 2006; Volume 186, Supplement 650
Joint Meeting of The German Society of Physiology and The Federation of European Physiological Societies 2006
3/26/2006-3/29/2006
Ludwig-Maximilians-University, Munich


INVOLVEMENT OF GABAA-MEDIATED TRANSMISSION IN STIMULUS-INDUCED SHARP WAVE-RIPPLE COMPLEXES IN HIPPOCAMPAL AREA CA3 IN VITRO
Abstract number: PM01A-9

Behrens1 CJ, van den Boom1 LP, Richter1 JP, Heinemann1 U

1Institute for Neurophysiology, Charit-Universittsmedizin Berlin

Generation of sharp wave-ripple complexes (SPW-R) within hippocampal area CA3 was induced by repeated stimulation of orthodromic as well as antidromic pathways of adult rat hippocampal brain slices. SPW-R originated in CA3 and propagated throughout the hippocampus. Intracellular recordings showed that their induction involves time-dependent changes in interactions between clusters of neurons in the CA3 associational network. In about 50 percent of recorded CA3 pyramidal cells synaptic input during SPW-R caused an EPSP generation followed by 1–4 action potentials whereas the remaining cells responded with a compound IPSP. Blocking GABAA-mediated inhibition during SPW-R activity led to a gradual transition of SPW-R into prolonged hypersynchronous bursts within area CA3. In comparison to stimulus-induced SPW-R the SR-95531-mediated bursts showed a significantly higher amplitude, duration and frequency content as well as >10-fold higher increases in [K+]o. Intracellular recordings of all recorded cells during GABAA receptor blockade showed that the bursts were characterized by a large, prolonged depolarization envelop giving rise to 20–40 action potentials. Applying the the gap junction blocker mefloquine during hypersynchronous network activity largely reduced fast ripple oscillations (~300 Hz) without blocking recurrent bursts.

To cite this abstract, please use the following information:
Acta Physiologica 2006; Volume 186, Supplement 650 :PM01A-9

Our site uses cookies to improve your experience.You can find out more about our use of cookies in our standard cookie policy, including instructions on how to reject and delete cookies if you wish to do so.

By continuing to browse this site you agree to us using cookies as described in our standard cookie policy .

CLOSE