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J Neurophysiol 90: 2106-2114, 2003. First published April 23, 2003; doi:10.1152/jn.00894.2002
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Modulation of Rat Corticohippocampal Synaptic Activity by High Pressure and Extracellular Calcium: Single and Frequency Responses

Adolfo E. Talpalar and Yoram Grossman

Department of Physiology, Faculty of Health Sciences and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel

Submitted 7 October 2002; accepted in final form 15 April 2003

High pressure (>1.5 MPa) induces a series of disturbances of the nervous system that are generically termed high-pressure nervous syndrome (HPNS). HPNS is characterized by motor and cognitive impairments. The neocortex and the hippocampus are presumably involved in this last disorder. The medial perforant path (MPP) synapse onto the granule cells of the dentate gyrus is the main connection between these structures. We have studied high-pressure (HP) effects on single and frequency response of this synapse. Since effects of HP on various synapses were mimicked by reducing [Ca2+]o, results under these conditions were compared. Medial perforant path-evoked field excitatory postsynaptic potentials (fEPSPs) were recorded from granule cells in rat brain slices. Slices were exposed to high pressure of helium (0.1–10.1 MPa) at 30°C. HP depressed single fEPSPs by 35 and 55% at 5.1 and 10.1 MPa, respectively, and increased paired-pulse facilitation (PPF) at 10- to 40-ms inter-stimulus intervals. Frequency-dependent depression (FDD) was enhanced by HP during trains of stimuli at 50 but not at 25 Hz. Depression of single fEPSPs by reduction of [Ca2+]o from 2 mM control to 1 mM at normal pressure was equivalent to the effect of 10.1 MPa at control [Ca2+]o. However, this low [Ca2+]o induced greater enhancement of PPF, and in contrast, turned FDD at 25–50 Hz into frequency-dependent potentiation. These results suggest that HP depresses single synaptic release by reducing Ca2+ entry, whereas slowing of synaptic frequency response is independent of Ca2+. These findings increase our understanding of HPNS experienced by deep divers.


Address for reprint requests and other correspondence: Y. Grossman, Dept. of Physiology, Faculty of Health Sciences, Ben-Gurion Univ. of the Negev, Beer-Sheva 84105, Israel (E-mail: ramig{at}bgumail.bgu.ac.il).




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A. E. Talpalar and Y. Grossman
Enhanced Excitability Compensates for High-Pressure-Induced Depression of Cortical Inputs to the Hippocampus
J Neurophysiol, December 1, 2004; 92(6): 3309 - 3319.
[Abstract] [Full Text] [PDF]




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