ELECTROPHYSIOLOGICAL PROPERTIES OF RAT HIPPOCAMPAL PRINCIPAL CELLS ARE UNALTERED BY PRENATAL PROTEIN-MALNUTRITION

Citation
J. Rushmore et al., ELECTROPHYSIOLOGICAL PROPERTIES OF RAT HIPPOCAMPAL PRINCIPAL CELLS ARE UNALTERED BY PRENATAL PROTEIN-MALNUTRITION, Hippocampus (New York, N.Y.), 8(4), 1998, pp. 380-389
Citations number
14
Categorie Soggetti
Neurosciences
ISSN journal
10509631
Volume
8
Issue
4
Year of publication
1998
Pages
380 - 389
Database
ISI
SICI code
1050-9631(1998)8:4<380:EPORHP>2.0.ZU;2-E
Abstract
There is growing evidence that prenatal protein malnutrition alters th e development of the hippocampal formation in rats (Morgane et al., 19 93; Galler et al., 1996; Almeida et al., 1996, for reviews). Little is known, however, of the possible functional consequences of prenatal m alnutrition on the physiology of principal cells in the hippocampus. W e have addressed this issue by comparing the electrophysiological prop erties of hippocampal neurons (dentate granule cells and CA1 pyramidal cells) in slices prepared from control and from prenatally protein ma lnourished adult male and female Sprague-Dawley rats. We found no sign ificant effect of the prenatal protein malnutrition insult upon a numb er of intrinsic membrane properties measured with whole-cell current c lamp recordings, including: resting membrane potential, input resistan ce, and membrane time constant, or on action potential characteristics such as threshold, amplitude, and/or firing frequency. Additionally, we saw no effect of prenatal malnutrition upon extracellular measures of glutamatergic synaptic transmission such as the presynaptic fiber v olley, excitatory postsynaptic potential or population spike amplitude at the perforant path to dentate granule cell synapse or at the Schaf fer collateral to CA1 pyramidal cell synapse. In conclusion, we have d emonstrated that prenatal protein malnutrition does not result in sign ificant alterations of the cellular physiological properties of these two types of principal neurons in the adult rat hippocampus. Hippocamp us 1998;8:380-389. (C) 1998 Wiley-Liss, Inc.