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J Neurophysiol 85: 699-707, 2001;
0022-3077/01 $5.00
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The Journal of Neurophysiology Vol. 85 No. 2 February 2001, pp. 699-707
Copyright ©2001 by the American Physiological Society

Effect of Adrenalectomy on Membrane Properties and Synaptic Potentials in Rat Dentate Granule Cells

M. Joëls, C. Stienstra, and Y. Karten

Institute for Neurobiology, University of Amsterdam, 1098 SM Amsterdam, The Netherlands

Joëls, M., C. Stienstra, and Y. Karten. Effect of Adrenalectomy on Membrane Properties and Synaptic Potentials in Rat Dentate Granule Cells. J. Neurophysiol. 85: 699-707, 2001. Adrenalectomy is known to accelerate both neurogenesis and cell death of granule cells located in the suprapyramidal blade of the rat dentate gyrus. Three days after adrenalectomy, some granule cells have already died by apoptosis while newly formed cells are not yet incorporated in the cell layer, resulting in a temporary loss of granule cells. Concomitantly, the field response to stimulation of perforant path afferents is reduced. While the temporary cell loss is likely to attenuate synaptic field responses, adrenalectomy-induced changes in properties of the surviving cells may also contribute to the reduction in field response amplitude. To address this possibility, we here investigated the membrane properties and synaptic responses of dentate granule cells, 3 days after adrenalectomy. We found that passive and most of the active membrane properties of granule cells in adrenalectomized rats were not significantly different from the cell properties in sham-operated controls. However, intracellularly recorded synaptic responses from surviving granule cells were markedly reduced after adrenalectomy. The N-methyl-D-aspartate (NMDA)- and the non-NMDA receptor-mediated components were reduced to a similar extent, suggesting that the attenuation of synaptic transmission after adrenalectomy could be partly of presynaptic origin. The data indicate that the earlier observed attenuation of synaptic field responses after adrenalectomy may be partly due to a diminished glutamatergic input to the dentate gyrus and not exclusively to a loss of granule cells participating in the synaptic circuit.






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