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Role of GABAA-mediated inhibition in controlling the responses of regular spiking cells in turtle visual cortex

Published online by Cambridge University Press:  10 April 2001

JAIME G. MANCILLA
Affiliation:
Committee on Neurobiology and Department of Organismal Biology and Anatomy, University of Chicago, Chicago
PHILIP S. ULINSKI
Affiliation:
Committee on Neurobiology and Department of Organismal Biology and Anatomy, University of Chicago, Chicago

Abstract

The visual cortex of freshwater turtles contains pyramidal cells, which have a regular spiking (RS) firing pattern, and several categories of aspiny, inhibitory interneurons. The interneurons show diverse firing patterns, including the fast spiking (FS) pattern. Postsynaptic potentials (PSPs) evoked in FS cells by visual stimulation of the retina reach their peak amplitudes as much as 200 ms before PSPs in RS cells (Mancilla et al., 1998). FS cells could, consequently, control the amplitudes of light-evoked PSPs in RS cells by producing disynaptic, feedforward inhibitory postsynaptic potentials (IPSPs) that overlap in time with geniculocortical excitatory postsynaptic potentials (EPSPs). Since FS cells receive recurrent, excitatory inputs from RS cells, they could also control the amplitudes of light-evoked PSPs in RS cells via polysynaptic, feedback inhibition. The in vitro geniculocortical preparation of Pseudemys scripta was used to characterize the temporal relationships of EPSPs and IPSPs produced in RS cells by electrical activation of geniculate afferents and by diffuse light flashes presented to the retina. GABAA receptor-mediated inhibition was blocked using extracellular application of bicuculline (3.5 mM) or intracellular perfusion of picrotoxin (1 μM) in individual RS cells. Electrical stimulation of thalamic afferents produced compound PSPs. Blockade of GABAA receptor-mediated IPSPs with either bicuculline or picrotoxin provided evidence for both early and late IPSPs in RS cells. Analysis of the apparent reversal potentials of light-evoked PSPs indicated the existence of early IPSPs during the first 140–300 ms following light onset. Light responses of cells perfused with picrotoxin diverged from control light responses at about 300 ms after light onset and had maximum amplitudes that were significantly different from control light responses. These experiments indicate that the responses of RS cells to both electrical and natural stimulation of geniculate afferents are controlled by both early and late IPSPs, consistent with activation of both feedforward and feedback pathways.

Type
Research Article
Copyright
2001 Cambridge University Press

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