The function and nature of inhibition of neurons in the visual cortex have been the focus of both experimental and theoretical investigations. There are two ways in which inhibition can suppress synaptic excitation. In hyperpolarizing inhibition, negative and positive currents sum linearly to produce a net change in membrane potential. In contrast, shunting inhibition acts nonlinearly by causing an increase in membrane conductance; this divides the amplitude of the excitatory response. Visually evoked changes in membrane conductance have been reported to be nonsignificant or weak, supporting the hyperpolarization mode of inhibition. Here we present a new approach to studying inhibition that is based on in vivo whole-cell voltage clamping. This technique allows the continuous measurement of conductance dynamics during visual activation. We show, in neurons of cat primary visual cortex, that the response to optimally orientated flashed bars can increase the somatic input conductance to more than three times that of the resting state. The short latency of the visually evoked peak of conductance, and its apparent reversal potential suggest a dominant contribution from gamma-aminobutyric acid ((GABA)A) receptor-mediated synapses. We propose that nonlinear shunting inhibition may act during the initial stage of visual cortical processing, setting the balance between opponent 'On' and 'Off' responses in different locations of the visual receptive field.

This phenomenon has also been recorded in the mammalian brain in vivo. Hippocampal pyramidal cells in behaving rats fire brief bursts of 2-10 action potentials at frequencies of 100-300 Hz, so-called 'complex spikes', during which the spikes typically become broader towards the end of the burst (Fox & Ranck, 1981). Intracellular recordings from hippocampal pyramidal cells in anaesthetized cats also showed spontaneous and evoked spike bursts with prominent spike broadening (Kandel & Spencer, 1961). Since most of the influx of Ca¥ typically occurs during the late part of each action potential (Llinas et al. 1982), spike broadening is an efficient way of increasing Ca¥ influx, thus modulating intracellular Ca¥ signals and Ca¥-dependent ion channels, enzymes, second messenger cascades, gene transcription, and release of transmitters or hormones (Jackson et al. 1991;Byrne & Kandel, 1996;Sabatini & Regehr, 1997). Previous studies have indicated that spike broadening during repetitive firing in neurones is often due to cumulative inactivation of voltage-gated K¤ channels, including slowly inactivating 'delayed rectifier' K¤ channels (Aldrich et al. 1979) and fast-inactivating K¤ channels (A_channels) (Jackson et al. 1991;Ma & Koester, 1996). Cumulative inactivation during a spike train can cause a progressive decline in the K¤ current that is available for spike repolarization, thus causing spike broadening. This mechanism has been described in a variety of neurones, including molluscan somata (Aldrich et al. 1979;Ma & Koester, 1996), magnocellular hypothalamic neurones (Bourque & Renaud, 1985) and pituitary neurosecretory terminals (Jackson et al. 1991). An enhanced activation of voltage-gated Ca¥ channels late in the train, can also contribute to the spike broadening during repetitive firing in some cases (Aldrich et al. 1979).

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Directional selectivity is a response that is greater for a visual stimulus moving in one (PREF) direction than for the opposite (NULL) direction, and its computation in the vertebrate retina is a classical issue in functional neurophysiology. To date, most quantitative experimental studies have relied on extracellular responses for identifying properties of the directionally selective circuit. Here I describe an intracellular analysis using whole-cell patch recordings of the synaptic events underlying the spike response in directionally selective ganglion cells of the turtle retina. These quantitative measurements allowed me to distinguish among various explicit classes of circuit models that can, in principle, account for ganglion cell directional selectivity. I found that ganglion cell directional selectivity is due to an excitatory input that itself is directionally selective, and that the crucial shunting inhibition implicated in this computation must act on cells presynaptic to the ganglion cell.

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