Direction-selective responses of units in the dorsal terminal nucleus of cat following intravitreal injections of bicuculline (original) (raw)
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Brain Research, 1990
Retinal application of ),-aminobutyric acid (GABA) antagonists block direction-sensitive (DS) responses in turtle in two ways: (1) the selectivity of DS retinal ganglion cells in vitro, and (2) the eye's ability to track the direction of full field image motion. The experiments described below demonstrate that an important locus for retinal slip computation by the accessory optic system (AOS) occurs in the retina. Visual responses were measured physiologically and behaviorally from turtles which had their telencephalon removed. Physiological responses to visual field movement were recorded in the AOS using an in vitro brain preparation. DS responses of single cells were blocked by intravitreal application of bicuculline. The behavioral approach was to measure optokinetic nystagmus (OKN) in lesioned animals. OKN occurred in the absence of the telencephalon, yet was disrupted following an intravitreai injection of bicucuUine. Thus, both experimental approaches showed that DS processing exists without the telencephalon, yet is disrupted by GABA antagonists applied to the retina.
Brain Research, 1984
Rearing cats with surgically induced strabismus resulted in an abnormally high percentage (80%) of monocularly driven neurons in visual cortex. Microiontophoretic application of the GABA antagonist bicuculline restored binocular responses to over 50% of these monocular cells. Elevation of spontaneous rate by glutamate failed to produce binocularity. These results indicate that intracortical inhibition plays a role in the abnormal ocular dominance distribution of strabismic cats.
European Journal of Neuroscience, 1994
The contribution of GABA-mediated inhibition to the generation of directional selectivity of neurons in the nucleus of the optic tract (NOT) and the dorsal terminal nucleus of the accessory optic system (DTN) was examined in anaesthetized rats by iontophoretic application of the GABAA receptor antagonist bicuculline methiodide. Spontaneous and visually evoked NOT-DTN cell activities were always increased by bicuculline application. The directional selectivity of NOT-DTN cells to slowly moving whole-field stimuli, expressed as the direction index, was reduced for most neurons. However, the difference between firing rates during stimulus movements in the preferred and in the non-preferred direction did not change systematically. On average, this difference was not significantly affected in the majority of the neurons, although bicuculline more strongly increased the activity during movement in the preferred or non-preferred direction in some of the neurons. These results indicate that directionally selective neurons in the rat NOT-DTN receive GABAergic inhibition which is most likely tonic and independent of the stimulus direction.
Comparative pharmacological effects on visual cortical neurons in monocularly deprived cats
Brain Research, 1985
Monocularly deprived (MD) cats show a loss of responsiveness to visual stimulation of the deprived eye among visual cortical neurons. Several lines of evidence suggest that this effect involves, at least in part, a suppression of deprived eye input, possibly mediated by GABA inhibition. In order to better understand the nature of this suppression we have evaluated the effectiveness of different types of disinhibitory and excitatory agents to reverse the effects of MD. We investigated bicuculline (a GABA antagonist); picrotoxin (a GABA antagonist with a different mechanism of action from bicuculline); strychnine (a glycine antagonist); ammonium ion (a blocker of membrane chloride channels); physostigmine (a cholinesterase inhibitor); and naloxone (an opiate antagonist and also a GABA antagonist). All drugs were given intravenously. Bicuculline restored binocularity to 50% of the visual cortical neurons tested and naloxone to 36%. With both drugs, receptive fields of the normal eye tended to lose specificity. The emergent deprived eye receptive fields were usually similar to those of the normal eye after drug administration. Ammonium ion produced binocular responses in 27% of neurons tested, but receptive fields were grossly abnormal; moreover, ammonium infusion tended to depress neuronal responsiveness. All other drugs tested failed to restore binocularity. These experiments lend further credence to the hypothesis that GABA inhibition contributes to the cortical effects of MD, since only drugs with GABA antagonistic action were effective in restoring neuronal responsiveness to the deprived eye. ness to the deprived eye can be restored by the GABA antagonist bicuculline, administered either
Action and localization of gamma-aminobutyric acid in the cat retina
The Journal of Physiology, 1985
1. The effects of iontophoretically applied GABA (y-aminobutyric acid) and bicuculline on retinal ganglion cells were studied in the optically intact eye of the anaesthetized cat. 2. GABA suppressed both the spontaneous activity and light-evoked discharge of all retinal ganglion cells, regardless of their type and regardless of the visual stimulus used. 3. Bicuculline antagonized the action of iontophoretically applied GABA. Bicuculline enhanced the spontaneous activity of on-centre cells, but suppressed the spontaneous activity of most off-centre cells. The light-evoked response of on-centre cells was increased by bicuculline. A more complicated picture emerged for off-centre cells. Weak light responses were suppressed by bicuculline, but during strong light responses the initial transient phase of the response was dramatically enhanced. 4. Amacrine cells of the inner nuclear layer and displaced amacrine cells of the ganglion cell layer were labelled, using glutamic acid decarboxylase (GAD) immunohistochemistry and [3H]muscimol uptake. GAD-positive dendrites were found throughout the inner plexiform layer and no sign of dendritic stratification was detected.
Brain Research, 1983
Key words: X and Y cells --dorsolateral geniculate nucleus --centre surround antagonism --GABA --inhibitory processes Visually elicited inhibitory processes, underlying the receptive field structure of cells in layers A and A 1 of the cat dorsal lateral geniculate nucleus (dLGN), have been examined by a combination of visual neurophysiological and iontophoretic techniques. Discrete visual stimulation of both centre and surround mechanisms, produced a powerful suppression of the elevated background discharge levels induced by iontophoretic application of an excitatory amino acid. These observations are consistent with the activation of a postsynaptic inhibitory input, a view supported by the fact that the suppressive effects were blocked by iontophoretic application of bicuculline, an antagonist of GABA, a putative inhibitory transmitter in the dLGN. These inhibitory effects were always elicited by the opposite phase of a flashed stimulus to that eliciting responses associated with the receptive field region. That is 'on' inhibitory effects were elicited from 'off' excitatory regions and 'off' inhibitory effects from 'on' excitatory regions.
Vision Research, 1973
A~C~KD~NG to the superposition model of k3DrECK and STONE (1965) and Griisser (WUTTKE and G~i_kx~, 1966) the output of the retinal ganglion cell in the cat is controlled by two spatially overla~~in g mechanisms~ fin Rodieck's terms) a "center mecba~ismi' and a "surround mechanism". For an on-center, off-surround cetf the center mechanism would cause excitation during the period when the light is on and inhibition after the stimulus is terminated. The surround mechanism would cause inhibition when the light is on and excitation after stirnu~~s termination. The Gaussian curves, which are used to describe both mechanisms, have their maximum strength in the center of the receptive field. The Gaussian fur the center mechanism has a higher mean and lower standard deviation than the Gaussian for the surround mechanism. According to RODIECK and STONE (1965) the surround mechanism has a latency which is about 50 msec longer than the Iatency of the center mechanism.