The Role of GABA in Inhibitory Synaptic Inputs on Inhibitory Burst Neurons in the Cat
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The electrical responses of 25 cells suggested to be hippocampal inhibitory interneurons to stimulation of two afferent fibre systems originated in contralateral hippocampus were investigated in nonanesthetized curarized rabbits. It is stated that the neurons under study have not only high-effective excitatory input but also a weak inhibitory one. The background and evoked activities of the neurons were under predominating influence of the excitatory input which plays a determining role in their behaviour.
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The effect of isoflurane on inhibitory postsynaptic potentials (IPSPs) was studied in rat hippocampal slices by intracellular recordings from pyramidal neurons (n = 34). The amplitude of the IPSP was transiently increased and subsequently reduced in a dose-dependent manner. The duration of the IPSP was increased. The reduction in the IPSP persisted after correction was made for the anesthetic-induced hyperpolarization. The reversal potential for the IPSP was slightly displaced in the depolarizing direction. The depolarizing γ-aminobutyric acid (GABA) response was unaltered, while the hyperpolarizing GABA response was reduced, suggesting a postsynaptic action. The reduction in the IPSP produced by isoflurane is at least partly due to an altered reversal potential for the IPSP (EIPSP).
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Neocortex
Electrical Synapses
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In computational neural network models, neurons are usually allowed to excite some and inhibit other neurons, depending on the weight of their synaptic connections. The traditional way to transform such networks into networks that obey Dale's law (i.e., a neuron can either excite or inhibit) is to accompany each excitatory neuron with an inhibitory one through which inhibitory signals are mediated. However, this requires an equal number of excitatory and inhibitory neurons, whereas a realistic number of inhibitory neurons is much smaller. In this letter, we propose a model of nonlinear interaction of inhibitory synapses on dendritic compartments of excitatory neurons that allows the excitatory neurons to mediate inhibitory signals through a subset of the inhibitory population. With this construction, the number of required inhibitory neurons can be reduced tremendously.
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1. Since the inhibitory effect of direct or indirect cortical stimulation on cortical units can be overcome by excitation with even more L ‐glutamate, it is not likely to be due to an excessive depolarization. 2. Further evidence that surface stimulation has a hyperpolarizing action on cortical cells was obtained by intracellular recording from over 120 pericruciate cells. Inhibitory post‐synaptic potentials (IPSPs) are seen in most cells, which are comparable in threshold and duration with the inhibitory effect observed extracellularly. The IPSPs are usually not preceded by a discharge of the same cells. 3. The extracellular slow wave corresponding to the inhibitory effect varies considerably with different preparations and different depths within the cortex. A predominantly positive wave is only seen occasionally. In general, the relevant wave recorded deep in the cortex tends to be mainly negative. 4. This negative slow wave can be much potentiated by tetanic stimulation, or, especially, by a large local release of L ‐glutamate; the last procedure is most effective either very near the surface, or below a depth of 1·0 mm. These observations suggest that inhibitory synapses occur more profusely in the superficial half of the grey matter. 5. Unlike L ‐glutamate, GABA tends to depress the ‘inhibitory’ slow wave. 6. The inhibitory effect must be produced by intracortical neurones, since it is fully preserved in isolated cortical slabs. In both acute and chronic slabs, the inhibition is particularly well marked and long lasting, partly because spontaneous activity and the usual post‐inhibitory rebound of excitability are absent. 7. The intracortical pathways responsible for the spread of inhibition cannot be situated mainly in the superficial layers, as they are not readily blocked by surface cooling or the application of local anaesthetics. 8. One can record unit discharges immediately after a surface shock. Some of these discharges could be from inhibitory interneurones, but they do not last more than 10‐20 msec. 9. We conclude from the observations described in this and a previous paper (Krnjević, Randić & Straughan, 1966 a ) that a widespread system of intracortical interneurones can be activated by direct or indirect stimulation of the cortex; these interneurones have a powerful and prolonged inhibitory action on most cortical cells. 10. The identity and distribution of the postulated inhibitory interneurones is discussed in the light of some relevant morphological evidence.
Tetanic stimulation
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In neural networks, both excitatory and inhibitory cells play important roles in determining the functions of systems. Various dynamical networks have been proposed as artificial neural networks to study the properties of biological systems where the influences of excitatory nodes have been extensively investigated while those of inhibitory nodes have been studied much less. In this paper, we consider a model of oscillatory networks of excitable Boolean maps consisting of both excitatory and inhibitory nodes, focusing on the roles of inhibitory nodes. We find that inhibitory nodes in sparse networks (small average connection degree) play decisive roles in weakening oscillations, and oscillation death occurs after continual weakening of oscillation for sufficiently high inhibitory node density. In the sharp contrast, increasing inhibitory nodes in dense networks may result in the increase of oscillation amplitude and sudden oscillation death at much lower inhibitory node density and the nearly highest excitation activities. Mechanism under these peculiar behaviors of dense networks is explained by the competition of the duplex effects of inhibitory nodes.
Oscillation (cell signaling)
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The most typical and well known inhibitory action in the cortical microcircuit is a strong inhibition on the target neuron by axo-somatic synapses. However, it has become clear that synaptic inhibition in the cortex is much more diverse and complicated. Firstly, at least ten or more inhibitory non-pyramidal cell subtypes engage in diverse inhibitory functions to produce the elaborate activity characteristic of the different cortical states. Each distinct non-pyramidal cell subtype has its own independent inhibitory function. Secondly, the inhibitory synapses innervate different neuronal domains, such as axons, spines, dendrites and soma, and their IPSP size is not uniform. Thus cortical inhibition is highly complex, with a wide variety of anatomical and physiological modes. Moreover, the functional significance of the various inhibitory synapse innervation styles and their unique structural dynamic behaviors differ from those of excitatory synapses. In this review, we summarize our current understanding of the inhibitory mechanisms of the cortical microcircuit.
Pyramidal cell
Dendritic spike
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