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Two different responses of hippocampal pyramidal cells to application of gamma-amino butyric acid.

TLDR
The results support the idea that the hyperpolarizing basket cell inhibition at the soma is mediated by the release of GABA, and propose the term discriminative inhibition for this postulated new type of control of pyramidal cell discharges.
Abstract
1. Extra- and intracellular recordings were made from CA1 cells in hippocampal slices in vitro. The effects of ionophoretically applied GABA on somatic and dendritic regions were studied. 2. Ionophoresis of GABA at dendritic sites gave a reciprocal effect by inhibiting the effect of excitatory synapses close to the dendritic application, while facilitating those lying further away. For example, GABA delivered to the mid-radiatum dendritic region reduced the population spike generated by a radiatum volley, while facilitating the population spike evoked by oriens fibre stimulation. Similarly, when single cells were recorded from, mid-apical dendritic delivery of GABA abolished the synaptically driven discharges evoked by fibres terminating at this part of the dendritic tree, but facilitated the responses to input from fibres terminating on the basal dendrites of the same cell. 3. With intracellular recording two effects were observed. Applied near the soma, GABA induced a hyperpolarization associated with an increased membrane conductance. When applied to dendrites, GABA caused a depolarization also associated with an increased membrane conductance. Both types of GABA applications could inhibit cell discharges, although in some cases the depolarizing response could facilitate other excitatory influences or cause cell firing by itself. 4. Both the hyperpolarizing and depolarizing GABA responses persisted after blockade of synaptic transmission by applying a low calcium high magnesium solution, indicating mediation via a direct effect upon the cell membrane. 5. The reversal potential for the hyperpolarizing GABA effect was similar to the equilibrium potential for the i.p.s.p. evoked from alveus or orthodromically, and was 10-12 mV more negative than the resting potential. The size of the depolarizing response was also dependent upon the membrane potential. By extrapolation an estimated equilibrium potential was calculated as about -40 mV. 6. Our results support the idea that the hyperpolarizing basket cell inhibition at the soma is mediated by the release of GABA. This hyperpolarizing response causes a general inhibition of firing. The dendritic effects of GABA, however, seem to represent another type of inhibition, which by shunting synaptic currents makes possible a selective inhibitory influence on afferents synapsing locally while facilitating more remotely placed excitatory synapses. We propose the term discriminative inhibition for this postulated new type of control of pyramidal cell discharges.

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Citations
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Journal ArticleDOI

Synaptic mechanisms of synchronized gamma oscillations in inhibitory interneuron networks

TL;DR: Experimental analysis in the hippocampus and the neocortex and computational analysis suggests that synaptic specialization turns interneuron networks into robust gamma frequency oscillators.
Journal ArticleDOI

Cellular bases of hippocampal EEG in the behaving rat.

TL;DR: Movement-related RSA was correlated with a decrease in firing rate of pyramidal cells and an increase in the firing of both interneurons and granule cells, and Gradual phase-shifts of RSA were observed both in CA1 and the dentate gyrus.
Journal ArticleDOI

Giant synaptic potentials in immature rat CA3 hippocampal neurones.

TL;DR: In neurones in which evoked GDPs were blocked by bicuculline, a NMDA‐mediated component was revealed by increasing the strength or the frequency of stimulation, and during the second week of postnatal life, superfusion with bicuciulline induced, as in adult slices, interictal discharges.
Journal ArticleDOI

GABA: A Pioneer Transmitter That Excites Immature Neurons and Generates Primitive Oscillations

TL;DR: It is suggested that an evolutionary preserved role for excitatory GABA in immature cells provides an important mechanism in the formation of synapses and activity in neuronal networks.
References
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Journal ArticleDOI

Immunocytochemical localization of glutamic acid decarboxylase in neuronal somata following colchicine inhibition of axonal transport

TL;DR: A reasonable explanation for the failure of earlier immunocytological studies to detect somal GAD in certain GABAergic neurons is that the axonal transport of GAD appears to occur at a sufficiently rapid rate to limit the somal concentration of G AD to low, undetectable levels.
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Antagonism between bicuculline and GABA in the cat brain.

TL;DR: The relatively high degree of specificity of bicuculline as a GABA antagonist indicates that this alkaloid is of considerable value in determining whether or not a particular inhibitory pathway could operate by releasing GABA as an inhibitory transmitter.
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Characterization and ionic basis of GABA-induced depolarizations recorded in vitro from cat primary afferent neurones.

TL;DR: Of the twelve structurally related compounds investigated, GABA was the most effective in its ability to produce a depolarization of the cell membrane.
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Micro-electrophoretic studies of neurones in the cat hippocampus.

TL;DR: Drugs have been applied micro‐electrophoretically to units in the hippocampal cortex of the anaesthetized cat, and their effects on cell firing were recorded simultaneously.
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