The dendritic response to GABA in CA1 of the hippocampal slice

Djørup, Allan; Jahnsen, Henrik; Laursen, Arne Mosfeldt

doi:10.1016/0006-8993(81)90282-1

Cited by 68 publications

(11 citation statements)

References 13 publications

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“…Similar differences in the responses to dendritic and somatic GABA application have been demonstrated in CA3 pyramidal cells (Lebeda, Hablitz & Johnston, 1982) and in cultured mouse spinal neurones (Barker & Ransom, 1978). There have been several attempts to clarify the mechanisms by which these different responses are produced in the hippocampus (Alger & Nicoll, 1982; Dj0rup, Jahnsen & Laursen, 1983), but these remain inconclusive. Brown & Scholfield (1979), found that bath-applied GABA produced a response in olfactory pyriform cells that reversed between -50 and -60 mV.…”

Section: Discussionmentioning

confidence: 71%

Actions and Interactions of Gaba and Benzodiazepines in the Mouse Hippocampal Slice

Biscoe¹,

Duchen²

1985

Exp Physiol

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SUMMARYIntracellular recordings have been made from CAl, CA3 and dentate cells of the mouse hippocampal slice. y-aminobutyric acid (GABA) and the water-soluble benzodiazepines, midazolam and flurazepam were applied close to the impaled cell somata by microelectrophoresis. GABA always caused a fall in input resistance, although the associated changes in membrane potential were variable. These were consistent with reports which have defined a hyperpolarizing response to somatic and a depolarizing response to dendritic application of GABA to CAl and CA3 cells in the rat and guinea-pig. In this study, the phenomenon was seen in CAl, CA3 and dentate cells. The reversal potential for the hyperpolarizing, somatic response to GABA lay between -70 and -75 mV, similar to the reversal potential ofthe evoked recurrent inhibitory post-synaptic potential (i.p.s.p.). The change in cell input conductance caused by GABA was larger at membrane potentials positive to the resting potential and smaller at hyperpolarized membrane potentials. Extracellular recordings of action potential frequency were made from ten cells in which the application of either midazolam or flurazepam increased the inhibitory potency of GABA. In three of these cells, the benzodiazepine reduced action potential frequency slightly when applied alone. Neither midazolam nor flurazepam had a consistent effect on membrane potential, resting input resistance or the current-voltage (I-V) relations of the cells when ejected alone. In twenty-eight of forty-one cells examined in detail, ejection of either midazolam or flurazepam was found to increase the response to GABA. In six cells, the response to GABA was significantly reduced by the benzodiazepine tested whilst in the remainder, no interaction of the drugs could be demonstrated. Examination of the doseresponse relation for GABA alone and in the presence of midazolam or flurazepam showed that the maximal response to GABA was increased by the benzodiazepine in some cells while it was unchanged in others. When intracellular electrodes were filled with potassium chloride, spontaneous depolarizing GABA-mediated post-synaptic potentials (p.s.p.s) were seen. Measurement of the interval and amplitude distributions of these events showed that flurazepam increased their amplitude but not their frequency.

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Section: Discussionmentioning

confidence: 71%

Actions and Interactions of Gaba and Benzodiazepines in the Mouse Hippocampal Slice

Biscoe¹,

Duchen²

1985

Exp Physiol

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“…Functional and regional heterogeneity in GABA systems may also play a role, since GABA systems may not all be inhibitory. It has been reported that GABA produces depolarizations in hippocampal pyramidal neurons (Djorup et al 1981). The recent finding of more than one gene for the alpha subunit of the GABA receptor (Levitan et al 1988) lends yet another perspective to the intricacies of GABA-ETOH interactions, one based on heterogeneity of the GABA-A receptor, this is especially relevant since the genetic control of LS and SS sensitivity to ETOH is known to be polygenic (Dudek and Abbott 1984).…”

Section: Discussionmentioning

confidence: 98%

Genotype-dependent effects of GABAergic agents on sedative properties of ethanol

Dudek

Phillips

1989

Psychopharmacology

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Two lines of mice, selectively bred for differential sensitivity to the soporific effects of ethanol (ETOH), were administered GABAergic drugs in an effort to evaluate a role for GABA in ETOH sensitivity. ETOH sensitive Long-Sleep mice (LS) showed potentiated ETOH sedation when administered bicuculline, muscimol and aminooxyacetic acid (AOAA). ETOH-insensitive SS mice exhibited reduced ETOH sedation in the presence of the antagonists, bicuculline and picrotoxin, and potentiated sedation in the presence of muscimol and AOAA. These changes in narcosis duration were interpreted as central effects, since blood ethanol levels at waking from ETOH sedation varied with GABAergic drug treatment. Picrotoxin antagonized pentobarbital-induced narcosis in both lines, but to a greater extent in SS mice. These and other experiments with a genetically heterogeneous stock suggest GABA involvement in genotype-dependent ETOH sensitivity, but do not support a simple role of GABA receptor involvement.

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“…Application of GABA to the dendrites of pyramidal cells produces a depolarization rather than a hyperpolarization (Alger andNicoll, 1979, 1982b;Andersen et at., 1980a;Thalmann et at., 1981;Dj¢rup et at., 1981;. This dendritic depolarizing response reverses at about -40 m V, is associated with a decreased input resistance, appears to be mediated via an increased conductance to chloride and some cation(s), and is more sensitive to blockade by GABA antagonists than is the typical somatic hyperpolarizing response.…”

Section: Electrophysiol· Ogy Of Hippocam· Pal Neuronsmentioning

confidence: 94%