Local and diffuse synaptic actions of GABA in the hippocampus

Isaacson, Jeffry S.; Solı́s, José M.; Nicoll, Roger A.

doi:10.1016/0896-6273(93)90308-e

Cited by 649 publications

(541 citation statements)

References 62 publications

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“…In this study, we have provided original evidence that the heterosynaptic CA3-inhibition of the distal dendrites at long intervals (150-400 ms) involves GABA B Rs (Fig. 6), extending previous reports showing similar CA3 inhibition on the mid-and proximal dendrites of CA1 pyramidal cells (Tsai and Leung, 2006;Olpe et al, 1993;Isaacson et al, 1993;Leung et al, 2008). The suppression of the MPP-evoked distal dendritic sink only with high-intensity CA3 conditioning stimulus (Fig.…”

Section: Reduction Of Ca1 Distal Dendritic Inhibition After Hyperthersupporting

confidence: 87%

“…IPI profiles were created by varying the delay between pulses from 20 to 400 ms while keeping the intensity of stimuli fixed; CA3 stimulation was adjusted to evoke ∼70% of the maximal population spike (PS) in CA1, and MPP stimulation was adjusted to evoke ∼70% of the maximal PS in the dentate gyrus or near maximal MPP-evoked distal dendritic sinks in CA1 (Leung et al, 1995). The IPI was varied to help differentiate between an early ionotropic GABA A receptormediated inhibition at <100 ms (Steffensen and Henriksen, 1991) and a metabotropic GABA B receptor-mediated inhibition at >100 ms (Tsai and Leung, 2006;Olpe et al, 1993;Isaacson et al, 1993).…”

Section: Electrophysiological Recordingsmentioning

confidence: 99%

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Loss of dendritic inhibition in the hippocampus after repeated early-life hyperthermic seizures in rats

Boyce

Leung

2013

Epilepsy Research

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"Loss of dendritic inhibition in the hippocampus after repeated early-life hyperthermic seizures in rats." (2013) Summary Seizures are relatively common in children and are a risk factor for subsequent temporal lobe epilepsy. To investigate whether early-life seizures themselves are detrimental to the proper function of the adult brain, we studied whether dendritic excitation and inhibition in the hippocampus of adult rats were altered after hyperthermia-induced seizures in immature rats. In particular, we hypothesized that apical dendritic inhibition in hippocampal CA1 pyramidal cells would be disrupted following hyperthermia-induced seizures in early life. Seizure rats were given three hyperthermia-induced seizures per day for three days from postnatal day (PND) 13 to 15; control rats were handled similarly but not heated. At PND 65-75, paired-pulse inhibition in area CA1 was evaluated under urethane anesthesia, using CA3 and medial perforant path (MPP) stimulation to excite the proximal and distal apical-dendrites, respectively, and the evoked field potentials were analyzed by current source density. There was no difference in the CA1 response to single-pulse stimulation of CA3 or MPP. In control rats, a high-intensity CA3 stimulus inhibited a subsequent MPP-evoked CA1 distal dendritic excitatory sink, and the inhibition at 150-200 ms was blocked by a GABA B receptor antagonist. Seizure as compared to control rats showed a decrease in a CA3-evoked inhibition of the CA1 distal dendritic excitation, 30-400 ms after the CA3 stimulus. In addition, seizure as compared to control rats showed a reduced early (20-80 ms) inhibition of a CA1 mid-apical dendritic sink following paired-pulse CA3 stimulation. In conclusion, long-term alterations in dendritic inhibition in CA1 were found following early-life seizures.

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Section: Reduction Of Ca1 Distal Dendritic Inhibition After Hyperthersupporting

confidence: 87%

Section: Electrophysiological Recordingsmentioning

confidence: 99%

Loss of dendritic inhibition in the hippocampus after repeated early-life hyperthermic seizures in rats

Boyce

Leung

2013

Epilepsy Research

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“…However, at present, much less is known about the function of GABA transport during synaptic transmission. It has been demonstrated that in the hippocampus, pharmacological block of GABA transport results in a notable increase in the time course of the GABA A receptor-mediated response (Dingledine and Korn 1985;Draguhn and Heinemann 1996;Isaacson et al 1993;Lambert 1992, 1994;Thompson and Gähwiler 1992). However, it is unclear whether these transporters have a neuronal or glial localization.…”

Section: Introductionmentioning

confidence: 99%

“…Block of transporter action has been shown to increase the duration of synaptically evoked responses in numerous systems, presumably by increasing the duration of the neurotransmitter transient (Barbour et al 1994;Isaacson et al 1993;Mager et al 1993;Mennerick et al 1999;Otis et al 1996;Overstreet et al 1999;Thompson and Gäh-wiler 1992). In addition to the role transporters play in the regulation of synaptic events at the nerve terminal, they may be important in regulating "spillover" of transmitter from neighboring nerve terminals at certain synapses within the brain (Barbour et al 1994;Isaacson et al 1993;Rossi and Hanaman 1998). Thus neurotransmitter transporters may be critically important in the determination of the time course of synaptic responses, the termination of the actions of transmitter following release, and the regulation of excitability and excitotoxicity throughout the brain.…”

Section: Introductionmentioning

confidence: 99%

Synaptically Evoked GABA Transporter Currents in Neocortical Glia

Kinney

Spain

2002

Journal of Neurophysiology

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. The presence, magnitude, and time course of GABA transporter currents were investigated in electrophysiologically characterized neocortical astrocytes in an in vitro slice preparation. On stimulation with a bipolar-tungsten stimulating electrode placed nearby, the majority of cells tested displayed long-lasting GABA transporter currents using both single and repetitive stimulation protocols. Using subtype-specific GABA transporter antagonists, long-lasting GABA transporter currents were identified in neocortical astrocytes that originated from at least two subtypes of GABA transporters: GAT-1 and GAT-2/3. These transporter currents displayed slow rise times and long decay times, contrasting the time course observed for glutamate transporter currents, and are indicative of a long extracellular time course of GABA as well as a role for glial GABA transporters during synaptic transmission.

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“…(3) Tonic G-protein inhibition of calcium channels may be relieved during repetitive stimulation (Bean, 1989;Elmslie et al, 1990;Herlitze et al, 1996;Ikeda, 1996;Brody et al, 1997), also leading to increased calcium influx during a train. (4) Neuromodulators can accumulate and act presynaptically to inhibit release, often through an inhibition of calcium channels (Isaacson et al, 1993;Yawo and Chuhma, 1993;Dittman and Regehr, 1997;Scanziani et al, 1997). (5) A transient decrease in the probability of release or a decrease in the number of readily releasable vesicles could depress synaptic strength during a train (Takeuchi, 1958;Elmqvist and Quastel, 1965;Betz, 1970;Silver et al, 1998).…”

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confidence: 99%

Modulation of Transmission during Trains at a Cerebellar Synapse

Kreitzer

Regehr

2000

J. Neurosci.

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Activity-dependent processes dynamically regulate synapses on the time scale of milliseconds to seconds. Here, we examine the factors governing synaptic strength during repetitive stimulation, both in control conditions and during presynaptic inhibition. Field recordings of presynaptic volleys, optical measurements of presynaptic calcium, and voltage-clamp recordings of postsynaptic currents were used to examine parallel fiber to Purkinje cell synapses in cerebellar brain slices at 34°C. In control conditions, regular stimulus trains (1-50 Hz) evoked up to a 250% peak synaptic enhancement, whereas during irregular stimulation, a threefold variability in EPSC amplitude was observed. When initial EPSC amplitudes were reduced by 50%, either by lowering external calcium or by activating adenosine A 1 or GABA B receptors, the peak enhancement during regular trains was 500%, and synaptic variability during irregular trains was nearly sixfold. By contrast, changes in fiber excitability and calcium influx per pulse were small during trains. Presynaptic calcium measurements indicated that by pulse 10, stimulusevoked calcium influx had increased by ϳ15%, which on the basis of the measured relationship between calcium influx and release corresponds to an EPSC enhancement of 50%. This enhancement was the same in all experimental conditions, even in the presence of N 6 -cyclopentyladenosine or baclofen, suggesting that repetitive stimulation does not relieve the G-protein inhibition of calcium channels by these modulators. Therefore, for our experimental conditions, changes in synaptic strength during trains are primarily attributable to residual calcium (Ca res )-dependent short-term plasticities, and the actions of neuromodulators during repetitive stimulation result from their inhibition of initial calcium influx and the resulting effects on Ca res and calcium-driven processes.

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Local and diffuse synaptic actions of GABA in the hippocampus

Cited by 649 publications

References 62 publications

Loss of dendritic inhibition in the hippocampus after repeated early-life hyperthermic seizures in rats

Loss of dendritic inhibition in the hippocampus after repeated early-life hyperthermic seizures in rats

Synaptically Evoked GABA Transporter Currents in Neocortical Glia

Modulation of Transmission during Trains at a Cerebellar Synapse

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