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PubMed1989

Disinhibitory actions of the GABAA agonist muscimol in immature hippocampus.

Bath application of muscimol (10-20 microM) to hippocampal slices obtained from rats on postnatal days 10-15 produced epileptiform activity in the form of multiple population spikes in 20% of slices tested, concurrent with marked disinhibition. The disinhibition occurred in nearly 100% of cases tested at muscimol concentrations that produced epileptiform activity. Paired pulse analysis of GABAergic recurrent inhibition revealed a muscimol-induced disinhibitory effect involving a decrease in maximum possible inhibition. Spontaneous and antidromically elicited inhibitory postsynaptic potentials (IPSPs) recorded intracellularly were suppressed by muscimol. Current-voltage analysis of the recurrent IPSPs suggests that muscimol acted at a number of sites to produce disinhibition. The input conductance of the postsynaptic pyramidal cell increased due to muscimol, creating a current shunt which likely decreased the efficacy of synaptic currents. Muscimol also caused a decrease in the conductance due to the IPSP as well as a shift in the depolarizing direction of the equilibrium potential of the IPSP. The data indicate that muscimol, a GABAA agonist, can produce disinhibition resulting from the multiple consequences of its action. We conclude that the physiologic consequences of GABAA agonist treatment are complex. On the other hand, neurons are likely to be inhibited by a tonic increase in membrane conductance. However, since recurrent inhibition is simultaneously compromised, excitatory vollies of sufficient intensity may overcome the tonic inhibition and produce a hyperexcitable state. In some cases, this disinhibition may induce epileptiform activity. These observations are relevant in light of the proposed use of GABA agonists clinically to control seizures.

Animals↗

PubMed1989

Actions of arachidonic acid and hepoxilin A3 on mammalian hippocampal CA1 neurons.

The effects of arachidonic acid and its lipoxygenase metabolites, the hepoxilins, were investigated in rat hippocampal CA1 neurons in vitro by intracellular electrophysiological recordings. Both arachidonic acid and the hepoxilins cause a hyperpolarization which is sometimes followed by a later depolarization, augment the postspike train long-lasting afterhyperpolarization (AHP) and increase orthodromic inhibitory postsynaptic potentials (IPSPs). These data show that this arachidonic acid metabolic pathway has significant actions on mammalian central neurons, and may represent an important mechanism of neuromodulation.

8,11,14-Eicosatrienoic Acid↗

PubMed1989

Optic tract stimulation evokes GABAA but not GABAB IPSPs in the rat ventral lateral geniculate nucleus.

The inhibitory postsynaptic potentials (IPSPs) evoked in neurons of the rat ventral geniculate nucleus (vLGN) by electrical stimulation of the optic tract and the action of GABA and baclofen on the same cells were studied using intracellular recording technique in an in vitro slice preparation. A short latency short duration IPSP always followed the monosynaptic excitatory postsynaptic potential (EPSP). This IPSP reversed in polarity at about -65 mV and was reversibly blocked by bicuculline (50 microM) thus indicating that it represents a GABAA receptor-mediated IPSP. No long-lasting IPSP was evoked in vLGN cells by stimulation of the optic tract, while in the same slice, long-lasting GABAB IPSPs were routinely recorded in the dorsal lateral geniculate nucleus. GABA applied by ionophoresis evoked a hyperpolarization that had a reversal potential close to -70 mV and was antagonized by bicuculline. Baclofen hyperpolarized vLGN neurons and its action was reversibly blocked by the selective GABAB antagonist phaclofen (1 mM). In the presence of bicuculline GABA also produced a hyperpolarization that had properties similar to that evoked by baclofen. These results indicate that, although functional GABAA and GABAB receptors are present on vLGN neurons, stimulation of the optic tract evokes only GABAA but not GABAB mediated IPSPs. The lack of long-lasting GABAB IPSPs could explain the absence of long-lasting inhibition observed in vLGN neurons in vivo following stimulation of the optic tract.

Action Potentials↗

PubMed1989

Localization of a leech inhibitory synapse by photo-ablation of individual dendrites.

An inhibitory motor neuron (cell 1) in the leech nervous system has a powerful inhibitory connection onto an excitatory motor neuron (cell 3) that is functionally important in behaviours such as swimming and local bending. The anatomical location of this connection was explored using focal ultraviolet irradiation of cell 3 dendrites filled with Lucifer yellow. Ablation of the main neurite of cell 3 in the middle of the ganglion eliminated 72% of the inhibitory postsynaptic potential (IPSP), showing that most of the synaptic contacts are in the dendritic field contralateral to the cell body. Ablation of a particular dendritic branch (d1), one of several that run anteriorly from the main neurite in the contralateral ganglion, eliminated 70% of the IPSP in some cases but only 4% in others. In these latter cases, subsequent ablation of a more distal dendrite (d2) eliminated from 41% to 83% of the IPSP. These findings suggest that the synapses onto cell 3 from cell 1 are primarily mediated by either one of these dendrites or the other, but not both. This synaptic specificity might be due to a developmental mechanism involving competition between dendrites for occupation of synaptic sites.

Action Potentials↗

PubMed1990

3-Aminopropanephosphinic acid is a potent agonist at peripheral and central presynaptic GABAB receptors.

The actions of the GABA analog 3-aminopropanephosphinic acid (3-APA) were studied in the guinea-pig isolated ileal preparation and at synapses between cultured rat hippocampal neurons. Like the GABAB receptor agonist, baclofen, 3-APA inhibited the electrically evoked ileal twitch. The EC50 for 3-APA was 0.8 microM; the EC50 for baclofen was 9 microM. In addition, the depressant responses to 3-APA and baclofen were blocked by the GABAB receptor antagonists phaclofen, saclofen, 2-hydroxy-saclofen and delta-aminovaleric acid. 3-APA also mimicked the presynaptic action of baclofen at GABAergic synapses between embryonic rat hippocampal neurons in culture. 3-APA reduced the amplitude of inhibitory postsynaptic potentials (IPSPs) and currents (IPSCs) by greater than 50% at a concentration of 1 microM, while baclofen reduced synaptic transmission to a similar degree at 10 microM. 3-APA did not alter membrane conductance, nor did the drug alter postsynaptic responses to GABA. These data show that 3-APA is a potent agonist at presynaptic GABAB receptors in the periphery and on GABAergic neurons from the central nervous system. The activity of 3-APA at central postsynaptic GABAB receptors remains to be studied.

Amino Acids↗

PubMed1990

In vivo intracellular analysis of rat dentate granule cells.

In vivo intracellular recordings and dentate EEG were obtained in urethanized-curarized rats. Granule cells (GCs) were identified by antidromic activation as well as by intracellular staining with Lucifer yellow (LY). GCs fired spikes which, in 43.6% of the cases, had brief post-hyperpolarization. Slow spikes were recorded at hyperpolarized levels during the rebound of hyperpolarizing pulses or during inhibitory postsynaptic potentials (IPSPs). Medial septal nucleus or perforant pathway stimulation evoked an excitatory postsynaptic potential (EPSP)-IPSP sequence. During theta (theta) rhythm, the membrane potential of 80.3% of the GCs showed rhythmic sine-like waves of up to 15 mV at a theta frequency which were phase-locked with extracellular theta. GCs were classified into 3 types: type 1 (67.1%) showed intracellular theta and rhythmic firing; type 2 (13.2%) revealed intracellular theta and random firing, but spikes tended to occur at a preferred phase of the dentate theta; and type 3 (19.7%) had neither intracellular theta nor rhythmic firing. Intracellular theta amplitude was wider during injection of the hyperpolarizing current and narrower during depolarizing ones, indicating that rhythmic EPSPs contribute to theta genesis. Intracellular theta was unaffected by Cl- or Cs+ diffusion, suggesting that IPSP is not essential to theta genesis.

Action Potentials↗

PubMed1990

Suppression of the PGO-related lumbar motoneuron IPSP by strychnine.

Intracellular recordings from lumbar motoneurons in chronic unanesthetized cats revealed that a distinct inhibitory postsynaptic potential (IPSP) occurs following pontogeniculooccipital (PGO) waves during active sleep. Strychnine, when applied juxtacellularly by microiontophoresis, was found to block this IPSP. These data suggest that glycine is likely to be the neurotransmitter that is responsible for the inhibition of lumbar motoneurons that occurs in conjunction with the PGO waves of active sleep.

Action Potentials↗

PubMed1990

Synaptic contributions to theta rhythm genesis in rat CA1-CA3 hippocampal pyramidal neurons in vivo.

The effects of intracellular Cl- diffusion and hyperpolarizing current pulses on inhibitory postsynaptic potentials (IPSPs) and the transmembrane theta rhythm of CA1-CA3 pyramidal neurons were tested in urethanized and curarized rats. Cl- diffusion and hyperpolarizing currents decreased the amplitude of IPSPs evoked by fornix stimulation without modifying the theta rhythm amplitude and phase. The membrane conductance was typically 22-46% higher at the positive than negative intracellular theta peaks. Results indicate that in curarized rats excitatory postsynaptic potentials were the main components of intracellular theta without an important participation of IPSPs in theta rhythm genesis.

Animals↗

PubMed1990

Electrophysiological properties of pedunculopontine neurons and their postsynaptic responses following stimulation of substantia nigra reticulata.

Membrane properties and postsynaptic responses to stimulation of the substantia nigra reticulata (SNr) of the neurons in rat pedunculopontine nucleus (PPN) were studied in an in vitro parasagittal slice preparation using intracellular recording techniques. Based on electrical membrane properties, PPN neurons were classified into 3 types (types I, II and II). The unique feature of the type I neuron was the low threshold calcium spike while the type II neuron had various inward and outward rectifications. The type III neuron showed no such features as those observed in type I or II neurons. Some recorded neurons were intracellularly labeled with biocytin to study their morphology, and their transmitter phenotype was investigated by immunocytochemistry for choline acetyltransferase (ChAT). The type I and III neurons were found to be non-cholinergic, but 50% of the labeled type II neurons were immunopositive for ChAT. Morphological features of type II neurons were also different from type I or III neurons. The soma of the type II neuron was almost always more than twice as large as that of type I and III neurons. Inhibitory postsynaptic potentials (IPSPs) were induced in all 3 types of PPN neurons following stimulation of SNr. SNr-induced IPSPs were usually followed by a slow depolarizing potential from which rebound spikes were triggered. These rebound excitations were found only in type I and II neurons. These data indicate that heterogeneous groups of neurons exist in the PPN in terms of morphology, transmitter phenotypes and electrical membrane properties.

Action Potentials↗

PubMed1991

Valproate suppresses N-methyl-D-aspartate-evoked, transient depolarizations in the rat neocortex in vitro.

Effects of the antiepileptic drug sodium valproate (VPA) were studied on neocortical pyramidal cells (layer II/III) of the rat in vitro by intracellular recording. VPA (0.1-1 mM) in a dose-related manner suppressed the characteristic transient depolarizations induced by N-methyl-D-aspartate (NMDA) applied iontophoretically Higher concentrations of VPA (5-10 mM) also reduced L-glutamate responses. At these concentrations VPA increased the duration of orthodromically evoked inhibitory postsynaptic potentials and reduced repetitive spike firing induced by depolarizing currents. All effects were fully reversible within about 30 min. These results suggest that an essential mode of action for the anticonvulsant VPA is the attenuation of NMDA receptor-mediated excitation.

Animals↗

PubMed1991

Strychnine antagonizes jaw-closer motoneuron IPSPs induced by reticular stimulation during active sleep.

In chronic, unanesthetized, normally respiring cats, stimulation of the nucleus reticularis pontis oralis induced inhibitory postsynaptic potentials (IPSPs) in masseter motoneurons during active sleep, but not during wakefulness or quiet sleep. Strychnine, when applied juxtacellularly by microiontophoresis to masseter motoneurons, specifically suppressed the active sleep-dependent IPSPs. In contrast, bicuculline did not suppress the active sleep-dependent IPSPs. These results indicate these IPSPs are mediated by the putative neurotransmitter glycine.

Action Potentials↗

PubMed1991

High CO2-bicarbonate buffer modifies GABAergic inhibitory effect at the crayfish neuromuscular synapse.

gamma-Aminobutyric acid (GABA) activated channels have a considerable permeability to bicarbonate ions (HCO3-), which might alter the efficacy of chloride-dependent synaptic inhibition. Saturation of the bicarbonate-buffered physiologic solution with 15% CO2/85% O2 increased the depolarizing inhibitory postsynaptic potential (IPSP) amplitude in crayfish muscle by 290% due to a shift of +8.33 mV in its reversal potential. Consequently, the normal inhibition exerted by the IPSP on the excitatory postsynaptic potential is reversed to large excitation.

Animals↗

PubMed1992

Synaptic inhibition of accessory motoneurons evoked by stimulation of the trigeminal nerve in the cat.

Stimulation of the trigeminal nerve produced polysynaptic inhibitory postsynaptic potentials (IPSPs) in accessory motoneurons of the cat. This contrasts with the observation that dorsal cervical motoneurons responded with EPSPs to trigeminal stimulus. Stimulation of the rostral part of spinal trigeminal nucleus elicited di- or polysynaptic IPSPs in accessory motoneurons. Transection of the anterior funiculus at the upper cervical cord selectively abolished the IPSPs. The IPSPs were antagonized by systematically administrated strychnine but not bicuculline.

Accessory Nerve↗

PubMed1993

GABAA receptor-mediated mechanisms contribute to frequency-dependent depression of IPSPs in the hippocampus.

Intracellular recordings from in vitro guinea-pig hippocampal slices were obtained to investigate the mechanisms underlying activity-dependent depression of inhibitory postsynaptic potentials (IPSPs) in CA1 pyramidal neurons. IPSPs were studied following blockade of glutamatergic transmission. Attenuation of both fast and slow IPSP components was apparent at stimulus rates of > 0.2 Hz, but the late IPSP showed depression at even lower rates of stimulation. Overlap of these events made resolving response components during depression difficult. Fast IPSPs were isolated using CsCl-filled microelectrodes, blocking slow potassium-dependent IPSPs and reversing the chloride gradient. Under this condition repetitive stimulation did not induce IPSP depression. Other experiments showed slow IPSP depression at stimulus rates of < 0.5 Hz was relieved in the presence of picrotoxin which antagonizes GABAA events. These results suggest that activity-dependent depression of the fast IPSP results largely from chloride accumulation as a consequence of repetitive activation. Depression of the slow IPSP appears to arise from at least two components: (1) a masking of the slow hyperpolarization resulting from an apparent increase in the depolarizing GABA response due to chloride accumulation; and (2) a novel process involving GABAA receptors, perhaps mediated through presynaptic inhibition.

Amino Acids↗

PubMed1994

Loss of calbindin-immunoreactivity in CA1 hippocampal stratum radiatum and stratum lacunosum-moleculare interneurons in the aged rat.

Alterations in hippocampal circuitry may underly age-related learning and memory impairment. We showed in a previous study that the GABAB-mediated slow inhibitory postsynaptic potential (IPSP) induced in CA1 pyramidal neurons by electrical stimulation of stratum radiatum, is depressed in the hippocampus of the aged rat. This could be due to alterations in GABAergic interneuron functions. We report in this study that the number of hippocampal calbindin-immunoreactive (CaBP-IR) GABAergic interneurons is decreased in the aged rat. The mean number of CaBP-IR interneurons per slice decreases by 50% in the aged rat. The most severe loss was observed in the stratum radiatum of CA1 (78%), with a less consistent loss of immunoreactivity in CA3 (35%). In contrast, the mean number of interneurons containing parvalbumin (PV), was not significantly decreased in the aged rat. Our results show a loss of CaBP immunoreactivity in a population of GABAergic interneurons, which might be related to an altered function of these interneurons and consequently of GABAergic synaptic transmission in the aged rat. In contrast, PV immunoreactivity in interneurons located close to the pyramidal layer does not decrease in the hippocampus of the aged rat.

Aging↗

PubMed1994

Effects of serotonin on hilar neurons and granule cell inhibition in the guinea pig hippocampal slice.

Intracellular recordings in guinea pig hippocampal slices were used to study the effects of serotonin (5-HT) on presumed inhibitory hilar neurons and on postsynaptic inhibition of granule cells. 5-HT applied by the bath hyperpolarized only 50% of the hilar neurons tested but all CA3 neurons and granule cells, presumably by activating a K-conductance. The bath application of 4-aminopyridine (4-AP, 50 microM) induced burst discharge activity in hilar neurons and giant inhibitory postsynaptic potentials (IPSPs) in granule cells consisting of a Cl- and K-component. 5-HT (5-10 microM) reversibly blocked the K-component of giant IPSPs in granule cells, but not their Cl-component. In the majority of hilar neurons 5-HT increased the frequency of 4-AP induced burst discharges even when hilar neurons were hyperpolarized. Only in a few hilar neurons 5-HT blocked 4-AP induced burst discharges. We conclude that the changes in burst discharge pattern of hilar neurons correspond with the differential effect of 5-HT on Cl- and K-mediated inhibition of granule cells.

4-Aminopyridine↗

PubMed1987

Mianserin blocks alpha 2 adrenoceptors in submucous neurones of the guinea-pig caecum.

Intracellular recordings were made from submucous plexus neurones of the guinea-pig caecum in vitro. The peak amplitude of the adrenergic inhibitory postsynaptic potential (IPSP) was depressed by mianserin in a dose-dependent manner (300 nM-100 microM). This was due to a direct blockade of postsynaptic alpha 2 adrenoceptors. The nicotinic excitatory postsynaptic potential (EPSP) and the non-cholinergic EPSP were not affected by mianserin (100 microM). The presynaptic inhibition of the release of acetylcholine, mediated by presynaptic alpha 2 receptors, was also blocked by mianserin (30 microM). The results suggest that mianserin antagonizes both pre- and post-synaptic alpha 2 adrenoceptors in enteric plexus neurones.

Adrenergic alpha-Antagonists↗

PubMed1981

Development of rabbit hippocampus: anatomy.

The postnatal development of the CA1 region of rabbit hippocampus was studied using a variety of light and electron microscopic (EM) techniques. Nissl and Golgi stains showed high cellular density, small cell soma area, and sparse dendritic branching in neurons of immature animals (less than 1 week old); dendritic spines were also relatively infrequent during this period. Cell branching and spine frequency reached near-adult levels by 3 weeks, with the major area of hippocampal expansion seen in the apical dendritic layer. EM examination of synapse patterns was made using osmicated and E-PTA-treated tissue. Both techniques showed that the vast majority of synapses in immature animals (less than 2 weeks old) occurred in the dendritic region and were of the asymmetric type. Axosomatic synapses became less rare by 2 weeks; they were usually of the symmetric synapse type. The pattern of synaptic contacts in immature hippocampus resembled the mature pattern by 3-4 weeks. These data suggest a relatively late development of inhibitory postsynaptic potentials in CA1 pyramidal cells.

Aging↗