Baclofen: Effects on evoked field potentials and amino acid neurotransmitter release in the rat olfactory cortex slice

Kainic Acid-Induced Seizures Enhance Dentate Gyrus Inhibition by Downregulation of GABABReceptors

“…There are three GABA B receptor populations presynaptic to granule neurons in the polysynaptic feedback inhibitory circuit that could control disinhibition and for which downregulation would enhance inhibition: (1) autoreceptors on GABAergic terminals synapsing directly on granule cells (Davies et al, 1990;Mott et al, 1993), (2) presynaptic receptors on glutamatergic terminals, which synapse on inhibitory interneurons (Collins et al, 1982), and (3) somatic or dendritic receptors directly on inhibitory interneurons (Misgeld et al, 1989). In the hippocampus, the release of both GABA (Davies et al, 1990;Mott et al, 1993) and glutamate (Harrison et al, 1990) has been shown to be suppressed by the activation of GABA B receptors on presynaptic terminals.…”

“…In the polysynaptic recurrent inhibitory circuit, mossy fiber collaterals either directly activate inhibitory interneurons or activate glutamatergic mossy cells, which then drive the interneurons. Activation of presynaptic GABA B receptors on mossy fiber terminals or axonal terminals of mossy cells would suppress glutamate release and, therefore, decrease excitation of inhibitory interneurons (Collins et al, 1982). A decrease of these presynaptic GABA B receptors on glutamate terminals would allow more glutamate release and heightened activation of interneurons.…”

“…GABA B receptors that suppress neurotransmitter release have been found on presynaptic terminals of both GABAergic (Davies and Col-lingridge, 1993;Mott et al, 1993) and glutamatergic (Harrison et al, 1990;Scanziani et al, 1992; neurons in the hippocampus. Therefore, inhibition of granule neurons also could be enhanced either by raising the excitatory drive on inhibitory interneurons (Collins et al, 1982) or by reducing GABA B receptor-mediated suppression of GABA release from inhibitory terminals (Davies et al, 1990;Mott et al, 1993).…”

Anticonvulsant‐like actions of baclofen in the rat hippocampal slice

“…Baclofen acts by inhibiting excitatory transmission in the spinal cord, apparently by reducing the release of neurotransmitter from synaptic terminals (Davidoff & Sears, 1974;Fox, Krnjevic, Morris, Puil & Werman, 1978;Curtis, Lodge, Bornstein & Peet, 1981;Ault & Evans, 1981). Indeed, biochemical studies have demonstrated its ability to depress the Ca2'-dependent release of excitatory amino acids from various CNS preparations (Potashner, 1979;Johnston, Hailstone & Freeman, 1980;Collins, Anson & Kelly, 1982). It has been proposed that baclofen interacts with a novel GABA receptor that is insensitive to bicuculline (Bic) (Bowery, Hill, Hudson, Doble, Mid-dlemiss, Shaw & Tumbull, 1980;Bowery, Doble, Hill, Hudson, Shaw, Turnbull & Warrington, 1981; Hill and is localized mainly on certain excitatory amino acid-releasing terminals.…”

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“…Rat OC slices (500p.m thick) were preincubated and perfused at room temperature (Pickles & Simmonds, 1976) in a solution containing 25gM picrotoxin to abolish GABA-mediation inhibition (Collins et al, 1982). The surface fields evoked on lateral olfactory tract (LOT) stimulation (50psec pulse width; supramaximal voltage, 0.0033Hz) were recorded using chlorided silver ball electrodes.…”