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Strychnine and L-allylglycine but not bicuculline and picrotoxin induce transsynaptic degeneration following transection of the inferior alveolar nerve in adult rats.

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The effects of the convulsants strychnine, bicuculline, picrotoxin and L-allylglycine on the transsynaptic destruction of medullary dorsal horn neurons were examined following transection of the inferior alveolar nerve in adult rats. Strychnine and L-allylglycine enhanced the transsynaptic effect of

Intracellular calcium accumulation in rat hippocampus during seizures induced by bicuculline or L-allylglycine.

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Using electron microscopy and the combined oxalate-pyroantimonate technique, free calcium ions were located in the hippocampus of control rats and of those that had undergone status epilepticus induced by L-allylglycine or bicuculline. The validity of this technique was established by the use of the

Dramatic increase in nigral t-[35S]butylbicyclophosphorothionate binding sites elicited by the degeneration of the striato-nigral GABAergic pathway: reversal by diazepam.

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In rats, the degeneration of the striato-nigral GABAergic pathway caused by the intrastriatal injection of kainic acid induced a marked decrease (65%) of GABA content and glutamic acid decarboxylase (GAD) activity and a dramatic increase (225%) in the binding of t-[35S]butylbicyclophosphorothionate

Dopaminergic mechanisms underlying the reduction of electrical coupling between horizontal cells of the turtle retina induced by d-amphetamine, bicuculline, and veratridine.

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Previous studies have shown that dopamine, bicuculline, or d-amphetamine reduce the electrical and dye-coupling between the axon terminals of the horizontal cells of the turtle retina (see Piccolino et al., 1984). In the present study we observed similar effects following the application of

Bicuculline increases the intracellular calcium response of CA1 hippocampal neurons to synaptic stimulation.

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Intracellular calcium levels were measured by ratio imaging of Fura-2-injected CA1 pyramidal neurons during repetitive electrical stimulation of the Schaffer collaterals in rat hippocampal slices. Baseline intracellular calcium levels of 102 nM increased to 190 nM during a 3-s stimulus train of 5

Regional and differential expression of gelatinases in rat brain after systemic kainic acid or bicuculline administration.

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Indirect evidence from in vitro studies implicates a functional role for matrix metalloproteinases (MMPs) in the central nervous system (CNS), including induction of neuronal migration during development and enhancement of neurite extension. Few reports have documented the expression of these

Effect of hypoxia on bicuculline seizures of rat: NMR spectroscopy and bioluminescence imaging.

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Previous studies suggested that hypoxia reduces the severity of brain injury after epileptic seizures. To test this hypothesis, the effect of hypoxic arrest of epileptic seizures on brain metabolism was investigated in rats by combining in vivo NMR spectroscopy with imaging techniques for the

Metabolic changes in cerebral cortex, hippocampus, and cerebellum during sustained bicuculline-induced seizures.

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The objective of the present experiments was to study metabolic correlates to the localization of neuronal lesions during sustained seizures. To that end, status epilepticus was induced by i.v. administration of bicuculline in immobilized and artificially ventilated rats, since this model is known

Degeneration of cholinergic basal forebrain nuclei after focally evoked status epilepticus.

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Status epilepticus (SE) of limbic onset might cause degenerative phenomena in different brain structures, and may be associated with chronic cognitive and EEG effects. In the present study SE was evoked focally by microinfusing picomolar doses of cyclothiazide+bicuculline into the anterior extent of

Effects of reduced cerebral blood flow upon EEG pattern, cerebral extracellular potassium, and energy metabolism in the rat cortex during bicuculline-induced seizures.

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Progressive cerebral ischemia was induced by blood pressure (BP) reduction in rats during status epilepticus, and the sequence of cerebral functional (EEG, extracellular K+ activity) and metabolic (levels of high energy phosphates, glucose, glucose-6-phosphate, lactate, pyruvate,

Translamellar disinhibition in the rat hippocampal dentate gyrus after seizure-induced degeneration of vulnerable hilar neurons.

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Longitudinally restricted axonal projections of hippocampal granule cells suggest that transverse segments of the granule cell layer may operate independently (the "lamellar" hypothesis). Longitudinal projections of excitatory hilar mossy cells could be viewed as antithetical to lamellar function,

[Effect of stimulation of the facial nucleus on discharge of respiratory neurons in the pre-Bözinger complex and its neurotransmitter mechanism in rats].

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The experiments were carried out on adult Sprague-Dawley rats. We investigated the discharge response of respiratory neurons (RNs) in the pre-Bözinger complex (PBC) to electrical stimulation of the facial nucleus in which the motor neurons were retrogradely degenerated and the antagonistic effects

The pyramidal neurons in the medial prefrontal cortex show decreased response to 5-hydroxytryptamine-3 receptor stimulation in a rodent model of Parkinson's disease.

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In the present study, effect of SR 57227A, a selective 5-hydroxytryptamine-3 (5-HT(3)) receptor agonist, on the firing activity of pyramidal neurons in the medial prefrontal cortex (mPFC) was studied in normal rats and rats with 6-hydroxydopamine lesions of the substantia nigra pars compacta by

Quantification of zinc toxicity using neuronal networks on microelectrode arrays.

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Murine neuronal networks, derived from embryonic frontal cortex (FC) tissue grown on microelectrode arrays, were used to investigate zinc toxicity at concentrations ranging from 20 to 2000 microM total zinc acetate added to the culture medium. Continual multi-channel recording of spontaneous action

The role of Akt-GSK-3beta signaling and synaptic strength in phencyclidine-induced neurodegeneration.

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N-methyl-D-aspartate (NMDA) receptor antagonists such as phencyclidine (PCP) can induce positive and negative symptoms of schizophrenia in humans and related effects in rodents. PCP treatment of developing rats induces apoptotic neurodegeneration and behavioral deficits later in life that mimic some

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