Nuciferine and central glutamate receptors.
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Biomedical subjects
Publications and source records attributed to D Lodge.
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1. The firing of spinal interneurones and Renshaw cells by microelectrophoretic (+/-)-ibotenate, which was approximately eight times more active as an excitant than L-glutamate, was followed by prolonged depression of the sensitivity of the neurones to excitant amino acids and acetylcholine. 2. The depression, which lasted for 15--30 min when ibotenate was ejected for 3--6 min, was blocked by the GABA-antagonist bicuculline methochloride, and was independent of prior firing since it occurred with subthreshold concentrations of ibotenate and when ibotenate firing had been blocked by DL-alpha-aminoadipate. 3. When administered electrophoretically for 5 min, muscimol, a potent GABA agonist, reduced neuronal excitability for prolonged periods and this effect was also prevented by bicuculline methochloride. 4. The depression of neuronal excitability produced by GABA, taurine, isoguvacine or 3-aminopropane sulphonate, ejected for periods of 5--6 min, recovered rapidly. 5. It is suggested that ibotenate is converted in vivo to muscimol or a related compound which has a prolonged, bicuculline-sensitive depressant action on the excitability of neurones.
1. The electrical threshold of the terminations of single group Ia and II afferent fibers was transiently reduced by the antidromic discharge of the initial segment of spinal motoneurons in the cat. 2. This depolarization of the terminals of afferent fibers known to synapse on motoneurons confirms previous observations of antidromic electrical interaction between these structures.
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Arecaidine and guvacine, constituents of the nut of Areca catechu, inhibited the uptake of GABA and beta-alanine, but not that of glycine, by slices of cat spinal cord. In cats anesthetised with pentobarbitone, electrophoretic arecaidine enhanced the inhibitory actions of GABA and beta-alanine, but not those of glycine or taurine, on the firing of spinal neurones. Similarly, electrophoretic guvacine enhanced the inhibition of spinal neurones by GABA but not that by glycine. The uptake of GABA by slices of cat cerebellum was inhibited by arecaidine, and the effect of electrophoretic GABA on the firing of cerebellar Purkinje cells was enhanced by electrophoretic arecaidine. When administered intravenously arecaidine failed to affect synaptic inhibitions considered to be mediated by GABA. Intravenous arecaidine had no effect on either spinal prolonged (presynaptic) inhibition (20mg/kg), dorsal root potentials (20mg/kg) or basket cell inhibition of Purkinje cells (250 mg/kg), although topical arecaidine (6.6-10 x 10(-3) M) blocked this latter inhibition. Large doses of arecaidine (1 g/kg subcutaneous) marginally reduced the lethal effects of bicuculline in mice but appeared to have little or no anticonvulsant activity.
In cats anaesthetized with pentobarbitone a pharmacological investigation was made of the inhibition by volleys in afferent fibres and ventral roots of physiologically identified Ia interneurones in the ventral horn. The recurrent inhibition of Ia interneurones by Renshaw cells, and the "mutual" inhibition between Ia interneurones, were suppressed by electrophoretic strychnine and are presumably mediated by glycine. Short latency and duration inhibitions by impulses in muscle and cutaneous afferents were also suppressed by strychnine. Electrophoretic GABA inhibited the firing of Ia interneurones and the effects of bicuculline methochloride suggested that this amino acid mediates longer latency and duration inhibition produced by afferent impulses of muscle and cutaneous origin.
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Experiments were performed on 39 male albino rats anaesthetized with pentobarbitone sodium and paralyzed with gallamine triethiodide. Facial motoneurones consistently showed a progressive alteration of spike shape and decrease in spike firing frequency during the continuous microelectrophoretic application of the excitant amino acids D,L-homocysteate, L-glutamate, L-aspartate, and kainate, but infrequently during that of N-methyl-D-aspartate. The relative potencies of these excitants on facial motoneurones are reported. The potential usefulness of N-methyl-D-aspartate to produce amino acid-evoked motoneurone action potentials is discussed. The microelectrophoretically-applied depressant amino acid antagonist strychnine selectively and reversibly blocked the depressant effects of glycine on facial motoneurones. The depression of amino acid-induced firing of facial motoneurones by stimuli to the lingual or glossopharyngeal nerves were reversibly antagonized by microelectrophoretically applied strychnine but not by bicuculline.
The facial nucleus of the rat can be divided into 5 morphological subdivisions. Using a method for the correlation of the observed subdivisions with antidromic field profiles, the orgins of the major muscle branches of the facial nerve in the motor nucleus were determined. The posterior auricular branch is in the medial, the cervical in the ventromedial, the inferior and superior buccolabiales in the lateral, the zygomatic in the dorsal and the temporal and digastric in the intermediate subdivision. The results are consistent with an organization of the motor nucleus reflecting a corresponding topographic organization of the facial musculature.
1. Hemicholinium-3 (HC-3) has at least two presynaptic effects at cholinergic synapses between motor acon collaterals and spinal Renshaw cells, neither of which influenced non-cholinergic excitatory synapses on dorsal horn interneurones. 2. One, which occurred independently of repetitive activity of the synapses and which resulted in increased latency of synaptic excitation, presumably involved changes in the properties of presynaptic fibres and terminals which influenced transmitter release. 3. The other, which depended on continuous repetitive synaptic activity, was consistent with depletion by HC-3 of presynaptic stores of acetylcholine (ACh).
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