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Biomedical subjects

J H Wolstencroft

Publications and source records attributed to J H Wolstencroft.

At least 19 recordsLinked to original sources
PubMed1985

Electrophysiological studies of a rostral projection from the nucleus raphe magnus to the hypothalamus in the rat and cat.

Neurones in nucleus raphe magnus (NRM) and the adjacent reticular formation with rostral projections were identified by their antidromic responses to stimulation at periventricular forebrain sites in rats and cats. In subsequent experiments, the effects of stimulation in the midline of the ventral medulla were tested on the activities of periventricular forebrain neurones. Taken together, the results of these experiments suggest that a direct inhibitory projection may exist from NRM to ventromedial forebrain structures including the anterior hypothalamus/preoptic region in rats in addition to polysynaptic pathways which mediate both excitations and inhibitions in rats and cats.

Animals↗
PubMed1985

A microiontophoretic study of the actions of the putative sleep factor, piperidine, in the rat brainstem.

By means of microiontophoresis, we have compared the actions of a putative sleep substance, piperidine, with other neurotransmitters in the rat anaesthetized with urethane. In the pons and midbrain, piperidine mimicked the actions of acetylcholine on more than 200 neurones. Piperidine- and acetylcholine-induced excitations were equally effectively antagonized by hexamethonium or atropine. In 32 neurones piperidine showed no affinity for the receptors for the excitatory amino acid agonists, quisqualate and N-methyl-D-aspartate, piperidine-evoked excitations being unaffected by the antagonists glutamate diethylester or 2-amino-5-phosphonovalerate. Similarly, piperidine-evoked excitations in 23 neurones were unaffected by alpha-methylnoradrenaline, suggesting that piperidine does not act at receptors for noradrenaline. Twenty per cent of neurones responsive to piperidine were inhibited. These inhibitions in 12 neurones were insensitive to either strychnine or bicuculline indicating that piperidine does not act on receptors for glycine or gamma-aminobutyric acid. In a further 68 neurones, neither hexamethonium (4 out of 59 cells) nor atropine (0 out of 9 cells) was effective in antagonizing the inhibitions evoked by piperidine or by acetylcholine. It is suggested that piperidine may exert its central hypnogenic effects by an action at cholinoceptors in brainstem areas involved in sleep regulation.

Acetylcholine↗
PubMed1983

The C-terminal dipeptide of beta-endorphin: a neuropeptide with inhibitory activity.

Glycylglutamine, the C-terminal dipeptide of beta-endorphin, has previously been shown to be present in porcine pituitary. Evidence is given that this dipeptide occurs in ovine brain stem where its concentration was shown to be similar to that of the complementary fragments of beta-endorphin determined by chromatography and radioimmunoassay. Using the technique of microiontophoresis an inhibitory activity of the dipeptide was demonstrated on neurones located in the reticular formation of rat brain stem.

Animals↗
PubMed1983

Actions of GABA, glycine, methionine-enkephalin and beta-endorphin compared with electrical stimulation of nucleus raphe magnus on responses evoked by tooth pulp stimulation in the medial reticular formation in the cat.

In decerebrate, cerebellectomized cats, a comparison was made between the effects of electrical stimulation in nucleus raphe magnus (NRM) and iontophoretic application of GABA, glycine, met-enkephalin and beta-endorphin on the responses of neurones in the medial brain stem reticular formation to tooth pulp stimulation. NRM stimulation, GABA, glycine and enkephalin produced a short lasting inhibition of tooth pulp evoked responses whilst the time course of the inhibition produced by beta-endorphin was much slower, often lasting up to 1 h following a 3-7 min ejection period. The effects of GABA and glycine could be antagonised by iontophoresis of bicuculline and strychnine respectively whilst intravenous injection of naloxone antagonised the inhibition induced by the opioid peptides. In most neurones tested, inhibition of tooth pulp evoked responses by NRM stimulation was blocked by iontophoretic application of bicuculline but not by strychnine or naloxone (i.v.). We conclude that GABA may act as a transmitter which mediates the inhibitory effects of NRM on the responses of reticular neurones to tooth pulp stimulation. Thus GABA may be involved in stimulation produced analgesia.

Animals↗
PubMed1982

An excitatory input to nucleus raphe magnus from the red nucleus in the cat.

In chloralose-anaesthetized cats, with the cerebellum removed, stimulation in the red nucleus excited the majority (60-65%) of neurones in nucleus raphe magnus (NRM), including raphespinal neurones. Evidence was obtained for both monosynaptic and polysynaptic excitation. The projection was confirmed by recording antidromic responses in the red nucleus to stimulation in NRM. It is suggested that the role of NRM in motor control is to inhibit spinal flexion responses to peripheral stimuli so that commands from the red nucleus and other motor control regions may take place without interruption.

Animals↗
PubMed1976

The reduced responsiveness of neurones in nucleus reticularis gigantocellularis following their excitation by peripheral nerve stimulation.

1. Post-stimulus histograms of neuronal activity, constructed from extracellular recordings in decerebrate, decerebellate cats, have been used to investigate the responsiveness of neurons in nucleus reticularis gigantocellularis following their excitation by a peripheral nerve stimulus. 2. The response to a testing stimulus applied to a peripheral nerve was depressed following the response to a conditioning stimulus applied to the same or a different peripheral nerve. This reduction in responsiveness was maximal within 50 msec of the peak of the response to the conditioning stimulus. Response latencies to the testing stimulus were increased during the period of reduced responsiveness. 3. Responsiveness to a peripheral nerve stimulus was also reduced following a spontaneous or an antidromically evoked spike, but this effect was weaker and much shorter-lasting than that following a nerve-evoked spike. Thus, the reduced responsiveness cannot be solely due to phenomena which are an inevitable consequence of an action potential in the neurone. 4. In spontaneously firing neurones, the duration of the reduced responsiveness to a testing stimulus generally outlasted the depression of spontaneous activity which often followed an excitation evoked by a peripheral nerve conditioning stimulus. 5. The reduction in responsiveness to a testing stimulus applied to the same nerve as the conditioning stimulus was greater and longer-lasting than that to a testing stimulus applied to a different nerve. 6. When stimuli were applied to one nerve at a relatively high rate, the neurone became much less responsive to that input, but simultaneously became more responsive to low rate stimulation of other nerves. 7. It is concluded that the greater part of the reduced responsiveness is due to events occurring on the input pathway to a reticular neurone, or possibly in the region of the afferent endings on its dendrites. These processes may allow selective changes in responsiveness to different inputs, and enable the units to act as novelty detectors.

Action Potentials↗