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Biomedical subjects

R J Boakes

Publications and source records attributed to R J Boakes.

At least 19 recordsLinked to original sources
PubMed1992

Physiological and biochemical studies on the cerebellar cortex of the murine mutants "jolting" and "motor end-plate disease".

The activity of cerebellar Purkinje cells in the murine mutants "jolting" and "med" has been determined using extracellular electrical recordings in vivo and in isolated cerebellar slices. Most of the cells in the mutant brains failed to generate simple spontaneous action potentials, but they responded to climbing fibre inputs by generating complex potentials. The few mutant cells that were spontaneously active exhibited much lower firing frequencies than normal cells, and interval histograms of spontaneous activity were skewed towards longer intervals. The silent cells in mutant cerebellar slices could be activated by direct intracellular stimulation, by antidromic excitation and by the application of glutamate and high [K+]0. Activity was not restored by the application of bicuculline. It seems that the failure of the cerebellar Purkinje cells to generate simple spontaneous action potentials is not due to an inherent inexcitability of the soma or to the excessive activity of GABA-ergic inputs onto the cells. It is suggested that an abnormality in the behaviour of a Ca2+ channel is the most likely origin for the deficit in these mutant mice.

Aging↗
PubMed1988

Transmission of burst responses through slices of rat cerebral cortex.

1. Slices of rat's forebrain, 400 micron thick, have been cut and maintained in a bath perfused with warm oxygenated Krebs solution. Records were made with extracellular micropipettes of the neural responses to local stimulation of the cortex itself or the underlying white matter. 2. Single stimuli at either of these sites could produce an all-or-nothing burst response among nearby neurones. This response usually lasted 0.2-0.5 s during which repetitively discharging cortical units could be recorded at all cortical depths. 3. This burst response was transmitted from the stimulated point across the cortex in all directions with a velocity of roughly 0.1 m s-1. 4. Complete recovery of excitability among neurones generating the burst response took about 10 s. 5. Removal of Ca2+ from the perfusate prevented transmission of this response, as did a high concentration of Mg2+ or 160 mg/100 ml of ethanol. 6. Propagation of the burst response was not dependent upon the integrity of the underlying white matter; it required only that any 20% of the cortical thickness was intact and undamaged. 7. In coronal sections of brain the response could be transmitted from one hemisphere to the other provided that the corpus callosum was intact.

Action Potentials↗
PubMed1987

Efflux of putative transmitters from superfused rat brain slices induced by low chloride ion concentrations.

Slices of rat cerebral cortex, preloaded with [14C]gamma-aminobutyric acid (GABA) and either [3H]5-hydroxytryptamine (5-HT) or [3H]noradrenaline, were superfused with media in which varying concentrations of Cl- had been replaced with other monovalent anions. Rapid reduction of [Cl-], by superfusion with media containing instead the impermeant anions propionate, isethionate, gluconate, or methyl sulphate, caused increases in the efflux of tritiated biogenic amines, but the increase in that of [14C]-GABA was not significant. The increased efflux of [3H]5-HT evoked by superfusion with low Cl- levels when propionate was the replacement anion, was transient and was linearly related to the log[Cl-]-1. It was not affected by removal of Ca2+ or by addition of 10 mM Mg2+ and was delayed but not abolished by tetrodotoxin. The low Cl(-)-evoked efflux of [3H]5-HT was not affected by pretreatment with neuronal reuptake blockers but was inhibited by picrotoxin, strychnine, and 4-acetamido-4-isothiocyanostilbene-2,2-disulphonic acid and was enhanced by glycine. Muscimol and GABA were without effect. These observations are taken to indicate that the efflux of biogenic amines is brought about by terminal depolarisation due to outward movement of Cl- in low chloride-containing media. They are of relevance to other physiological and pharmacological studies in which anion concentrations are manipulated and suggest that the anion-evoked release phenomenon may provide a model for the analysis of Cl(-)-dependent mechanisms in nerve terminals.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1986

Failure of carbachol to influence the release of somatostatin from slices of rat cerebral cortex.

A [K+]-related, Ca2+-dependent efflux of immunoreactive somatostatin (IRS) from superfused slices of rat cerebral cortex has been observed; this release paralleled the release of both [14C]noradrenaline and [14C]GABA. However IRS release in this preparation was not stimulated by the muscarinic agonist carbachol at low (10 microM) or high (500 microM) concentrations. Furthermore, 100 or 500 microM carbachol did not affect the IRS efflux from rat cortex slices incubated in the presence of 12, 25 or 53 mM K+.

Animals↗
PubMed1986

Cerebellar structure and function in the murine mutant "jolting".

The morphology of the cerebellar cortex of the murine mutant "jolting" and its phenotypically normal littermate was studied. The general organisation of the cerebellum of normal mice was similar in all respects to that described for other vertebrate species. In "jolting" mice aged 4 months or more there was a marked loss of Purkinje cells and spheroids were present on Purkinje cell axons. An ultrastructural examination showed that the spheroids contained randomly orientated neurofilaments, degenerating mitochondria and autophagic vacuoles. The abnormalities in the cerebellum appeared confined to the Purkinje cells. Extracellular recordings were made of the electrical activity of the cerebellar cortex of anaesthetised mice. In the cerebellar cortex of "jolting" animals, Purkinje cells generated little spontaneous activity, but complex discharges resulting from climbing fibre inputs were indistinguishable from normal. The abnormal electrical activity of Purkinje cells in "jolting" mice could be seen in animals as young as 3 weeks. It was concluded that the "jolting" mouse suffers from a cerebellar ataxia.

Action Potentials↗
PubMed1985

Abnormal behavioural changes associated with vasopressin-induced barrel rotations.

Arginine-8-vasopressin (AVP) was injected into the cerebral ventricles of rats in order to characterize the dose-response relations of the convulsant actions of AVP and to obtain a detailed description of other acute behavioural effects. The incidence of barrel rotations, a violent and apparently uncontrolled motor activity during which rats rotate about their long axis, was found to be dose dependent, with a threshold of between 1 and 10 ng per rat. Other behavioural effects of AVP including immobility, titubation, ataxia, backward walking, and inhibition of exploratory activities and of grooming were seen at doses as low as 100 pg. These behavioural effects occurred within 9 min after injection, and thus have the same time course as barrel rotations. These acute actions of AVP may be significant in interpreting the effects of AVP on cognitive processes and memory and should also be taken into consideration in the clinical use of AVP as an anti-amnestic.

Animals↗
PubMed1984

Release of aspartate and glutamate caused by chloride reduction in synaptosomal incubation media.

Release of the amino acid neurotransmitter candidates aspartate and glutamate from synaptosomes can be stimulated by reduction of [Cl-] in the incubation medium by replacement with the impermeant anions propionate and isethionate. Replacement by the permeant anion Br- is without effect on amino acid release. This release offers a biochemical method of studying the Cl-ion channel in CNS membrane.

Animals↗
PubMed1979

Interactions of (+)-amphetamine and chlorpromazine on neurones in the lower brain stem of the rat.

1 The ability of chlorpromazine to antagonize the effects of iontophoretic application of (+)-amphetamine to single neurones in the medulla and lower pons of anaesthetized rats has been studied. 2 Chlorpromazine, administered systemically or iontophoretically, consistently and specifically antagonized the excitatory actions of (+)-amphetamine, but not those of noradrenaline on the same neurone. 3 It is concluded that chlorpromazine reduces the effect of (+)-amphetamine by a presynaptic mechanism. 4 (+)-Amphetamine did not mimic the prolonged inhibitory response of some neurones to noradrenaline but often excited these neurones and chlorpromazine blocked these excitatory responses to (+)-amphetamine.

Acetylcholine↗
PubMed1972

A neuronal basis for the alerting action of (+)-amphetamine.

1. (+)-Amphetamine mimicked the excitatory and inhibitory actions of (-)-noradrenaline on single neurones in the brain stem of acute halothaneanaesthetized rats when these compounds were applied by iontophoresis. (+)-Amphetamine had no actions on neurones unaffected by (-)-noradrenaline.2. These mimicking actions of (+)-amphetamine could not be observed 20 h after treatment of the animals with reserpine 5 mg/kg.3. The enzyme inhibitors alpha-methyl-p-tyrosine and FLA 63 also greatly reduced the number of (-)-noradrenaline-mimicking responses to (+)-amphetamine.4. In animals pretreated with alpha-methyl-p-tyrosine, but not in those pretreated with FLA 63, excitatory actions of (+)-amphetamine on neurones excited by (-)-noradrenaline could be elicited 45-90 min after systemic injection of L-DOPA.5. These results indicate that (+)-amphetamine can release noradrenaline from presynaptic sites in the brain stem, which may be a basis for its alerting actions.

Action Potentials↗