Search PubMed⌕ Search

Biomedical subjects

P Bevan

Publications and source records attributed to P Bevan.

At least 19 recordsLinked to original sources
PubMed1979

The action of microelectrophoretically applied (3,4-dihydroxy-phenylamino)-2-imidazoline (DPI) on single cortical neurones.

1. The technique of microelectrophoresis was used in order to compare the actions of the imidazoline derivative, (3,4-dihydroxy-phenylamino)-2-imidazoline (DPI), with those of dopamine and phenylephrine on single neurones in the cerebral cortex of the rat anaesthetized with halothane. 2. DPI and phenylephrine were almost exclusively excitatory, whereas dopamine could evoke both excitatory and depressant responses. 3. In the case of excitatory responses, DPI appeared to be more potent than dopamine, and was approximately equipotent with phenylephrine. 4. The dopamine antagonist, haloperidol, could discriminate between excitatory responses to DPI and dopamine: responses to dopamine were abolished, whereas responses to DPI, and to a control agonist, acetylcholine, were unaffected. 5. The alpha-adrenoceptor antagonist, phenoxybenzamine, antagonized equally excitatory responses to DPI and phenylephrine. Responses to acetylcholine were not affected. 6. It is concluded that DPI does not stimulate dopamine receptors on cortical neurones; the excitatory responses of these cells to DPI may be mediated by alpha-adrenoceptors.

Animals↗
PubMed1978

Comparison of the responses of single cortical neurones to tyramine and noradrenaline: effects of desipramine.

1 The technique of microelectrophoresis was used in order to compare the actions of tyramine and noradrenaline on single neurones in the cerebral cortex of the rat.2 Tyramine could both excite and depress cortical neurones. Each tyramine-sensitive cell was also sensitive to noradrenaline. There was a high correlation between the directions of responses to tyramine and noradrenaline, most cells excited by tyramine being excited by noradrenaline, and most cells depressed by tyramine being depressed by noradrenaline.3 In the case of both excitatory and depressant responses, tyramine appeared to be less potent than noradrenaline.4 Tyramine evoked ;slower' responses than noradrenaline, both the latencies to onset and the recovery times being longer for responses to tyramine than for responses to noradrenaline.5 When the rates of release of tyramine and noradrenaline from micropipettes were measured in vitro, no significant difference could be observed between the transport numbers of the two drugs. Thus the difference in potency between the two drugs, and the difference in the time courses of responses to the two drugs, are presumably of biological origin.6 Desipramine could discriminate between neuronal responses to tyramine and noradrenaline: responses to tyramine were antagonized, while responses to noradrenaline were either potentiated or unaffected. Responses to DL-homocysteic acid were not affected by desipramine.7 The results are consistent with the hypothesis that tyramine is an indirectly acting sympathomimetic amine in the brain, and desipramine acts by blocking the uptake of both tyramine and noradrenaline into presynaptic noradrenergic nerve terminals.

Animals↗
PubMed1977

The pharmacology of adrenergic neuronal responses in the cerebral cortex: evidence for excitatory alpha- and inhibitory beta-receptors.

1. The technique of microelectrophoresis was used to compare the actions of a range of adrenoceptor agonists on single cortical neurones in the rat anaesthetized with halothane. 2. Phenylephrine and methoxamine were exclusively excitatory, whereas salbutamol was entirely depressant. Noradrenaline and isoprenaline could evoke both excitatory and depressant responses. Lower doses of isoprenaline usually evoked depressions, whereas higher doses, on the same cell, evoked excitatory responses. 3. The alpha-adrenoceptor blocking agents, phentolamine and phenoxybenzamine, reversibly antagonized excitatory responses to adrenoceptor agonists, without affecting depressant responses to adrenoceptor agonists or excitatory responses to acetylcholine. 4. The beta-adrenoceptor blocking agents, propranolol and sotalol, reversibly antagonized both depressant and excitatory responses to adrenoceptor agonists, without affecting responses to acetylcholine. When the effect of sotalol on excitatory and depressant responses to adrenoceptor agonists was compared on the same cell, the depressant responses could be selectively antagonized, without affecting the excitatory responses. 5. It is concluded that (a) responses of cortical neurones to adrenoceptor agonists are mediated by both alpha- and beta-receptors; (b) these alpha- and beta-receptors give rise to opposite effects: the alpha-receptors being excitatory and the beta-receptors being inhibitory; and (c) responses of many neurones reflect the presence of both types of receptor.

Adrenergic alpha-Agonists↗
PubMed1976

Potentiation by desipramine of neuronal responses to mescaline.

The effect of desipramine on responses of single cortical neurones to mescaline was studied by the microelectrophoretic technique. Both potentiation and antagonism of responses to mescaline by desipramine were observed. The antagonism may be related to the alpha-adrenolytic action of desipramine. The potentiation is unlikely to reflect the uptake blocking action of desipramine, since desipramine does not block the uptake of mescaline in the cerebral cortex. It is suggested that the potentiation may be due to a post-synaptic action of desipramine.

Animals↗
PubMed1976

The action of microelectrophoretically applied L-3,4-dihydroxyphenylalanine (DOPA) on single cortical neurones.

The technique of microelectrophoresis was used in order to compare the actions of L-3,4-dihydroxyphenylalanine (DOPA) and noradrenaline on single neurones in the cerebral cortices of cats and rats. DOPA could both excite and depress cortical neurones. Cells excited by DOPA were also excited by noradrenaline and cells depressed by DOPA were also depressed by noradrenaline. In the case of both excitatory and depressant responses, DOPA appeared to be less potent than noradrenaline. Responses to DOPA and noradrenaline could be antagonized by phentolamine and propranolol. Responses to acetylcholine were not affected. Responses to acetylcholine, but not responses to DOPA, were antagonized by atropine. The results indicate that locally applied DOPA may mimic the actions of noradrenaline on cortical neurones. Possible mechanisms for these effects of DOPA are discussed.

Acetylcholine↗