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Biomedical subjects

P Bevan

Publications and source records attributed to P Bevan.

At least 55 records · Page 3Linked to original sources
PubMed1977

Effect of punishment on human variable-interval performance.

Three female human subjects pressed a button for monetary reinforcement in a range of variable-interval schedules specifying different frequencies of reinforcement. On alternate days, responding was also punished (by subtracting money) according to a variable-ratio 34 schedule. In the absence of punishment, rate of responding was an increasing negatively accelerated function of reinforcement frequency; the relationship between response rate and reinforcement frequency conformed to Herrnstein's equation. The effect of the punishment schedule was to suppress responding at all frequencies of reinforcement. This was reflected in a change in the values of both constants in Herrnstein's equation: the value of the theoretical maximum response-rate parameter was reduced, while the parameter describing the reinforcement frequency corresponding to the half-maximal response rate was increased.

Journal Article↗
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↗
PubMed1976

Behavior of humans in variable-interval schedules of reinforcement.

During Phase I, human subjects pressed a button for monetary reinforcement in five variable-interval schedules, each of which specified a different frequency of reinforcement. The rate of responding was an increasing, negatively accelerated function of reinforcement frequency; the data conformed closely to Herrnstein's equation. During Phase II, the same five schedules were in operation, but in addition a concurrent variable-interval schedule (B) was introduced, responses on which were always reinforced at the same frequency. Response rate in component A increased while the response rate in B decreased, as a function of the reinforcement frequency in component A. Relative response rates in the two component schedules matched the relative frequencies of reinforcement. Comparing the absolute response rates in component A during Phase I and Phase II it was found that introduction of the concurrent schedule did not affect the value of the theoretical maximum response rate, but did increase the value of the reinforcement frequency needed to obtain any particular submaximal response rate.

Journal Article↗
PubMed1975

The effect of tricyclic antidepressants on cholinergic responses of single cortical neurones.

1 The technique of microelectrophoresis was used in order to study the effects of tricyclic antidepressants on responses of single cortical neurones to acetylcholine. 2 Both potentiation and antagonism of excitatory responses to acetylcholine could be observed after a brief application of imipramine or desipramine. A higher dose of the antidepressant was required to evoke antagonism than to evoke potentiation. 3 Responses to carbachol were affected by desipramine similarly, suggesting the inhibition of cholinesterase is not responsible for the potentiation of cholinergic responses. 4 A brief application of atropine also had a dual effect on responses to acetylcholine. 5 It is suggested that the potentiation of excitatory cholinergic responses by atropine and the antidepressants may be due to the blockade of masked inhibitory receptors.

Acetylcholine↗
PubMed1975

Effects of desipramine on neuronal responses to dopamine, noradrenaline, 5-hydroxytryptamine and acetylcholine in the caudate nucleus of the rat.

1 The sensitivity of single neurones to microelectrophoretically applied dopamine, noradrenaline (NA), 5-hydroxytryptamine (5-HT) and acetylcholing (ACh) was investigated in the caudate nucleus of the rat, anaesthetized with halothane. Both excitatory and depressant responses could be observed to each of the agonists. There was a high correlation between the direction of responses to dopamine and noradrenaline, whereas there was no significant correlation between the direction of responses to dopamine and ACh. 2 The effect of desipramine was studied on both excitatory and depressant responses to dopamine, NA and 5-HT, and on excitatory responses to ACh. Both potentiation and antagonism of neuronal responses to monoamines and ACh could be observed after a brief application of desipramine. 3 Excitatory responses to glutamate were not affected by desipramine. 4 The observation that responses to dopamine and NA can be potentiated by desipramine in the caudate nucleus suggests that uptake blockade is not a prerequisite for potentiation. 5 It is suggested that the potentiation of neuronal responses to dopamine by desipramine may be responsible for the therapeutic efficacy of desipramine in Parkinson's disease.

Acetylcholine↗
PubMed1975

Effects of iprindole on responses of single cortical and caudate neurones to monoamines and acetylcholine.

1 The technique of microelectrophoresis was used to study the effects of iprindole on single neurones in the cerebral cortex and caudate nucleus of the rat. 2 Iprindole, when applied for a brief period, did not affect the firing rate of the vast majority of neurones tested. 3 Both potentiation and antagonism of neuronal responses to noradrenaline, dopamine, and 5-hydroxytryptamine could be observed after a brief application of iprindole. Potentiation and antagonism often occurred after the same application of iprindole, antagonism always preceding potentiation. 4 Responses to acetylcholine were affected by iprindole similarly: both potentiation and antagonism of the responses could be observed. 5 Responses to glutamate were not affected by iprindole. 6 It is concluded that the potentiation of responses to monoamines by iprindole cannot be explained on the basis of uptake blockade; this potentiation may be due to the blockade of masked receptors on the post-synaptic cell. 7. It is suggested that the common pharmacological action of the tricyclic antidepressants may be the ability to block both monoamine and acetylcholine receptors in the brain.

Acetylcholine↗