Behavioral Actions of Neuroleptics

Fielding, Stuart; Lal, Harbans

doi:10.1007/978-1-4613-4042-3_3

Cited by 56 publications

(16 citation statements)

References 42 publications

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“…It has previously been suggested that complex behavioural acts, or behaviours that require more effort, are more sensitive to attenuating effects of neuroleptics (Ettenberg et al, 1981;Fielding and Lal, 1978;Neill, 1982;Rolls et al, 1974). An interesting comparison can therefore be made between the attenuation caused by haloperidol and SCH 23390 in this complex and more requiring paradigm and the attenuation caused under conditions of continuous reinforcement using the same lever (c.f.…”

Section: Discussionmentioning

confidence: 98%

“…A decreased dopaminergic transmission, produced either by a lesion or by administration of DA antagonists, is, for example, known to attenuate food and water intake (Ungerstedt, 1970;Rolls et al, 1974;Fielding and Lal, 1978;Dourish, 1983;Ljungberg, 1987Ljungberg, , 1989b. The DA neurotransmission is also known to be important for the initiation and/or execution of orientation movements towards sensory stimuli (Marshall et al, 1974;Ljungberg and Ungerstedt, 1976;Carli et al, 1985).…”

Section: Introductionmentioning

confidence: 97%

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Effects of dopamine D-1 and D-2 antagonists on decision making by rats: No reversal of neuroleptic-induced attenuation by scopolamine

Ljungberg

Enquist

1990

J. Neural Transmission

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The effects of the dopamine (DA) D-1 antagonist SCH 23390 and the D-2 antagonists haloperidol and sulpiride on decision making in thirsty rats were investigated. The problem given to the rats was to choose between two behaviours, locomoting or lever-pressing, in order to obtain rewards (water). SCH23390 and haloperidol dose-dependently reduced the number of rewards obtained. However, only minor effects were seen on the decision making parameters. DA is thus important for initiation and/or performance of learned behavioural acts, not for information sampling and processing leading to the decision of which behaviour to perform. There were no differences between D-1 and D-2 antagonism in this respect. After sulpiride, no significant effects were observed. A specific behavioural prolife obtained by extinction was not mimicked by any of the doses of neuroleptics tested. It has previously been shown that performance per se of the two behavioural options used in the task can be reinstated by scopolamine after haloperidol attenuation. However, when these options had to be organized into functional sequences to reach a goal, haloperidol-induced attenuation could not be counteracted by scopolamine.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 97%

Effects of dopamine D-1 and D-2 antagonists on decision making by rats: No reversal of neuroleptic-induced attenuation by scopolamine

Ljungberg

Enquist

1990

J. Neural Transmission

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“…3 Indeed, when used at clinical doses, such medication can induce parkinsonian symptoms such as rigidity and bradykinesia that can only be reversed by removal of the drug or addition of antiparkinsonian agents (see for example, Fielding and Lal19). It is well known that antipsychotic drugs have a delayed action on blocking presynaptic dopamine activity and that this closely mirrors the time course of their antipsychotic efficacy 4.…”

Section: Discussionmentioning

confidence: 99%

Effects of antipsychotic medication on electromyographic responses to transcranial magnetic stimulation of the motor cortex in schizophrenia

Davey

Puri

Lewis

et al. 1997

Journal of Neurology, Neurosurgery & Psychiatry

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Objective-To assess the eVect of antidopaminergic antipsychotic medication on the electromyographic (EMG) responses of thenar muscles to transcranial magnetic stimulation (TMS) of the motor cortex in schizophrenic patients. Methods-A group of nine drug naïve schizophrenic patients was compared with a group of nine schizophrenic patients established on neuroleptic medication. Surface EMG recordings were made from the thenar muscles while patients maintained a weak isometric voluntary contraction. TMS was applied using a 9 cm circular stimulating coil centred over the vertex. The EMG responses to up to 50 magnetic stimuli were rectified and averaged. Results-There was no diVerence in threshold TMS strength for eliciting compound motor evoked potentials (cMEPs), or in their latency, in drug naïve and medicated patients. In some patients the silent period (SP) was clearly made up of two parts and the percentage of control levels of voluntary EMG was measured in each component. During the early component of the SP there was a weaker (P<0.05) suppression of EMG in the medicated patients (mean 73.9 (SEM) 5.5% of control levels) compared with the drug naïve patients (54.7 (SEM) 7.3% of control levels). This resulted in the latency of maximum suppression of voluntary EMG being longer (P<0.05) in the medicated patients (38.3 (2.4) ms) than in the drug naïve patients (28.2 (0.7) ms). During the late component of the SP voluntary EMG was reduced to similar levels (P>0.05) in both medicated (48.2 (7.7)% of control levels) and drug naïve (58 (7.8)% of control levels) patients. Conclusion-The results are discussed with reference to the disrupted inhibition seen in the early part of the SP in Parkinson's disease and drug induced parkinsonism. The future uses of motor responses to TMS as a marker for the status of antipsychotic medication are considered. (J Neurol Neurosurg Psychiatry 1997;63:468-473) Keywords: antipsychotic drugs; schizophrenia; transcranial magnetic stimulation Since the report by Carlsson and Lindquist 1 that the typical antipsychotic drugs chlorpromazine and haloperidol give rise to an accumulation of dopamine metabolites in dopamine rich brain areas in mice, it has been found that all eVective antipsychotic drugs bind to dopamine receptors. The degree of dopamine D2 receptor binding correlates with the clinical eVectiveness of typical antipsychotic drugs.2 3 Furthermore, there are delayed actions of these drugs on presynaptic dopamine activity that closely parallel the time course of their therapeutic action. 4 The mode of action of this class of drugs remains uncertain, and more recent studies (see review 5 ) have implicated several other neurotransmitters and neurohormones.Transcranial magnetic stimulation (TMS) using a coil delivering a rapidly changing magnetic field 6 is a method that can be used safely and painlessly to stimulate the motor cortex through the intact skull. When stimulation is delivered using a circular coil centred over the vertex, compound motor evoked potentials (cMEPs) ar...

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“…However, the systemic administration of CLOZ exhibits moderate potency in antagonizing apomorphine-and amphetamine-induced hyperactivity (Costall and Naylor, 1975;Fielding and Lal, 1978;Ljungberg and Ungerstedt, 1985;Peuch et al, 1978;Worms and Lloyd, 1979;Worms et al, 1983) and apomorphine-induced climbing in mice (Peuch et al, 1978;Worms and Lloyd, 1979;Worms et al, 19831, which are believed to be mediated by the mesolimbic system (Worms et al, 1983). CLOZ is also more effective in blocking the behavioral effects produced by the microinjection of DA into various mesolimbic areas compared to the striatum (Costall and Naylor, 1975).…”

Section: Studies Addressing Cloz's Selectivity For the Mesolimbic Sysmentioning

confidence: 96%

Pharmacological actions of the atypical antipsychotic drug clozapine: A review

Ashby

Wang

1996

Synapse

167

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Clozapine [8-chloro- 11-(4-methyl- 1-piperazinyl)-3H-dibenzo (b,e)(1,4) diazepine], or clozaril, is a member of the dibenazepine class of antipsychotic drugs. Initially, studies in animals using a number of neurochemical, biochemical, electrophysiological, and behavioral paradigms indicated that clozapine was markedly different from various typical antipsychotic drugs such as haloperidol and chlorpromazine. Subsequently, clinical studies have shown that clozapine is effective in ameliorating the core symptoms, as well as the negative symptoms, in schizophrenia. However, clozapine has a much lower propensity for inducing neurological side effects after acute or repeated administration compared to various typical neuroleptics. Furthermore, clozapine is therapeutically effective in treating about 30% of schizophrenic patients who are resistant to standard antipsychotic drugs. Based on the above information, clozapine has been designated an atypical antipsychotic drug. However, at this time, it is not entirely clear why clozapine is such a unique antipsychotic drug. To date, there has not been a comprehensive review regarding clozapine's pharmacological profile. Therefore, we will review clozapine's profile in the following areas: 1) affinity for neurotransmitter receptors in the brain; 2) electrophysiology (in vivo, single-cell recording and iontophoresis; in vitro studies); 3) in vivo microdialysis and voltammetry; 4) monoamine turnover or metabolism; 5) intermediate early gene expression; 6) positron emission tomography studies; and 7) molecular biological studies. We will also compare and contrast clozapine's acute and chronic effects, and discuss the merits of various hypotheses that have been put forward to explain clozapine's unique profile.

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Behavioral Actions of Neuroleptics

Cited by 56 publications

References 42 publications

Effects of dopamine D-1 and D-2 antagonists on decision making by rats: No reversal of neuroleptic-induced attenuation by scopolamine

Effects of dopamine D-1 and D-2 antagonists on decision making by rats: No reversal of neuroleptic-induced attenuation by scopolamine

Effects of antipsychotic medication on electromyographic responses to transcranial magnetic stimulation of the motor cortex in schizophrenia

Pharmacological actions of the atypical antipsychotic drug clozapine: A review

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