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At least 523 records · Page 29Linked to original sources
PubMed1985

Dopamine agonist action in mesolimbic, cortical and extrapyramidal areas to modify spontaneous climbing behaviour of the mouse.

Dopamine and apomorphine were injected directly into limbic, extrapyramidal and cortical areas of mouse brain to determine relative sensitivities to the inhibitory effects of these agents on mouse spontaneous climbing behaviour. Injections of 0.06-2 micrograms apomorphine or dopamine into the nucleus accumbens, central area of the amygdala, septum or ventral tegmental nucleus caused dose-dependent motor inhibition with maximal reductions in the order of 60-70% of control value. In the extrapyramidal nuclei, caudate-putamen and globus pallidus, apomorphine and dopamine were required at 0.5-2.5 micrograms to produce inhibition, but the degree of inhibition never achieved 50% of control. Apomorphine and dopamine (0.001-10 micrograms) failed to cause any inhibition of mouse spontaneous climbing behaviour when injected into the anteromedial, supragenual or suprarhinal cortex. The higher doses of dopamine or apomorphine could effect stimulation of climbing behaviour from the limbic, extrapyramidal and cortical areas. Bilateral injections of haloperidol or (-)sulpiride (0.001-1 microgram) into the selected limbic and extrapyramidal areas caused dose-related depression of mouse spontaneous climbing, the limbic areas, particularly the nucleus accumbens, being the most sensitive. Doses of these neuroleptics selected as having minimal effect in their own right were shown to antagonise the marked motor inhibition effected by dopamine and apomorphine from the limbic areas, and the modest inhibition effected from the extrapyramidal areas. In contrast, intracerebral pretreatments with prazosin or yohimbine failed to antagonise the motor inhibitory effects of dopamine or apomorphine from any brain area.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

Neuropharmacological studies on D145 (1,3-dimethyl-5-aminoadamantan).

The effects of D145 (1,3-dimethyl-5-aminoadamantan) and amantadine on dopaminergic mechanisms in the rat were investigated by use of pharmacological agents known to disrupt dopamine function, by placing electrolytic lesions in the dopamine-containing areas of the extrapyrimidal and mesolimbic systems and by the direct application to dopamine sensitive areas. Stereotypy and circling behaviour were used as behavioural indices of dopaminergic stimulation and apomorphine and d-amphetamine were used as standard dopaminergic agonists. In addition, the possible importance of 5-hydroxytryptamine to the dopamine effects was investigated using electrolytic lesions of the midbrain raphé nuclei. Both D145 and amantadine caused a stereotyped behaviour characterized by periodic sniffing, repetitive limb movements and biting, but the effect of amantadine was far more periodic. In addition D145, but not amantadine, caused marked hyperactivity. These behavioural effects were resistant to pretreatment with alpha-methylparatyrosine but not to combined alpha-methylparatyrosine/reserpine or low doses of haloperidol. Also, the prior administration of D145 or amantadine inhibited the development of the biting components of apomorphine and d-amphetamine stereotypy. Both D145 and amantadine caused circling behaviour in animals with asymmetric lesions of the medial raphé nucleus or unilateral lesions of the substantia nigra but the action of D145 was more intense. Bilateral electrolytic lesions placed in the extrapyrimidal (caudate-putamen, globus pallidus, substantia nigra), mesolimbic (nucleus accumbens septi, tuberculum olfactorium, nucleus interstitialis stria terminalis, nucleus amygdaloideus centralis) nuclei or the neuronal pathways supplying them showed D145 and amantadine to act in both areas although their action on the extrapyrimidal system was most marked. However, of particular note was the significantly greater involvement of the substantia nigra with the D145 effect, and the greater involvement of the D145 effect with mesolimbic function. Lesions placed in the medial and/or dorsal raphé nucleus indicated some involvement of 5-hydroxytryptamine with the actions of both D145 and amantadine. The bilateral intrastriatal application of D145 or amantadine in nialamide pretreated animals failed to induce stereotyped or hyperactive behaviour although contralateral asymmetries, which were abolished by lesions of the substantia nigra, were recorded following the unilateral intrastriatal application of D145 or amantadine in haloperidol pretreated animals.

Amantadine↗
PubMed1979

The effects of 5,7-dihydroxytryptamine lesions of extrapyramidal and mesolimbic sites on spontaneous motor behaviour, and amphetamine-induced stereotypy.

5,7-Dihydroxytryptamine lesions of the nucleus accumbens septi, or substantia nigra, resulted in a twofold increase in spontaneous locomotor activity. Striatal 5HT depletion also raised basal activity levels, as well as increasing rearing behaviour in an open field. The sterotyped responses to all doses of amphetamine tested (2.5--10 mg/kg, i.p.) were enhanced by lesions of the nucleus accumbens or substantia nigra. Striatal lesions only affected the response to the lowest dose of amphetamine. Lesions of the tuberculum olfactorium were without effect on spontaneous or amphetamine induced responses. The results support the concept of a modulatory 5HT influence on nigro-striatal function, and suggest that 5HT in the nucleus accumbens has an antagonistic role with respect to dopamine function in this site.

5,7-Dihydroxytryptamine↗
PubMed1986

Calcineurin in human brain and its relation to extrapyramidal system. Immunohistochemical study on postmortem human brains.

Calcineurin immunoreactivity has been successfully detected in formalin-fixed paraffin-embedded postmortem human brain tissue using the peroxidase-antiperoxidase method. We have examined two autopsy cases with Huntington's disease (HD), three cases with Parkinson's disease, and two senile patients as controls. In the controls, calcineurin immunoreactivity was present in neuronal cells only and highly concentrated in the caudate nucleus, putamen, globus pallidus (striato-pallidal pathway), substantia nigra (striato-nigral pathway) and hippocampal formation. These localizations were similar to those identified in rat brain. There was a marked depletion of neurons containing calcineurin in the caudate nucleus and putamen, and a marked reduction of calcineurin-immunoreactive nerve fibers in the globus pallidus and substantia nigra were found in the cases with HD, but not in those with Parkinson's disease. These findings suggest that calcineurin can be a useful and specific index of neuronal degeneration in the caudato-putamen resulting from extrapyramidal disease, and that the calcineurin-immunostaining method can be a valuable tool for clarifying the anatomy of the human extrapyramidal system.

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