1,720,984 research outputs found
SYNTHESIS OF SOME 1-(3-HYDROXY-4-METHOXYBENZYL)-2-ALKYL-6,7-METHYLENEDIOXY-1,2,3,4-TETRAHY DROISOQUINOLINES AND THEIR BINDING AFFINITIES TO DA RECEPTOR SUBTYPES
No full textLesions of substantia nigra by kainic acid: effects on apomorphine-induced stereotyped behaviour
No full textFifteen days after bilateral lesions of the substantia nigra by local infusion of kainic acid (0.75 microgram) or after intranigral injection of vehicle, rats were administered 0.1, 0.25, 1.0 and 2.5 mg/kg s.c. of apomorphine and the stereotyped items (locomotion, sniffing and gnawing) were recorded on an event-recorder and motility was measured by a photocell apparatus. After low doses of apomorphine (0.1, 0.2 mg/kg), rats lesioned in the substantia nigra with kainic acid showed a degree of stimulation of motility and of sniffing similar to controls; on the other hand, in rats lesioned with kainic acid in the nigra, a dramatic reduction of gnawing and its replacement by sniffing was observed after administration of higher doses of apomorphine (1.0, 2.5 mg/kg). Bilateral infusion of kainic acid (0.75 microgram) into the reticular information, 2.0 mm dorsal to the substantia nigra, had no effect on apomorphine-induced stereotyped behaviour. These results are in agreement with the concept that the substantia nigra, through non-DA pars reticulata neurons, mediates motor and behavioural syndromes of striatal origin
Role of substantia nigra pars reticulata neurons in the expression of neuroleptic-induced catalepsy
No full textBilateral kainate-induced lesions of the substantia nigra prevented or dramatically reduced the catalepsy produced by haloperidol. In contrast, infusion of 1 or 4 micrograms 6-OHDA in the medial forebrain bundle, which decreased striatal DA by 30% and 80% respectively, failed to affect or actually potentiated haloperidol catalepsy. Since intranigral kainate, in contrast to 6-OHDA, destroys pars reticulata neurons it appears that these neurons are essential for the expression of haloperidol-catalepsy
Irreversible neuronal damage after intrastriatal injection of colchicine.
No full textIntrastriatal injection of 2 or 4 mg of colchicine results in loss of striatal perikarya without damage of mielinated boundies of passage. Neurochemical markers of intrinsle and afferent striatal neurons are markedly reduced on the lesioned sid
A re-evaluation of the role of superior colliculus in turning behaviour
No full textThere is much debate on the role of the superior colliculus (SC) in turning behaviour. In order to clarify this issue, unilateral kainate lesions were made by infusing 0.25 microgram of kainate at two different anterior planes (0.8 mm apart), in the lateral or in the medial aspects of the deep collicular layers (DLSC), in the dorsal mesencephalic reticular formation (MRF), or in the lateral periaqueductal grey (PAG), both in normal rats and in rats made unilaterally supersensitive to DA-receptor agonists by unilateral infusion of 6-OHDA in the rostral substantia nigra. The effect of kainate lesions on spontaneous and apomorphine-induced motor behaviour was studied. In normal rats, unilateral kainate lesions of lateral DLSC or dorsal MRF resulted in short-lasting, spontaneous ipsiversive turning and persistent ipsiversive circling after peripheral administration of apomorphine. In 6-OHDA rats, kainate lesions of lateral DLSC or of dorsal MRF ipsilateral to 6-OHDA denervation reduced or even reversed the contralateral circling normally elicited in these rats by peripheral administration of apomorphine. Lesions of dorsal MRF, when compared with lesions of lateral DLSC, were more effective in producing these changes. Kainate lesions restricted to medial DLSC or to the PAG failed to elicit motor asymmetries in normal rats or to significantly modify the intensity of contralateral turning in 6-OHDA rats. These results clearly indicate that the SC plays an important role in turning behaviour. Failure of previous studies to research this conclusion probably derives from inadequate localization of collicular lesions and from the use of bilateral lesions
Loss of striatal neurons after local microinjection of colchicine.
No full textIntrastriatal injections of colchicine (4 micrograms) produced irreversible striatal damage characterized 30 days later by loss of intrinsic striatal neurons, gliosis and shrinkage but no apparent damage to myelinated bundles of the internal capsule. This neuronal loss was associated with a dramatic reduction of striatal and nigral glutamate-decarboxylase (GAD), the marker of GABA-ergic synapses and of striatal choline-acetyltransferase (CAT), the marker of cholinergic synapses. The levels of dopamine (DA) and serotonin (5HT) in the striatum as well as those of their metabolites were also reduced, indicating that colchicine exerts toxic effects also on terminals of striatal afferent neurons
Substantia nigra as an efferent station for dopaminergic behavioral syndromes arising in the striatum
No full textOrigin of GABA-ergic strio-nigral neurons as studied by kainate-induced lesions
No full textKainic acid was used to clarify the source of nigral GABA-ergic terminals. Rats were microinjected unilaterally with kainic acid in the globus pallidus, head, body and tail of the caudate. Lesions of the pallidus resulted in a non-significative (5.5 %) reduction of nigral GAD. Kainic-lesions of the head of the caudate resulted in a significative (19%) drop of nigral GAD, while lesions of the caudate body resulted in the largest reduction of nigral GAD (53%). Lesions of the caudate tail were without effect. These results indicate that nigral GAD arises mostly from the body and in part, also from the head of the caudate but not from the globus pallidus or from the tail of the caudate
Evidence for selective and long-lasting stimulation of "regulatory" dopamine-receptors by bromocriptine (CB 154).
No full textBromocriptine, an ergot-derivate with DA-receptor stimulating properties in vivo, produces long-lasting hypomotility in mice not accustomed to the motility cage and decreases brain DOPAC and HVA without affecting brain DA. These effects are obtained with doses 25 times lower than those which produce hypermotility. The decrease of brain DOPAC is correlated to the hypomotility both on a dose- and on a time-basis. Potent neuroleptics as pimozide, benzperidol and droperidol, which are considered to be fairly specific DA-receptor blockers, antagonize the hypomotility and the decrease of brain DOPAC produced by bromocriptine. These effects are obtained with very low doses (0.05--0.3 mg/kg) of neuroleptics which per se do not affect motility or brain DOPAC. The maximal decrease of brain DOPAC and HVA produced by bromocriptine is similar to that produced by apomorphine and the combination of these drugs does not result in a further decrease of brain DOPAC or HVA. On the basis of these results it is postulated that bromocriptine decreases brain DA-turnover and produces hypomotility by acting on "regulatory" DA-receptors different from the post-synaptic ones of the "terminal" dopaminergic areas
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