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    Partial protection by CDP-choline against kainic acid-induced lesion in the rat caudate nucleus.

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    The acute intraperitoneal administration of CDP-choline to rats caused an increase in striatal dopamine (DA) synthesis, measured by DOPA accumulation after decarboxylase inhibition. Moreover, the chronic treatment with CDP-choline induced a decrease in the total number of 3H-spiroperidol binding sites, while partially antagonizing the disappearance of DA-sensitive adenylate cyclase activity elicited by intrastriatal kainic acid. These results suggest that CDP-choline may have a trophic and/or stimulant action on the function of nigrostriatal dopaminergic neurons

    Self-inhibitory dopamine-receptors and central effects of apomorphine.

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    Apomorphine, a central dopamine-receptor agonist, is well known to produce excitatory effects in animals. However, low doses exert depressant effects as hypomotility, sedation and sleep. The mechanism of these effects are discussed in terms of a stimulation by apomorphine of DA-receptors, different from the post-synaptic ones, provided of an inhibitory effect on DA-synthesis and on the firing of dopaminergic neurons

    Role of dorsal mesencephalic reticular formation and deep layers of superior colliculus in turning behaviour elicited from the striatum1

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    Kainate or electrolytic lesions were placed unilaterally in the dorsal mesencephalic reticular formation (MRF) or in the deep layers of the superior colliculus (DLSC) on the same side of a unilateral lesion of the medial forebrain bundle with 6-OHDA. Before the lesions the rats turned contralaterally when challenged with 0.25 mg/kg of apomorphine. After lesions of the MRF most rats turned ipsilaterally in response to the same dose of apomorphine. After lesions of the DLSC apomorphine-induced contralateral turning was significantly reduced but not abolished. The results indicate that the MRF and DLSC play a primary role in the expression of turning originated from the striatum

    Opposite turning effects of dainic and ibotenic acid injected in the rat substantia nigra

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    Unilateral intranigral administration of kainic and ibotenic acid, two putative stimulants of glutamatergic mechanisms, elicited turning behaviour starting from doses of 10 ng. While the turning produced by kainic acid was ipsilateral, that produced by ibotenic acid was contralateral to the injected side. Previous destruction of dopaminergic neurons on the side of the intranigral injection failed to reduce the turning behaviour. Peripheral treatment with picrotoxin did not reduce the turning in response to ibotenic acid. The results might suggest the existence of excitatory and inhibitory glutamate receptors which control nigral non-dopaminergic neurons mediating turning-behaviour
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