Cerebellar pathways to ventral midbrain and nigra.
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Biomedical subjects
Publications and source records attributed to S R Snider.
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The dopamine agonist, bromocriptine, produced either inhibition or stimulation of motor behaviour in rats depending upon the dose and time after administration. Stimulation of motor activity occurred only with high doses after a 1-2 h delay. Both inhibition and stimulation were associated with decreased turnover of dopamine in the brain. Release of noradrenaline in brain and noradrenaline plus adrenaline in adrenal varied with motor activity. It is suggested that low doses of bromocriptine inhibit behaviour by activating an inhibitory presynaptic receptor, resulting in reduced synthesis and release of dopamine, whilst high doses cause behavioural excitation by activating the post-synaptic dopamine receptor.
Forty-three of 101 outpatients with parkinsonism reported that they regularly experienced primary sensory symptoms, i.e., spontaneous abnormal sensations not caused by somatic disease. This is in contrast to similar symptoms reported by only 8 percent of a control population. The most striking and severe symptom was burning of the trunk and proximal extremities, occurring in 11 patients. Twenty-nine patients reported spontaneous pain; a variety of other paresthesialike sensations, e.g., tingling, numbness, and formication, occurred in 32 patients. These subjective sensory phenomena were not associated with sensory loss or autonomic or motor signs. In 20 percent of affected individuals (9 percent of the total), sensory symptoms preceded the onset of the movement disorder, causing difficulty in diagnosis. It is concluded that at least some sensory symptoms originate within the nervous system as a manifestation of the disease process and are not secondary effects of the motor disorder.
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Rats received intravenous injections of 3H-tyrosine and were killed at various time intervals thereafter. 3H-dopamine (DA) in the adrenals reached a maximum within 1.5 min after the administration of 3h=tyrosine. From the 15th min it disappeared with an apparent half life of 90 min. 3H-Adrenaline (A) plus 3H-noradrenaline(NA) increased much more slowly and reached a plateau 120-240 min after the injection. The approximate synthesis rate of adrenal A plus NA, calculated from the specific activity curves, ranged from 0.3 to 2.2 nmoles/h per kg b.w. The highest value was noted the first few minutes, the lowest 1-2 hrs after the administration of 3H-tyrosine. In some experiments subcellular fractionation of the adrenals was performed. In untreated animals the amount of DA and A plus NA recovered from the supernatant fraction was about 10 and 8 per cent, respectively, of the total amount recovered from the supernatant and particulate fractions. In the adrenals of animals receiving 3H-tyrosine 3.75 or 60 min beforehand these figures were significantly elevated whereas the DA and A plus NA of the particulate fraction did not deviate significantly from control values. The specific activities of 3H-DA were the same in the supernatant and particulate fractions within 3.75 min after the injection of 3H-tyrosine.
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