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Biomedical subjects

Y Agid

Publications and source records attributed to Y Agid.

At least 577 records · Page 32Linked to original sources
PubMed1977

Retrograde axonal transport of 125I-tetanus toxin as a tool for tracing fiber connections in the central nervous system; connections of the rostral part of the rat neostriatum.

After previous studies had shown that 125I-tetanus toxin is taken up with high efficiency by all (adrenergic, sensory and motor)peripheral nerve terminals and that it is transported retrogradely by intraaxonal transport to the corresponding cell bodies, the present experiments were designed to investigate whether 125I-tetanus toxin could be used as a tool for retrograde tracing of fiber connections in the central nervous system and how the results obtained compared with other available retrograde tracing methods. Three to 12 h after injection of 125I-tetanus toxin into the rostral part of the nucleus caudatus of the rat, heavily labeled nerve cells were found in the substantia nigra zona compacta, in Forel field H2 and parts of the zona incerta, and in specific thalamic intralaminar nuclei (nucleus medialis pars lateralis and nucleus parafascicularis). Moderately labeled neurons were observed in the nucleus ventralis thalami and its dorsomedial part, in the nucleus raphe dorsalis and in the frontal, cingular and occipital cortex. Besides the labeling by retrograde transport, orthograde transport of radioactivity occurred in a striatonigral system. The high sensitivity and reliability of this method, even after injection of very small amounts of protein in a very small volume, represent important advantages over most of the commonly used tracing methods.

Animals↗
PubMed1977

["Beginning and end of dose" dyskinesias caused by L-DOPA].

The four cases of dyskinesia at the "beginning and end of dose" caused by L-Dopa presented in this series were characterized by four essential features: 1) their onset at the beginning and end of the period of effectiveness of a dose of L-Dopa + IDC (benserazide); 2) their ballic and dystonic appearance associated with a reinforcement of Parkinsonian signs; 3) the possibility of their reduction by an increase and fractionning of the daily dose of L-Dopa; 4) the particular nature of the underlying Parkinsonian problem in which they were seen, i.e. the young age at onset of the disease, the severity of akinesia, and the quality of the clinical response to L-Dopa. Thus on the basis of the circumstances of their development, their appearance, and their treatment, such forms of dyskinesia at the "beginning and end of dose" appear to be different from classical "mid-dose" dyskinesia. In addition, they pose a new physiolopathological problem.

Benserazide↗
PubMed1976

Specificity of dopaminergic neuronal degeneration induced by intracerebral injection of 6-hydroxydopamine in the nigrostriatal dopamine system.

The neurotoxic specificity of injections of 6-hydroxydopamine (6-OHDA) into areas containing either dopamine (DA) cell bodies (substantia nigra) or DA axon terminals (striatum) was studied. This selective effect was compared to the unspecific effects of copper sulfate (CuSO4) injection and electrocoagulation. One to two days after unilateral nigral injection of 2 mug of either 6-OHDA or CuSO4 into the nigra the volume of the unspecific lesions around the tip of the cannula was very similar. Only the 6-OHDA-induced lesions were associated with elective degeneration of the nigral DA neurons. Ten days after the administration of the same compounds the gliosis in the substantia nigra was much more extensive in CuSO4-than in 6-OHDA-treated rats; however, the reduction of DA concentrations in the ipsilateral striatum was only noticeable after 6-OHDA (-62%). A somewhat similar decrease of striatal DA levels (-52%) was observed after large electrocoagulation of the substantia nigra. Ten days after 6-OHDA (8mug) or electrolytic lesion of the striatum the Km for DA, serotonin and choline uptakes were similar in the striata of both sides, suggesting that the uptake process in the non-damaged neurons of the lesioned side was functionally normal. Following electrolytic lesion of the striatum, serotonin and choline Vmax values were decreased to about the same extent as the striatal reduction in weight and DA levels. When directly administered into the striatum 6-OHDA also produced a decline in DA concentration and Vmax but in contrast did not affect serotonin and choline uptake (Vmax), suggesting that the drug specifically destroyed dopaminergic neurons. The present data confirm that selective DA denervation can be achieved when appropriate amounts of the drug are injected into brain tissue in order to limit the unspecific lesion.

Animals↗
PubMed1975

Oxotremorine- and atropine-induced changes of dopamine metabolism in the rat striatum.

The effects of various doses of oxotremorine and of atropine (30 min, i.p.) on the metabolism of dopamine were examined in the striatum of the rat. Changes in striatal dopamine metabolism were estimated by following either the accumulation of [3H] dopamine 15 min after intravenous injection of [3H] tyrosine or the accumulation of dopa (taken as an index of dopamine synthesis) in animals pretreated with a dopa decarboxylase inhibitor Ro4-4602. Oxotremorine, 0-1 mg kg-1, and atropine, 1 mg kg-1, did not affect dopamine metabolism. Oxotremorine, 0-5 and 1-5 mg kg-1, did not modify dopamine concentrations but increased the accumulation of [3H]dopamine. The drug enhanced dopa formation in animals pretreated with Ro4-4602. Atropine, 5 and 20 mg kg-1, increased the accumulation of [3H]dopamine but did not affect dopamine concentrations. The accumulation of dopa was not modified there being no difference from the saline value in animals pretreated with the dopa decarboxylase inhibitor at high dopamine metabolism and atropine reduced dopamine utilization.

Animals↗