Download Dyskinesia: Research and Treatment by P. Seeman (auth.), Daniel E. Casey MD, Thomas N. Chase MD, PDF

By P. Seeman (auth.), Daniel E. Casey MD, Thomas N. Chase MD, Anne Vibeke Christensen MSc Pharm, DSc, Jes Gerlach MD (eds.)

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When progabide was administered concomitantly with the neuroleptic the increase in the density of 3H-spiroperidol binding sites was almost totally prevented (Table 1). This suggests that progabide prevents the proliferation of striatal DA receptors induced by chronic neuroleptic treatment. These biochemical changes may explain pharmacological findings 41 Influence of GABA Mimetics and Lithium on Biochemical Manifestations Table 1. 1 % Tween 80) or with haloperidol (2 mgjkg IP) for 14 consecutive days.

Secondly, on a long-term basis, they antagonize the proliferation of striatal dopamine receptors subsequent to chronic neuroleptic treatment. Thirdly, they modulate the expression of dopamine receptor activation by acting distally to the dopaminergic synapse. Lithium and GABA mimetics have the last two properties in common. These effects may represent the biochemical basis for the therapeutic action of GABA mimetics in iatrogenic dyskinesias. Moreover, the similarity between the biochemical effects of GABA mimetics and lithium suggest that the former drugs may have a therapeutic potential in mania.

We have recently investigated the effect of Li on different neurochemical indices of striatal DA target cell supersensitivity (Le Douarin et al. 1983). g/h by means of osmotic minipumps) did not influence tolerance to the increase in DA turnover or to the diminution of ACh levels in the striatum of the rat, which normally occur during prolonged neuroleptic treatment. 01). These data taken together indicate a striking similarity between Li and GABA mimetics with respect to their effects on behavioral and neurochemical indices of striatal DA target cell hypersensitivity.

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