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Journal of neural transmission. General section

3 papers in the library · 26 citations · publishing 1993-1995

Papers

Evidence that ibogaine releases dopamine from the cytoplasmic pool in isolated mouse striatum.

Journal of neural transmission. General section January 1, 1994 L G Harsing, H Sershen, A Lajtha 26 citations

Ibogaine increases the release of dopamine from mouse striatum in a concentration-dependent way, primarily from the cytoplasmic pool rather than from vesicles, and this release is not regulated by presynaptic autoreceptors. The effect is reduced by dopamine uptake inhibitors but not by removing calcium or blocking sodium channels. Ibogaine does not affect dopamine uptake or retention. The dopamine-releasing action may contribute to its hallucinogenic effects observed in African ritual practices.

Delayed changes in neural visinin-like calcium-binding protein gene expression caused by acute phencyclidine administration.

Journal of neural transmission. General section January 1, 1995 Y Kajimoto, O Shirakawa, T Kuno et al.

In rats, the drug phencyclidine (PCP), which produces a schizophrenia-like state, reduced the expression of a calcium-binding protein called NVP-1 in the nucleus accumbens by 42% after 24 hours. This finding suggests that changes in calcium-binding proteins may contribute to the brain pathology underlying PCP-induced psychosis and possibly schizophrenia.

Phencyclidine treatment in mice: effects on phencyclidine binding sites and glutamate uptake in cerebral cortex preparations.

Journal of neural transmission. General section January 1, 1993 P Saransaari, S M Lillrank, S S Oja

Chronic treatment with phencyclidine (PCP), a psychotomimetic drug, alters glutamatergic neurotransmission in mice. After PCP administration via implanted minipumps (1 mg per mouse per day for 3 days), the binding capacity of TCP to cortical membranes increased, indicating more binding sites became available, while binding affinity remained unchanged. The actions of glutamate, its receptor agonists, and glycine were potentiated. Glutamate uptake showed changes in transport kinetics: the high-affinity component's transport constant increased and its maximal velocity increased, while the low-affinity component's maximal velocity decreased. Inhibition by structural analogues was also potentiated, suggesting modification of the glutamate transporter. These findings indicate that chronic PCP treatment, used as a psychosis model, markedly affects glutamatergic parameters.