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PubMed1984

Electroshock-induced increase in [3H]prazosin binding to cortical membranes in reserpinized rats.

Chronic, spaced electroconvulsive shock (ECS, 6 treatments at 72 h intervals) produced a moderate (16%) increase in the density of [3H]prazosin binding sites to rat cerebral cortical membranes. The increase was of borderline significance (0.1 greater than P greater than 0.05) and KD was not affected. The effect was similar but much more pronounced (increase in Bmax by 38%, P less than 0.01) in rats receiving reserpine pretreatment (4 mg/kg i.p.) 24 h before each ECS. Reserpine produced a transient increase in [3H]prazosin binding 24 h but not 48 h after the last dose, at the time when the ECT effect was measured.

Animals↗
PubMed1989

Redistribution of haloperidol after electroshock: experimental evidence.

We have previously reported that plasma and red blood cell levels of haloperidol, a neuroleptic agent, significantly increased immediately after electroconvulsive shock therapy (ECT) in schizophrenic patients on long term haloperidol treatment. To elucidate the mechanism of this increase, we attempted to reproduce this phenomenon in female Wistar rats. After 4 successive days of ip administration of haloperidol (10 mg/kg body weight, once daily), rats were given ECT through corneal electrodes on the fifth day (a.c. 50 Herz, 55 mA, 2.0 sec). Haloperidol levels were determined in plasma and other major tissues using a radioreceptor assay for haloperidol distribution before and after ECT at appropriate time intervals. Plasma haloperidol level was significantly increased 1 min after ECT but tended to return to the control level (without ECT) after 5 min. A significant decrease in haloperidol concentration in tissues was not observed in any of the tissues examined including frontal cerebrum, striatum, and muscle tissues (gluteal muscles). However, the relatively high haloperidol level and the large volume of muscle tissues suggested that the muscle could be the source of the transient increase in haloperidol levels in plasma. This conclusion was also supported by the data showing no significant rise of plasma haloperidol level after ETC in rats previously given a muscle relaxant, succamethonium chloride.

Animals↗
PubMed1990

PD117302, a selective non-peptide opioid kappa agonist, protects against NMDA and maximal electroshock convulsions in rats.

The pharmacological profile of PD117302 was studied in three rat models of experimental seizures. It was determined that PD117302 is a potent and efficacious anticonvulsant against NMDA (ED50 = 0.27 mg/kg, i.v.) and MES (ED50 = 16.3 mg/kg, s.c.), but not flurothyl, convulsions. Its anticonvulsant profile was dose- and time-dependent, stereospecific and sensitive to naloxone and the selective kappa opioid antagonist nor-binaltorphimine. Given these findings, we suggest that PD117302 acts via the kappa receptor to modulate seizure protection. Furthermore, in view of its marked ability to block NMDA excitotoxicity (including lethality) it seems possible that this drug, or related compounds, may have potential therapeutic utility as a neuroprotective agent.

Animals↗