Biomedical subjects

F C Tortella

Publications and source records attributed to F C Tortella.

93 records · Page 6Linked to original sources

PubMedDate not supplied

Repeated electroconvulsive shock or chronic morphine treatment increases the number of 3H-D-Ala2,D-Leu5-enkephalin binding sites in rat brain membranes.

Experiments were performed in rats to evaluate the possible mechanisms responsible for the pharmacological cross-sensitization observed between repeated electroconvulsive shock (ECS) and chronic morphine administration. Repeated daily ECS for 9 days as well as chronic morphine pellet implantation resulted in a significant increase in the number of 3H-DADLE binding sites (Bmax values of 231 and 196 fmoles/mg protein, respectively). By contrast, single ECS, repeated sham ECS, and placebo pellet-treated rats all had significantly lower Bmax values (approx. 170 fmoles/mg protein). Affinities were not significantly altered by these treatments (Kd values between 3.1 and 4.0 nM). These data may link pharmacological cross-sensitization (repeated ECS and chronic morphine treatment) with a functional increase in the number of available opioid receptors.

Animals↗

PubMedDate not supplied

Pituitary opioid involvement in ECS-postictal electrogenesis and behavioral depression in rats.

The role of pituitary opioids in electroconvulsive shock (ECS)-induced postictal electrogenesis and behavioral depression was investigated in sham-hypophysectomized and hypophysectomized rats. These animals were divided into two subgroups and injected SC with either saline or naloxone (3 mg/kg) 10 min prior to transauricular ECS. Sham-hypophysectomized rats given saline responded to a single ECS with a 65 +/- 18% (s.e.) increase in postictal electrogenesis and a behavioral depression lasting 3840 +/- 530 sec. Naloxone significantly antagonized both the postictal increase in EEG voltage output and behavioral depression. Hypophysectomy by itself was without effect on EEG patterns and only partially attenuated the ECS-induced electrogenesis and postictal depression (31.9 +/- 9% and 2360 +/- 511 sec, respectively). However, in hypophysectomized rats, naloxone did not further antagonize these effects of ECS. Thus, it appears that pituitary opioids may, at least in part, mediate postictal electrogenesis and behavioral depression. Alternatively, since hypophysectomy only partially attenuates these phenomena, central or nonpituitary opioid peptide systems may be involved. In view of the observed decrease in responsiveness to naloxone in hypophysectomized rats, nonopioid systems cannot be ruled out as contributors to the opioid-like effects of ECS in these animals.

Animals↗

PubMedDate not supplied

Anticonvulsant effects of mu (DAGO) and delta (DPDPE) enkephalins in rats.

The effects of highly selective mu and delta opioid peptide agonists were determined in two rat models of experimentally-induced convulsions, the flurothyl threshold test and the maximal electroshock test. Intracerebroventricular injections of the mu selective enkephalin DAGO (0.3-2.2 nmol) resulted in a dose-related protection in both seizure models. Pretreatment with a low dose of naloxone (29 nmol) or the irreversible mu antagonist beta-FNA (21 nmol), but not the delta opioid antagonist ICI 154,129 (50 nmol), antagonized the anticonvulsant actions of DAGO. Intracerebroventricular injections of the delta selective enkephalin DPDPE (70-140 nmol) also resulted in seizure protection. These effects were selectively antagonized by the delta antagonist ICI 174,864 (2.8 nmol), but not by pretreatment with beta-FNA. Thus, using agonists and antagonists highly selective for mu and delta opioid receptors, anticonvulsant actions of enkephalin have been described against chemically- and electrically-induced convulsions in rats.

Animals↗