Rats chronically implanted with push-pull cannulas were injected with a pulse of 14C-norepinephrine (NE) into the lateral cerebroventricle under a variety of pretreatment and behavioral conditions. Animals pretreated intraventricularly with 6-hydroxydopamine (Group A) or ascorbic acid vehicle (Group B) were subsequently perpised imder fpur conditions: (1) presentation of a novel, visual stimulus in a one-way avoidance chamber; (2) presentation of the light (CS) followed by shock; (3) training to a high level of avoidance behavior, after which the CS was presented in the absence of opportunity for an avoidance response and in the absence of shock; and (4) after forced extinction, followed by CS without opportunity to aboid and with out presentation of shock. Samples of perfusate from rats subjected to the four test conditions were analyzed by thin-layer chromatography for total 14C in a scintillation counter and for proportion of NE and normetanephrine (NM). During Tests 1 and 4 the 14C perfusion wash-out did not differ from control values for either Group A or B. During Test 2, total radioactivity as well as the proportions of NE and NM increased in the perfusate for both Groups A and B. Presenting the CS without shock (3) resulted in 14C and NE and NM for Group B (vehicle), but not for Group A (6-OHDA). To test for non-specific release unrelated to a brain catecholaminergic function, another group of rats was subjected to identical treatments with the exception that 14C-urea replaced 14C-NE as a pulse-label. In these animals Test 2 (shock) induced an increase in 14C in the perfusate, while Tests 1, 3 and 4 yielded wash-out curves essentially identical to controls.

Animals↗

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Comparison of 2, 5-dimethoxy-4-methylamphetamine (DOM) and d-amphetamine for in vivo efflux of catecholamines from rat brain.

The neurochemical effects of DOM and d-amphetamine were compared under several conditions in unanesthetized rats implanted with chronic-indwelling push-pull cannulae in a cerebral lateral ventricle. Brain catecholamine storage sites were previously pulse-labelled with 14-C-norepinephrine administered intraventricularly. During the perfusion of the lateral ventricles with artificial cerebrospinal fluid, the animals were injected i.p. with 1.5 mg/kg of DOM, 2.0 mg/kg of d-amphetamine or 1.0 ml/kg of isotonic saline. Analysis of the perfusate in successive samples indicated an increased efflux of 14-C-radioactivity in rats administered DOM or d-amphetamine. Increased proportions of 14-C-norepinephrine and 14-C-normetanephrine were detected in samples of perfusate 15 to 30 min after drug injection. Pretreatment of other animals with 6-hydroxydopamine intraventricularly, which decreased brain levels of both norepinephrine and dopamine, blocked the increased efflux of 14-C-radioactivity induced by DOM or d-amphetamine. Pretreatment of rats with 6-hydroxydopa i.p., which depleted brain norepinephrine selectively, reduced to about half the d-amphetamine-induced efflux of 14-C-radioactivity for all samples during the time course of the effect. However, animals pretreated with 6-hydroxydopa and then tested for DOM effects showed a different pattern of 14-C-radioactivity efflux. The efflux for the initial samples was increased as with the DOM control, but the 6-hydroxydopa pretreatment attuated the DOM-induced efflux for the later samples. The results suggest DOM and d-amphetamine share qualitatively similar effects in releasing and/or blocking the reuptake of catecholamines at brain periventricular nerve terminals. Nevertheless, DOM appears to differ from d-amphetamine in the temporal pattern of net catecholamine release.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗

PubMedDate not supplied

Developmental neurotoxicity of polybrominated biphenyls.

Female F0 generation Sprague-Dawley rats received daily oral doses of 0, 0.2, or 2 mg/kg polybrominated biphenyls (PBB) as fireMaster BP-6 from Day 6 of gestation through Day 24 postpartum. Maternal parameters were assessed, and F1 generation offspring were evaluated for growth and survival, as well as physical and behavioral development. No adverse maternal effects were observed nor were there PBB-related effects on survival of the F1 generation or acquisition of developmental landmarks. Crown-rump length of 0.2 and 2 mg/kg male offspring was significantly less than that of controls and 2 mg/kg male and female offspring gained significantly less weight than did controls for the entire 60-day postnatal observation period. An overall evaluation of behavior by multivariate analysis of variance revealed significant PBB-related effects for acquisition of forward locomotion, cliff avoidance, cage emergence, and open-field activity of male and female offspring from dams administered 2 mg/kg. Delays in acquisition of forward locomotion and suppressed open-field activity were the most prominent effects. These indications of growth retardation and neurobehavioral toxicity occurred at concentrations of PBB in offspring body fat in the range of those which have been reported for highly exposed human subjects with neurological sequelae.

Aging↗

PubMedDate not supplied

Behavioral changes in rats after chronic aluminum and parathyroid hormone administration.

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Aluminum↗