Cannulae were implanted into forebrain loci of goldfish (Carassius auratus; 45-90 g) to determine (i) the effects and site of action of intracranial norepinephrine (NE) injections on behavioral thermoregulation and (ii) the mechanism and the types of adrenoreceptors involved in the thermoregulatory effect of NE. After 30 min in a thermal gradient, implanted fish were injected with norepinephrinebitartrate salt (2.5-500 ng NE) in a total volume of 0.2 ul (carrier was 0.7% NaCl). Injections of 5, 10, 25, and 50 ng NE into the anterior aspect of the nucleus preopticus periventricularis (NPP1 Peter and Gill 1975) led to consistent, dose-dependent decreases in selected temperature. No effect on temperature selection was observed following injections of 2.5 ng NE or control injections of 100 ng tartaric acid. The effects of injections into other loci, including intraventricular injections, were dependent upon the dose and proximity to the anterior NPP1 at sites adjacent to the anterior NPP, larger doses were required, and the effects became inconsistent. At sites further removed, no effect on selected temperature was observed1 included in this category were more caudal sites within the NPP and the nucleus preopticus.

Removal of the pineal gland from partially parathyroidectomized rats produces stereotyped violent seizures. Inasmuch as the neurotransmitter norepinephrine (NE) has been implicated in this experimental paradigm, the purpose of this study was to investigate the effect of specific alterations in catecholamine function on convulsions produced by pinealectomy (PinX). Additionally, the role of various pineal substances, sex differences and the caging paradigm in the convulsive response was studied. Male and female rats (grouped five per cage) were found to respond similarly to the convulsive stimulus of parathyroidectomy followed by PinX. Neither implants of melatonin nor ventricular injections of arginine vasotocin in isolated and grouped rats, respectively, produced consistent changes in convulsions from PinX. The method of caging the rats after PinX, however, dramatically influenced seizures. Isolated rats (one per cage) convulsed significantly later after PinX and did so less often than grouped (five per cage) controls. NE neurotransmission appears to play a strong role in influencing PinX-induced seizures. Augmenting NE function with desipramine suppressed seizures. Convulsions were enhanced by the (beta)-receptor antagonist timolol, while neonatal injections of the catecholamine neurotoxin 6-OHDA potentiated seizures so markedly that many rats died from just one convulsion. NE levels were significantly reduced in the telencephalons and increased in the brain stems of sham-pinealectomized rats which had also received neonatal 6-OHDA; telencephalic levels of DA were elevated by 6-OHDA. Both the proconvulsant effects of 6-OHDA and the alterations it produced in central catecholamine levels were prevented, for the most part, by pretreatment with DMI. Altering both NE and DA function with L-dihydroxyphenylalanine, (alpha)-methyl-p-tyrosine, FLA-63 or reserpine did not significantly affect PinX-induced seizures in isolated rats. NE appears to play a strong role in modulating PinX-induced seizures; however, a deficit in NE function per se does not seem to be the fundamental cause of the seizures since sham-pinealectomized rats having lowered NE and/or DA function did not convulse.