ABSTRACT
The purpose of this study was to investigate the role that mu and delta opioid receptor blockade has upon stimulant-induced behavior and neuropeptide gene expression in the striatum. Acute administration of amphetamine (2.5 mg/kg i.p.) caused an increase in behavioral activity and preprodynorphin, substance P, and preproenkephalin mRNA expression. Intrastriatal infusion of the mu opioid antagonist, H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH(2) (CTAP), or the delta opioid antagonist, H-Tyr-Tic[CH(2)NH]-Phe-Phe-OH (TIPPpsi), significantly decreased amphetamine-induced vertical activity. However, only CTAP reduced amphetamine-induced distance traveled. Quantitative in situ hybridization histochemistry revealed that CTAP blocked amphetamine-induced preprodynorphin and substance P mRNA. However, preproenkephalin mRNA levels in the dorsal striatum were increased to the same extent by CTAP, amphetamine, or a combination of the two drugs. In contrast, TIPPpsi significantly decreased amphetamine-induced mRNA expression of all three neuropeptides. These data indicate that both mu and delta receptor subtypes differentially regulate amphetamine-induced behavior and neuropeptide gene expression in the rat striatum.
Subject(s)
Amphetamine/pharmacology , Central Nervous System Stimulants/pharmacology , Corpus Striatum/drug effects , Neuropeptides/metabolism , Receptors, Opioid, delta/metabolism , Receptors, Opioid, mu/metabolism , Animals , Behavior, Animal/drug effects , Corpus Striatum/metabolism , Corpus Striatum/physiology , Drug Interactions , In Situ Hybridization , Male , Motor Activity/drug effects , Narcotic Antagonists/pharmacology , Neuropeptides/genetics , Oligopeptides/pharmacology , Peptide Fragments , Peptides/pharmacology , RNA, Messenger/metabolism , Radiographic Image Enhancement , Random Allocation , Rats , Rats, Sprague-Dawley , Receptors, Opioid, delta/antagonists & inhibitors , Receptors, Opioid, delta/physiology , Receptors, Opioid, mu/antagonists & inhibitors , Receptors, Opioid, mu/physiology , SomatostatinABSTRACT
Galanin (GAL) and nitric oxide synthase (NOS) have been implicated in the control of thermogenesis in mammals. An experimental protocol was designed to determine whether or not the expression of these molecules in the hypothalamus of the toad could be related to environmental temperature changes. Exposure of the animals to low temperature increased the number and intensity of NOS-positive neurons in the magnocellular hypothalamic region, in contrast to a weak immunoreactivity observed in control animals kept in a natural environment at a spring-summer temperature (23-27 degrees C). Also a significantly higher number of GAL-immunoreactive (-IR) cells was observed in the preoptic area as compared to that observed in controls, while no difference in the intensity of GAL immunostaining intensity was detected. These results show a temperature-related expression of GAL and NOS in the hypothalamus and preoptic area of the toad. The results suggest a possible role of GAL and NOS in the regulation of hibernation in these animals.
Subject(s)
Acclimatization/physiology , Bufo arenarum/metabolism , Galanin/metabolism , Hypothalamus/metabolism , Nitric Oxide Synthase/metabolism , Animals , Cell Count , Hypothalamus/cytology , Hypothalamus/enzymology , Immunohistochemistry , Male , TemperatureABSTRACT
The expression of the neuropeptide galanin was analyzed by immunohistochemistry in magnocellular and preoptic hypothalamic neurons of toads following hypophysectomy (HPX) and pars distalectomy (PDX). There was a marked increase in the galanin-like immunoreactive expression in magnocellular hypothalamic cells 3 days after HPX, followed by a decrease to normal levels after 7 days. No changes in the expression of galanin were detected after PDX in these neurons when compared to controls. Moreover, 7 days after HPX or PDX the number of cells expressing galanin was significantly increased in the preoptic area, where numerous intraependymal cells were intensely immunoreactive. The hypophysis grafts into the hind limb in HPX or PDX animals prevented increased galanin-like immunoreactivity in preoptic cells but not in magnocellular neurons. Similarly, PDX toads given growth hormone showed no GAL-LI in the intraependymal preoptic cells. These results suggest the presence of a region regulation of galanin expression in the preoptic area by hypophyseal hormones, in particular growth hormone.
