ABSTRACT
Neurotensin (NT), n active neuropeptide, and bicuculline, a GABA-A receptor antagonist, were microinjected into the rat hypothalaamus (MH) or the dorsal periaqueductal gray matter (DPAG). Bicuculline (80 pmol) produced behavioral activation which included jumping and NT (1-20 nmol) caused a dose-dependent behavioral activation accompanied by catalepsy rather than jumping. These results suggest that the behavioral activation produced by NT may be due to an interaction of the neuropeptide with specific receptors while its cataleptic effect may be attributed to the blockade of dopamine receptors
Subject(s)
Rats , Animals , Male , Bicuculline/pharmacology , Hypothalamus, Middle , Neurotensin/pharmacology , Runaway Behavior/drug effects , Periaqueductal Gray/physiology , DopamineABSTRACT
Eletrical stimulation or microinjection of GABA antagonists into the dorsal periaqueductal gray (DPAG) produces escape behavior. In order to determine whether the nigrocollicular gabaergic fibers exert some control over this behavior, rats bearing kainic acid lesion of the substantia nigra pars reticulata were submitted to microinjections of bicuculline or electrical stimulation of the DPAG at the escape threshold. Rats thus treated exhibited a significant decrease in the escape threshold while bicuculline increased the expression of flight behavior. These results suggest an inhibitory control of gabaergic fibers from the substantia nigra pars reticulata on aversive behavior induced by DPAG stimulation
Subject(s)
Rats , Animals , Male , Bicuculline/pharmacology , gamma-Aminobutyric Acid/antagonists & inhibitors , Runaway Behavior/drug effects , Substantia Nigra , Electric StimulationABSTRACT
In order to study the functional consequences of brain changes caused by early malnutrition, rats were fed a protein-deficient diet from birth until 49 days of age and a balanced diet from day 50 to day 70. The animals were submitted to a step-down inhibitory avoidance task and to the flinch-jump nociceptive test at 49 and 70 days of age. Malnourished rats showed longer step-down latencies and lower flinch and junp theresholds than eutrophic animals. Chlordiazepoxide (5 mg/Kg, ip) shortened step-down latency of well-nourished rats, whereas it failed to do so in malnourished rats. Since well-nourished animals also became resistant to chlordiazepoxide when tested with a higher shock intensity, generating avoidance latencies comparable to those of malnourished animals, we conclude that the drug resistance induced by malnutrition may be secondary to enhanced pain sensitivity and/or reactivity