ABSTRACT
The inferior colliculus (IC) is an important midbrain relay station for the integration of descending and ascending auditory information. In addition, it has also been implicated in the processing of acoustic information of aversive nature, as well as in sensory-motor gating. There is evidence that glutamate-mediated mechanisms at the IC level influence haloperidol-induced catalepsy. The present study investigated the influence of glutamate-mediated mechanisms in the IC on catalepsy induced by intrastriatal microinjection of haloperidol (10 µg/0.5 µl). Male Wistar rats received bilateral intracollicular microinjections of the glutamate receptor agonist NMDA (10 or 20 nmol/0.5 µl), the NMDA receptor antagonists MK-801 (15 or 30 nmol/0.5 µl) or physiological saline (0.5 µl), followed by bilateral microinjections of haloperidol (10 µg/0.5 µl) or vehicle (0.5 µl) into the dorso-rostral or ventro-rostral striatum. The catalepsy test was performed positioning both forepaws of the rats on an elevated horizontal wooden bar and recording the time during which the animal remained in this position. The results showed that the administration of physiological saline in the IC followed by the microinjection of haloperidol in the dorso-rostral region of the striatum was not able to induce catalepsy. However, when the bilateral administration of NMDA into the IC was followed by microinjection of haloperidol into the dorso-rostral striatum, catalepsy was observed. The microinjection of haloperidol into the ventro-rostral striatum induced catalepsy, counteracted by previous administration of MK-801 into the IC. These findings suggest that glutamate-mediated mechanisms in the IC can influence the intrastriatal haloperidol-induced catalepsy and that the IC plays an important role as a sensorimotor interface.
Subject(s)
Antipsychotic Agents/adverse effects , Catalepsy/chemically induced , Glutamic Acid/metabolism , Haloperidol/adverse effects , Inferior Colliculi/drug effects , Inferior Colliculi/physiopathology , Animals , Catalepsy/physiopathology , Corpus Striatum/drug effects , Corpus Striatum/physiopathology , Dizocilpine Maleate/pharmacology , Excitatory Amino Acid Antagonists/pharmacology , Male , N-Methylaspartate/metabolism , Rats, Wistar , Receptors, N-Methyl-D-Aspartate/agonists , Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors , Receptors, N-Methyl-D-Aspartate/metabolism , Synaptic Transmission/drug effects , Synaptic Transmission/physiologyABSTRACT
The zona incerta, located in the ventral thalamus, is a site of convergence of signals related to drinking. In the present experiments, agonists and antagonists of dopamine receptors were injected into the ZI of animals deprived of water overnight. Injection of 53 nM dopamine or the D2 dopamine receptor agonist PPHT caused a reduction of water and food intake, while the injection of the D1 receptor agonist SKF38393 had no effect. The current results suggest that dopamine injected into the ZI exerts inhibitory influences on drinking behavior mediated by D2 type receptor.
Subject(s)
Drinking/physiology , Receptors, Dopamine/physiology , Thalamic Nuclei/physiology , Thirst/physiology , Animals , Brain Mapping , Dopamine/physiology , Male , Neural Inhibition/physiology , Rats , Receptors, Dopamine D2/physiology , Water Deprivation/physiologyABSTRACT
Acute sodium depletion by peritoneal dialysis (PD) induces c-fos expression in the subfornical organ (SFO) and organum vasculosum laminae terminalis (OVLT), in conscious rats. Fos immunoreactive (Fos-ir) neurons detected by immunohistochemistry first appeared in these nuclei 60 min after PD, increased gradually in the next 4 h and remained high for 27 h following PD. Fos-ir cells were distributed throughout the body of SFO, being the core of the posterior sections preferentially activated, whereas Fos-ir neurons occurred around the periphery of OVLT (annular disposition). When rats were allowed to drink sodium salt (1.8% NaCl) 24 h after PD, there was a marked reversion of the c-fos expression in the OVLT and a comparatively smaller effect in the SFO. Intracerebroventricular infusion of hypertonic CSF (170 mM NaCl) from 30 min before and during 4 h after PD, significantly inhibited the c-fos expression in both nuclei. These results demonstrate that an acute body sodium deficit induces c-fos activity in SFO and OVLT neurons, indicating the special role of these structures in sodium balance regulation. They also show that the sodium-depletion-induced production of Fos in neurons of the lamina terminalis can be modulated by central or systemic reposition of sodium.
Subject(s)
Cerebral Ventricles/chemistry , Hypothalamus/chemistry , Nerve Tissue Proteins/analysis , Proto-Oncogene Proteins c-fos/analysis , Sodium/metabolism , Subfornical Organ/chemistry , Analysis of Variance , Animals , Evaluation Studies as Topic , Immunohistochemistry , Male , RatsABSTRACT
Physiological evidence indicates that the zona incerta (ZI) may be an important region for convergence of signals mediating drinking. It is known that the ZI receives neural influences from brain osmoreceptive zones. Also there are wide-spread projections from the ZI to the neocortex. In the present experiments, lidocaine (1 microliter, 20 ng/microliters) was injected into the rostral aspect of the ZI. The animals were previously stimulated for water drinking by: a) overnight water deprivation; b) 2 M NaCl IP; c) AII (50 ng) in the anteroventral wall of the third ventricle (AV3V). In every case, lidocaine administration significantly enhanced the volume of water drank. The results support the idea that ZI exerts an inhibitory influence upon the expression of drinking behavior.