The experimental evidence for the antipyretic action of arginine vasopressin (AVP) in guinea-pigs can be summarized as follows: The febrile response to a bacterial pyrogen can be reduced by a microinfusions of exogenous AVP into the ventral septal area of the limbic system. Immunohistochemical studies indicate increased activity of AVP terminals in the ventral septal area (VSA) and in parvocellular AVP neurones of the hypothalamic paraventricular nucleus (PVN) in several stressful situations accompanied by reduced febrile responses (late stage of pregnancy, immobilization, cold adaptation, osmotic stimulation). Also the peripheral and/or central release of AVP measured in some of these situations is increased. Electrical stimulation of the PVN suppresses fever, this suppression can, at least partly, be cancelled by simultaneous intraseptal application of the vasopressinergic VI receptor antagonist. The documented AVP pathways from the PVN to the septum receive noradrenergic afferents from the lower brainstem. Chronic destruction of these afferents by microinjections of 6-hydroxydopamine (6-OHDA) significantly reduced the fever responses to pyrogen application, while microinfusion of noradrenaline (NA) enhances the fever reaction.
Hippocampus is a brain structure containing vasopressin (AVP) fibers and specific binding sites for this peptide. There is growing evidence that AVP and its metabolites participate in glutamate-mediated plasticity of the hippocampus. The aim of the present study was to evaluate the influence of NMDA on AVP release in the rabbit hippocampus. Caudate nucleus was chosen as the reference structure. The mentioned brain structures were simultaneously microdialyzed with 0.9 % NaCl solution. AVP was determined in the outflowing fluid by radioimmunoassay. The mean basal AVP content in the fluid outflowing from the hippocampus was significantly greater than that from the caudate nucleus. The addition of K+ into the fluid perfusing the probes implanted into the hippocampus and caudate nucleus significantly increased AVP release into the extracellular fluid of both brain structures. NMDA applied into the mentioned brain structures increased AVP release only from the hippocampus but not from the caudate nucleus. Our findings indicate a role which NMDA receptors play in AVP release into the extracellular fluid of the hippocampus., M. Orłowska-Majdak, W. Z. Traczyk, D. Szymański., and Obsahuje bibliografii
Galanin (GAL) is suggested to be a neuropeptide involved in pain transmission. In this study we tried to determine, whether the increase of GAL concentration in brain cells affects impulse transmission between the motor centers localized in the vicinity of the third and fourth cerebral ventricles. The experiments were carried out on rats under chloralose anesthesia. The study objectives were realized using the method allowing to record the amplitude of evoked tongue jerks (ETJ) in response to noxious tooth pulp stimulation during the perfusion of the cerebral ventricles with solutions containing tested compounds. Perfusion of the cerebral ventricles with GAL concentration-dependently inhibited the ETJ amplitude. The antinociceptive effect of GAL was blocked by a galanin receptor antagonist, galantide (GLT) and by opioid antagonists: non-selective naloxone (Nal) and μ-selective β-funaltrexamine (β-FNA). In contrast, a δ-opioid receptor antagonist, naltrindole (NTI) or the κ-opioid receptor antagonist, nor-binaltrophimine (nor-BNI) did not inhibit the effect of GAL. The antinociceptive effect of GAL was more pronounced when GAL was perfused in combination with other neuropeptides/neurohormones, such as endomorphin-2 (EM-2), vasopressin (AVP) and oxytocin (OT). The present results demonstrate that in the orofacial area analgesic activity is modulated by GAL, OT and AVP and that EM-2-induced antinociception involves GAL., M. Zubrzycka, A. Janecka., and Obsahuje bibliografii a bibliografické odkazy
Previous studies have substantiated the antipyretic role played by extrahypothalamic limbic system (EXHY-LS) AVP during fever. Repeated attempts to elucidate other thermoregulatory functions of this hormone have failed. Circumstantial evidence, however, suggest central role for this hormone in thermoregulation under hypohydration. Hypohydration, hyperosmolarity and hypovolaemia induce upward shifts in temperature thresholds for activation of heat dissipating mechanisms. When hypovolaemia is superimposed on hyperosmolarity these shifts are additive. Analogously, these two stressors when combined, decrease the osmotic threshold for AVP release. In rats, the elevated temperature thresholds for evaporative cooling and peripheral vasodilation occurring with hypohydration are positively correlated with lower Hypothalamic/EXHY-LS AVP ratio. Reciprocal relations between limbic system and blood AVP contents suggest competitive interaction between central and peripheral demands. Hypothesis for the possible mode of action of central AVP in thermoregulation under hypohydration is discussed.