Distribution of melanin-concentrating hormone neurons projecting to the medial mammillary nucleus

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Temporal changes in calcium-binding proteins in the medial geniculate nucleus of the monkey Sapajus apella

The subdivisions of the medial geniculate complex can be distinguished based on the immunostaining of calcium-binding proteins and by the properties of the neurons within each subdivision. The possibility of changes in neurochemistry in this and other central auditory areas are important aspects to understand the basis that contributing to functional variations determined by environmental cycles or the animal's cycles of activity and rest. This study investigated, for the first time, day/night differences in the amounts of parvalbumin-, calretinin- and calbindin-containing neurons in the thalamic auditory center of a non-human primate, Sapajus apella. The immunoreactivity of the PV-IR, CB-IR and CR-IR neurons demonstrated different distribution patterns among the subdivisions of the medial geniculate. Moreover, a high number of CB- and CR-IR neurons were found during day, whereas PV-IR was predominant at night. We conclude that in addition to the chemical heterogeneity of the medial geniculate nucleus with respect to the expression of calcium-binding proteins, expression also varied relative to periods of light and darkness, which may be important for a possible functional adaptation of central auditory areas to environmental changes and thus ensure the survival and development of several related functions.

Effect of nicotinic stimulation of the amygdaloid complex on water and sodium chloride intake

We studied the nicotine stimulation of the amygdaloid complex (AMG) on sodium and water intake in satiated and water-deprived rats. Nicotine produced no change in sodium or water intake in satiated animals when injected directly into the AMG. In water-deprived animals, nicotine injected into the AMG (basolateral nuclei) only blocked sodium chloride intake. We have previously demontrated that carbachol inhibits water and sodium intake in both satiated and water-deprived animals injected into the AMG. Injection of hexamethonium into the AMG totally blocked water intake in satiated and water-deprived animals. Hexamethonium injected into the AMG prior to nicotine produced no change in sodium intake. Thus, the present data suggest that sodium and water intake are mediated by a specific population of cholinoceptive neurons in the amygdaloid complex.

Effect of adrenergic stimulation of the amygdaloid complex on water intake

The effect of noradrenaline, isoproterenol, phentolamine and propranolol, injected into the basolateral nuclei of the amygdala on water intake, was investigated in male Holtzman rats. The injection of noradrenaline (40 nmol) into the amygdaloid complex (AC) of satiated rats produced no change in water intake (0.05 ± 0.03 ml/1 hour). The injection of isoproterenol (40 nmol) produced an increase in water intake in sedated rats (1.93 ± 0.23 ml/1 hour). Noradrenaline injected into the AC produced a decrease in water intake in deprived rats (0.40 ± 0.19 ml/1 hour). The injection of isoproterenol into the AC of deprived rats produced no change in water intake in comparison with control (11.65 ± 1.02 and 10.92 ± 0.88 ml/1 hour, respectively). When compared with control values, phentolamine injected prior to noradrenaline blocked the inhibitory effect of noradrenaline on water intake in deprived rats (10.40 ± 1.31 ml/1 hour). Propranolol blocked the effect of isoproterenol in satiated rats (0.85 ± 0.49 ml/1 hour) and also blocked the water intake induced by deprivation (0.53 ± 0.38 ml/1 hour). In satiated and deprived animals the injection of phentolamine before hexamethonium blocked the inhibitory effect of hexamethonium on water intake. In satiated animals, when hexamethonium was injected alone, water intake was 0.39 ± 0.25 ml/1 hour and when hexamethonium was injected with phentolamine, water intake was 1.04 ± 0.3 ml/1 hour. In deprived animals, hexamethonium alone blocked water intake (0.40 ± 0.17 ml/1 hour) and when injected with phentolamine it elicited an intake of 9.7 ± 1.8 ml/1 hour. these results clearly demonstrate the participation of catecholaminergic receptors of the AC in the regulation of water intake.

The Edinger-Westphal nucleus II: Hypothalamic afferents in the rat

Numerous functions have been attributed to the Edinger-Westphal nucleus (EW), including those related to feeding behavior, pain control, alcohol consumption and the stress response. The EW is thought to consist of two parts: one controls accommodation, choroidal blood flow and pupillary constriction, primarily comprising cholinergic cells and projecting to the ciliary ganglion; and the other would be involved in the non-ocular functions mentioned above, comprising peptide-producing neurons and projecting to the brainstem, spinal cord and prosencephalic regions. Despite the fact that the EW is well known, its connections have yet to be described in detail. The aim of this work was to produce a map of the hypothalamic sources of afferents to the EW in the rat. We injected the retrograde tracer Fluoro-Gold into the EW, and using biotinylated dextran amine, injected into afferent sources as the anterograde control. We found retrogradely labeled cells in the following regions: subfornical organ, paraventricular hypothalamic nucleus, arcuate nucleus, lateral hypothalamic area, zona incerta, posterior hypothalamic nucleus, medial vestibular nucleus and cerebellar interpositus nucleus. After injecting BDA into the paraventricular hypothalamic nucleus, lateral hypothalamic area and posterior hypothalamic nucleus, we found anterogradely labeled fibers in close apposition to and potential synaptic contact with urocortin 1-immunoreactive cells in the EW. On the basis of our findings, we can suggest that the connections between the EW and the hypothalamic nuclei are involved in controlling stress responses and feeding behavior. © 2013 The Authors.

Cannabidiol administration into the bed nucleus of the stria terminalis alters cardiovascular responses induced by acute restraint stress through 5-HT1A receptor

Systemic administration of cannabidiol (CBD) is able to attenuate cardiovascular responses to acute restraint stress through activation of 5-HT1A receptors. Previous results from our group suggest that the bed nucleus of the stria terminalis (BNST) is involved in the antiaversive effects of the CBD. Moreover, it has been proposed that synapses within the BNST influence restraint-evoked cardiovascular changes, in particular by an inhibitory influence on the tachycardiac response associated to restraint stress. Thus, the present work investigated the effects of CBD injected into the BNST on cardiovascular changes induced by acute restraint stress and if these effects would involve the local activation of 5-HT1A receptors. The exposition to restraint stress increased both blood pressure and heart rate (HR). The microinjection of CBD (30 and 60nmol) into the BNST enhanced the restraint-evoked HR increase, in a dose-dependent manner, without affecting the pressor response. The selective 5-HT1A receptor antagonist WAY100635 by itself did not change the cardiovascular responses to restraint stress, but blocked the effects of CBD. These results showed that CBD microinjected into the BNST enhanced the HR increase associated with acute restraint stress without affecting the blood pressure response. Although these results are not in agreement with those observed after systemic administration of CBD, they are similar to effects observed after reversible inactivation of the BNST. Moreover, similar to the effects observed after systemic administration, CBD effects in the BNST seem to depend on activation of 5-HT1A receptors. © 2012 Elsevier B.V. and ECNP.

The control of sodium chloride intake: Functional relationship between hypothalamic inhibitory areas and amygdaloid complex stimulating areas

Sodium chloride intake was studied in rats submitted to different neurosurgical procedures. Intake decreased in animals submitted to bilateral destruction of the basolateral amygdaloid complex, and increased after the same animals were submitted to destruction of the anterior lateral hypothalamus, a procedure which is known to cause increased intake in intact rats. In the reverse experiment, where the anterior lateral hypothalamus was destroyed before the basolateral amygdaloid complex, the effect of increased sodium chloride intake induced by destruction of the hypothalamus overcame the decreased expected upon destruction of the amygdaloid complex. These results permit us to conclude that the hypothalamic areas which inhibit sodium chloride intake predominate over the stimulating areas of the amygdaloid complex in the control of sodium chloride intake. © 1981 ANKHO International Inc.

Damage to the central amygdala produces differential encephalic c-fos expression in the water deprivation-partial rehydration protocol

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Interaction between paraventricular nucleus and medial septal area on the renal effects induced by adrenaline

The aim of the present study was to analyze the role of alpha(1),alpha(2)-adrenoceptors, and the effects of losartan and PD123319 (selective ligands of the AT(1) and AT(2) angiotensin receptors, respectively) injected into the paraventricular nucleus (PVN) on the diuresis, natriuresis, and kaliuresis induced by administration of adrenaline into the medial septal area (MSA). Male Holtzman rats with a stainless steel cannula implanted into the MSA and bilaterally into the PVN were used. The administration of adrenaline into the MSA increased in a dose-dependent manner the urine, sodium, and potassium excretions. The previous administration of prazosin (an alpha(1)-adrenoceptor antagonist) injected into the PVN abolished the above effects of adrenaline, whereas yohimbine (an a-adrenoceptor antagonist) doesn't affect the diuresis, natriuresis, and kaliuresis induced by adrenaline. Pretreatment with losartan into the PVN decreased in a dose-dependent manner the urine, sodium, and potassium excretions induced by MSA administration of adrenaline (50 ng), while PVN PD123319 was without effect. These results indicate that urinary and electrolyte excretion effects induced by adrenaline into the MSA are mediated primarily by PVN AT, receptors. However, the doses of losartan were more effective when combined with the doses of PD123319 than given alone, suggesting that the urinary, natriuretic, and kaliuretic effects of MSA adrenaline may involve activation of multiple angiotensin II receptors subtypes into the PVN. (C) 2004 Elsevier B.V All rights reserved.

Role of the alpha(1)- and alpha(2)-adrenoceptors of the paraventricular nucleus on the water and salt intake, renal excretion, and arterial pressure induced by angiotensin II injection into the medial septal area

In this study we investigated the influence of cu-adrenergic antagonists injections into the paraventricular nucleus (PVN) of the hypothalamus on the thirst and salt appetite, diuresis, natriuresis, and presser effects of angiotensin II (ANG II) stimulation of medial septal area (MSA). ANG II injection into the MSA induced water and sodium intake, diuresis, natriuresis, and presser responses. The previous injection of prazosin (an alpha (1)-adrenergic antagonist) into the PVN abolished, whereas previous administration of yohimbine (an alpha (2)-adrenergic antagonist) into the PVN increased the water and sodium intake, urinary, natriuretic, and presser responses induced by ANG ii injected into the MSA. Previous injection of a nonselective alpha -adrenergic antagonist, regitin, into the PVN blocked the urinary excretion, and reduced the water and sodium intake, sodium intake, and presser responses induced by ANG II injected into the MSA. The present results suggest that alpha -adrenergic pathways involving the PVN are important for the water and sodium excretion, urine and sodium excretion, and presser responses, induced by angiotensinergic activation of the MSA. (C) 2001 Elsevier B.V.

Role of angiotensin II and vasopressin receptors within the supraoptic nucleus in water and sodium intake induced by the injection of angiotensin II into the medial septal area

In this study we investigated the effects of the injection into the supraoptic nucleus (SON) of non-peptide AT1- and AT2-angiotensin II (ANG II) receptor antagonists, DuP753 and PD123319, as well as of the arginine-vasopressin (AVP) receptor antagonist d(CH2)5-Tyr(Me)-AVP, on water and 3% NaCl intake induced by the injection of ANG II into the medial septal area (MSA). The effects on water or 3% NaCl intake were assessed in 30-h water-deprived or in 20-h water-deprived furosemide-treated adult male rats, respectively. The drugs were injected in 0.5 µl over 30-60 s. Controls were injected with a similar volume of 0.15 M NaCl. Antagonists were injected at doses of 20, 80 and 180 nmol. Water and sodium intake was measured over a 2-h period. Previous administration of the AT1 receptor antagonist DuP753 into the SON decreased water (65%, N = 10, P<0.01) and sodium intake (81%, N = 8, P<0.01) induced by the injection of ANG II (10 nmol) into the MSA. Neither of these responses was significantly changed by injection of the AT2-receptor antagonist PD123319 into the SON. on the other hand, while there was a decrease in water intake (45%, N = 9, P<0.01), ANG II-induced sodium intake was significantly increased (70%, N = 8, P<0.01) following injection of the V1-type vasopressin antagonist d(CH2)5-Tyr(Me)-AVP into the SON. These results suggest that both AT1 and V1 receptors within the SON may be involved in water and sodium intake induced by the activation of ANG II receptors within the MSA. Furthermore, they do not support the involvement of MSA AT2 receptors in the mediation of these responses.

Ibotenate lesion of the medial hypothalamus alters the salt intake and pressor responses to activation of the median preoptic nucleus in rats

We investigated the influence of ibotenic acid lesions of the medial hypothalamus (MH) on salt appetite and arterial blood pressure responses induced by angiotensinergic and adrenergic stimulation of the median preoptic nucleus (MnPO) of rats. Previous injection of the adrenergic agonists norepinephrine, clonidine, phenylephrine, and isoproterenol into the MnPO of sham MH-lesioned rats caused no change in the sodium intake induced by ANG II. ANG II injected into the MnPO of MH-lesioned rats increased sodium intake compared with sham-lesioned rats. Previous injection of clonidine and isoproterenol increased, whereas phenylephrine abolished the salt intake induced by ANG II into the MnPO of MH-lesioned rats. Previous injection of norepinephrine and clonidine into the MnPO of sham MH-lesioned rats caused no change in the mean arterial pressure (MAP) induced by ANG II. Under the same conditions, previous injection of phenylephrine increased, whereas isoproterenol reversed the increase in MAP induced by angiotensin II (ANG II). ANG II injected into the MnPO of MH-lesioned rats induce a decrease in MAP compared with sham-lesioned rats. Previous injection of phenylephrine or norepinephrine into the MnPO of MH-lesioned rats induced a negative MAP, whereas pretreatment with clonidine or isoproterenol increased the MAP produced by ANG II injected into the MnPO of sham- or MH-lesioned rats. These data show that ibotenic acid lesion of the MH increases the sodium intake and presser responses induced by the concomitant angiotensinergic, alpha(2) and beta adrenergic activation of the MnPO, whereas alpha(1) activation may have opposite effects. MH involvement in excitatory and inhibitory mechanisms related to sodium intake and MAP control is suggested.

Influence of angiotensin II receptor subtypes of the paraventricular nucleus on the physiological responses induced by angiotensin II injection into the medial septal area

Objective - We determined the effects of losartan and PD 123319 (antagonists of the AT1 and AT2 angiotensin receptors, respectively), and [Sar1, Ala8] ANG II (a relatively peptide antagonist of angiotensin receptors) injected into the paraventricular nucleus (PVN) on water and 3% NaCl intake, and the diuretic, natriuretic, and pressor effects induced by administration of angiotensin II (ANG II) into the medial septal area (MSA) of conscious rats. Methods - Holtzman rats were used. Animals were anesthetized with tribromoethanol (20 mg) per 100 grams of body weight, ip. A stainless steel guide cannula was implanted into the MSA and PVN. All drugs were injected in 0.5-μl volumes for 10-15 seconds. Seven days after brain surgery, water and 3% NaCl intake, urine and sodium excretion, and arterial blood pressure were measured. Results - Losartan (40 nmol) and [Sar1, Ala8] ANG II (40 nmol) completely eliminated whereas PD 123319 (40 nmol) partially blocked the increase in water and sodium intake and the increase in arterial blood pressure induced by ANG II (10 nmol) injected into the MSA. The PVN administration of PD 123319 and [Sar1, Ala8] ANG II blocked whereas losartan attenuated the diuresis and natriuresis induced by MSA administration of ANG II. Conclusion - MSA involvement with PVN on water and sodium homeostasis and arterial pressure modulation utilizing ANGII receptors is suggested.

Activation of the serotonergic 5-HT1A receptor in the paraventricular nucleus of the hypothalamus inhibits water intake and increases urinary excretion in water-deprived rats

The paraventricular nucleus (PVN) may be considered as a dynamic mosaic of chemically-specified subgroups of neurons. 5-HT1A is one of the prime receptors identified and there is expressed throughout all magnocellular regions of the PVN. Several reports have demonstrated that a subpopulation of the magnocellular neurons expressing 5-HT1A receptors are oxytocin (OT) neurons and activation of 5-HT1A receptors in the PVN increases the plasma OT. Increasing evidence shows that OT inhibits water intake and increases urinary excretion in rats. The aim of this study was to investigate the role of serotonergic 5-HT1A receptors in the lateral-medial posterior magnocellular region of the PVN in the water intake and diuresis induced by 24 h of water deprivation. Cannulae were implanted in the PVN of rats. 5-HT injections in the PVN reduced water intake and increased urinary excretion. 8-OH-DPAT (a 5-HT1A agonist) injections blocked the water intake and increased urinary output in all the periods of the observation. pMPPF (a 5-HT1A antagonist) injected bilaterally before the 8-OH-DPAT blocked its inhibitory effect on water intake and its diuretic effect. We suggest that antidipsogenic and diuretic responses seem to be mediated via 5-HT1A receptors of the lateral-medial posterior magnocellular region of the PVN in water-deprived rats. (C) 2008 Elsevier B.V. All rights reserved.