Lateral parabrachial nucleus and serotonergic mechanisms in the control of salt appetite in rats

This study investigated the effects of bilateral injections of serotonergic receptor agonist and antagonist into the lateral parabrachial nucleus (LPBN) on the ingestion of water and 0.3 M NaCl induced by intracerebroventricular angiotensin II (ANG II) or by combined subcutaneous injections of the diuretic furosemide (Furo) and the angiotensin-converting enzyme inhibitor captopril (Cap). Rats had stainless steel cannulas implanted bilaterally into the LPBN and into the left lateral ventricle. Bilateral LPBN pretreatment with the serotonergic 5-HT1/5-HT2 receptor antagonist methysergide (4 mu g/200 nl each site) increased 0.3 M NaCl and water intakes induced by intracerebroventricular ANG II (50 ng/mu l) and 0.3 M NaCl intake induced by subcutaneous Furo + Cap. Pretreatment with bilateral LPBN injections of a serotonergic 5-HT2A/2C receptor agonist DOI (5 mu g/200 nl) significantly reduced 0.3 M NaCl intake induced by subcutaneous Furo + Cap. Pretreatment with methysergide or DOI into the LPBN produced no significant changes in the water intake induced by subcutaneous Furo + Cap. These results suggest that serotonergic mechanisms associated with the LPBN may have inhibitory roles in water and sodium ingestion in rats.

Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetite

Central cholinergic mechanisms are suggested to participate in osmoreceptor-induced water intake. Therefore, central injections of the cholinergic agonist carbachol usually produce water intake (i.e., thirst) and are ineffective in inducing the intake of hypertonic saline solutions (i.e., the operational definition of sodium appetite). Recent studies have indicated that bilateral injections of the serotonin receptor antagonist methysergide into the lateral parabrachial nucleus (LPBN) markedly increases salt intake in models involving the activation of the renin-angiotensin system or mineralocorticoid hormones. The present studies investigated whether sodium appetite could be induced by central cholinergic activation with carbachol (an experimental condition where only water is typically ingested) after the blockade of LPBN serotonergic mechanisms with methysergide treatment in rats. When administered intracerebroventricularly in combination with injections of vehicle into both LPBN, carbachol (4 nmol) caused water drinking but insignificant intake of hypertonic saline. In contrast, after bilateral LPBN injections of methysergide (4 mug), intracerebroventricular carbachol induced the intake of 0.3 M NaCl. Water intake stimulated by intracerebroventricular carbachol was not changed by LPBN methysergide injections. The results indicate that central cholinergic activation can induce marked intake of hypertonic NaCl if the inhibitory serotonergic mechanisms of the LPBN are attenuated.

Effect of the bound nucleon form factors on charged-current neutrino-nucleus scattering

We study the effect of bound nucleon form factors on charged-current neutrino-nucleus scattering. The bound nucleon form factors of the vector and axial-vector currents are calculated in the quark-meson coupling model. We compute the inclusive C-12(nu(mu),mu(-))X cross sections using a relativistic Fermi gas model with the calculated bound nucleon form factors. The effect of the bound nucleon form factors for this reaction is a reduction of similar to8% for the total cross section, relative to that calculated with the free nucleon form factors.

Paraventricular nucleus administration of DuP753 or PD123319 inhibits the effects of angiotensin on water and sodium intake

We determined the effects of DuP753 and PD123319 (both nonpeptides and selective antagonists of the AT(1) and AT(2) angiotensin receptors, respectively), and [Sar(1), Ala(8)]ANG II (a non-selective peptide antagonist of angiotensin receptors) on water and 3%NaCl intake induced by administration of angiotensin II (ANG II) into the paraventricular nucleus (PVN) of sodium-depleted Holtzman rats weighing 250-300 g. Twenty hours before the experiments, the rats were depleted of sodium using furosemide (10 ng/rat, sc). The volume of drug solution injected was 0.5 mu l over a period of 10-15 sec. Water and sodium intake were measured at 0.25, 0.5, 1.0 and 2.0 h. Pre-treatment with DuP753 (14 rats) at a dose of 60 ng completely abolished the water intake induced by injection of 12 ng of ANG II (15 rats) (6.4 +/- 0.6 vs 1.4 +/- 0.3 ml/2 h), where [Sar(1), Ala(8)]ANG II (12 rats) and PD123319 (10 rats) at the doses of 60 ng partially blocked water intake (6.4 +/- 0.6 vs 2.9 +/- 0.5 and 2.7 +/- 0.2 ml/2 h, respectively). In the same animals, [Sar(1), Ala(8)]ANG II, DuP753, and PD123319 blocked the sodium intake induced by ANG II (9.2 +/- 1.6 vs 3.3 +/- 0.6, 1.8 +/- 0.3, and 1.4 +/- 0.2 ml/2 h, respectively). These results indicate that both DuP753 and PD123319, administered into the PVN, blocked the water and sodium intake induced by administration of ANG II into the same site.

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.

Effect of ibotenate lesions of the ventromedial hypothalamus on the water and salt intake induced by activation of the median preoptic nucleus in sodium-depleted rats

In this study we investigated the influence of a ventromedial hypothalamus (VMH) lesion with ibotenic acid on water and sodium intake and presser responses induced by combined treatment of the median preoptic nucleus (MnPO) with angiotensin Il (ANG II) and adrenergic agonists (phenylephrine, norepinephrine, isoproterenol and clonidine). Male Holtzman rats with a stainless steel cannula implanted into the MnPO and bilateral sham (vehicle) or VMH lesions with ibotenic acid were used. The ingestion of water and sodium and mean arterial pressure (MAP) were determined in separate groups submitted to sodium depletion with the diuretic furosemide (20 mg/rat). ANG II (10 pmol) injection into the MnPO of sham-lesioned rats induced water and sodium intake and presser responses. VMH-lesion reduced ANG II-induced water intake and increased saline intake, In sham rats phenylephrine (80 nmol) into MnPO increased, whereas norepinephrine (80 nmol) and clonidine (40 nmol) reduced ANG II-induced water intake while sodium intake was reduced only by clonidine into MnPO. In VMH-lesioned rats, phenylephrine reduced, noradrenaline increased and clonidine produced no effect on ANG II-induced water intake. In lesioned rats ANG II-induced sodium intake was reduced by phenylephrine and noradrenaline, whereas clonidine produced no change. ANG II-induced presser response was reduced in VMH-lesioned rats, but the presser response combining ANG II and phenylephrine or noradrenaline in VMH-lesioned rats was bigger than sham rats. These results show that the VMH is important for the changes in water and sodium intake and cardiovascular responses induced by angiotensinergic and adrenergic activation of the MnPO. (C) 1997 Elsevier B.V. B.V.

Cytoarchitecture and musculotopic organization of the facial motor nucleus in Cebus apella monkey

The architecture and musculotopic organization of the facial motor nucleus in the Cebus apella monkey (a New World primate) were investigated using histological techniques and a multiple labelling strategy, in which horseradish peroxidase-conjugated neuroanatomical tracers (CTB-HRP and WGA-HRP) and fluorescent tracers were injected into individual facial muscles. The facial motor nucleus was formed by multipolar motoneurons and had an ovoid shape, with its rostrocaudal axis measuring on average 1875 mum. We divided the nucleus into four different subnuclei: medial, intermediate, dorsal and lateral. Retrograde labelling patterns revealed that individual muscles were innervated by longitudinal functional columns of motoneurons. The columns of the orbicularis oculi, zygomaticus, orbicularis oris, auricularis superior, buccinator and platysma muscles were located in the dorsal, intermediate, lateral, medial, lateral and intermediate subnuclei, respectively. However, the motoneuron columns of the levator labii superioris alaeque nasi muscle and frontalis muscle could not be associated with a specific subnucleus. The present results confirm previous studies regarding the musculotopic organization of the facial motor nucleus. However, we observed some particularities in terms of the relative size of each column in C. apella, which might be related to the functional and behavioral importance of each muscle in the particular context of this primate.

Anxiolytic effect of estradiol in the median raphe nucleus mediated by 5-HT1A receptors

Estrogen deficiency has been associated with stress, anxiety and depression. Estrogen receptors have been identified in the median raphe nucleus (MRN). This structure is the main source of serotonergic projections to the hippocampus, a forebrain area implicated in the regulation of defensive responses and in the resistance to chronic stress. There is evidence showing that estrogen modulates 5-HT1A receptor functions. In the MRN, somatodendritic 5-HT1A receptors control the activity of serotonergic neurones by negative feedback. The present study evaluated the effect of intra-MRN injection of estradiol benzoate (EB) (600 or 1200 ng/0.2 mu l) on the performance of ovariectomised rats submitted to the elevated plus-maze test of anxiety and to the open-field test. Additionally, the same effect was evaluated with a previous intra-MRN injection of WAY 100635 (100 ng/0.2 mu l), an antagonist of 5-HT1A receptors. The results showed that both doses of EB increased the percentage of entries and the percentage of time spent into the open arms, suggestive of an anxiolytic effect. The highest dose of the drug also increased the number of entries into the enclosed arm and locomotion in the open field, indicating a stimulatory motor effect. WAY 100635 antagonised the effect of estradiol in the elevated plus-maze and in the open-field. The results show that estrogen receptors of the MRN are implicated in the regulation of anxiety-related behaviour. The results also support claims that the effect of estrogen involves a change in 5-HT1A receptor function. (C) 2005 Elsevier B.V. All rights reserved.

An algebraic q-deformed form for shape-invariant systems

A quantum deformed theory applicable to all shape-invariant bound-state systems is introduced by defining q-deformed ladder operators. We show that these new ladder operators satisfy new q-deformed commutation relations. In this context we construct an alternative q-deformed model that preserves the shape-invariance property presented by the primary system. q-deformed generalizations of Morse, Scarf and Coulomb potentials are given as examples.

NONLOCAL EFFECTS IN THE NUCLEUS-NUCLEUS FUSION CROSS-SECTION

Effects of the nonlocality of factorizable potentials are taken into account in the calculation of nucleus-nucleus fusion cross section through an effective mass approach. This cross section makes use of the tunneling factor calculated for the nonlocal barrier, without the explicit introduction of any result coming from coupled channel calculation, besides the approximations of Hill-Wheeler and Wong. Its new expression embodies the nonlocal effects in a factor which redefines the local potential barrier curvature. Applications to different systems, namely O-16 + Co-59, O-16,O-18 + Ni-58,Ni-60,Ni-64, and O-16,O-18 + Cu-63,Cu-65 are presented, where the nonlocal range is treated as a free parameter.

EFFECT OF LATERAL HYPOTHALAMUS LESIONS ON THE WATER AND SALT INTAKE, AND SODIUM AND URINE EXCRETION INDUCED BY ACTIVATION OF THE MEDIAN PREOPTIC NUCLEUS IN CONSCIOUS RATS

In this-study we investigated the influence of electrolytic lesion of the lateral hypothalamus (LH) on the water and salt appetite, and the natriuretic, diuretic and cardiovascular effects induced by angiotensinergic, cholinergic and noradrenergic stimulation of the median preoptic nucleus (MnPO) in rats. Male Holtzman rats were implanted with a cannula into the MnPO. Other groups of sham- and LH-lesioned rats received a stainless steel cannula implanted into the MnPO. ANGII injection into the MnPO induced water and sodium intake, and natriuretic, diuretic, presser and tachycardic responses. Carbachol induced water intake, and natriuretic, presser and bradycardic responses, whereas noradrenaline increased urine, sodium excretion and blood pressure, and induced bradycardia. In rats submitted to LH-lesion only, water and sodium intake was reduced compared with sham rats. LH lesion also reduced the sodium ingestion induced by ANGII (12 ng) into the MnPO. In LH-lesioned rats, the dipsogenic, diuretic and presser responses induced by ANGII (12 ng), carbachol (2 nmol) and noradrenaline (20 nmol) injection into the MnPO were reduced. The same occurred with sodium excretion when carbachol (2 nmol) and noradrenaline (20 nmol) were injected into the MnPO of LH-lesioned rats, whereas ANGII(12 ng) induced an increase in sodium excretion. These data show that electrolytic lesion of the LH reduces fluid and sodium intake, and presser responses to angiotensinergic, cholinergic and noradrenergic activation of the MnPO. LH involvement with MnPO excitatory and inhibitory mechanisms related to water and sodium intake, sodium excretion and cardiovascular control is suggested.