Effects of sinoaortic denervation on Fos expression in the brain evoked by hypertension and hypotension in conscious rabbits

We have previously shown [Li and Dampney (1994) Neuroscience 61, 613-634] that periods of sustained hypertension and hypotension each induces a distinctive and reproducible pattern of neuronal expression of Fos (a marker of neuronal activation) in specific regions of the brainstem and forebrain of conscious rabbits. The aim of this study was to determine the contribution of afferent inputs from arterial baroreceptors to the activation of neurons in these various brain regions that is caused by a sustained change in arterial pressure. Experiments were carried out on rabbits in which the carotid sinus and aortic depressor nerves were cut in a preliminary operation. Following a recovery period of seven to 10 days, a moderate hypertension or hypotension (increase or decrease in arterial pressure of 20-30 mmHg) was induced in conscious barodenervated rabbits for 60 min by the continuous infusion of phenylephrine or sodium nitroprusside, respectively. In control experiments, barodenervated rabbits were subjected to the identical procedures except that they were infused with the vehicle solution alone. Compared with the effects seen in barointact rabbits, [Li and Dampney (1994) Neuroscience 61, 613-634] the number of neurons that expressed Fos in response to hypertension was reduced by approximately 90% in the nucleus of the solitary tract and in the caudal and intermediate parts of the ventrolateral medulla. In supramedullary regions, baroreceptor denervation resulted in a reduction of approximately 60% in hypertension-induced Fos expression in the central nucleus of the amygdala and in the bed nucleus of the stria terminalis, but no significant reduction in the parabrachial complex in the pons. Following hypotension, the number of neurons that expressed Fos in barodenervated rabbits, compared with barointact rabbits, [Li and Dampney (1994) Neuroscience 61, 613-634] was reduced by approximately 90% in the nucleus of the solitary tract, area postrema, and caudal, intermediate and rostral parts of the ventrolateral medulla. Baroreceptor denervation also resulted in a similar large reduction in hypotension-induced Fos expression in many supramedullary regions (locus coeruleus, midbrain periaqueductal grey, hypothalamic paraventricular nucleus, and in the central nucleus of the amygdala and the bed nucleus of the stria terminalis in the basal forebrain). In the supraoptic nucleus, hypotension-induced Fos expression in barodenervated rabbits was reduced by 75% compared to barointact animals, but was still significantly greater than in control animals. There was also a high level of Fos expression, much greater than in control animals, in the circumventricular organs surrounding the third ventricle (subfornical organ and organum vasculosum lamina terminalis). The results indicate that in conscious rabbits the activation of neurons that occurs in several discrete regions at all levels of the brain following a sustained change in arterial pressure is largely dependent upon inputs from arterial baroreceptors, with the exception of neurons in the circumventricular organs surrounding the third ventricle that are activated by sustained hypotension. The latter group of neurons are known to project to vasopressin-secreting neurons in the supraoptic nucleus, and may therefore via this pathway trigger the hypotension-induced release of vasopressin that occurs in the absence of baroreceptor inputs.     

Alteration of limb and brain patterning in early mouse embryos by ultrasound-guided injection of Shh-expressing cells

Injection of the fructose analogue, 2,5-anhydro-d-mannitol (2,5-AM), increases food intake and Fos-like immunoreactivity (Fos-li) in both brainstem and forebrain structures. Because of the interconnections between brainstem and forebrain areas, it has not been possible to determine whether or to what extent induction of Fos-li in a given region reflects brainstem-forebrain interactions. We addressed this issue using chronic decerebrate (CD) rats with complete transections of the neuroaxis at the meso-diencephalic juncture. CD and neurologically intact control rats were injected (i.p.) with saline or 400 mg/kg 2,5-AM and brains were examined for Fos-li. Both intact and CD rats showed increased Fos-li in the nucleus of the solitary tract (NTS) after injection of 2,5-AM as compared with saline. 2, 5-AM treatment increased Fos-li in the external lateral division of parabrachial nucleus (PBNel) in intact but not in CD rats, suggesting that descending projections from the forebrain may play a role in the activation of PBNel neurons after 2,5-AM injection. Decerebration eliminated significant 2,5-AM-induced Fos-li responses in forebrain structures, including the paraventricular nucleus, supraoptic nucleus, bed nucleus of the stria terminalis and central nucleus of the amygdala. The results are consistent with the hypothesis that the activation of forebrain structures after 2,5-AM treatment is due to stimulation by ascending projections from the brainstem.     

Recognition and management of childhood cardiac arrhythmias

Axonal connections between the amygdala and the hypothalamic paraventricular nucleus were examined by combined anterograde-retrograde tract tracing. Iontophoretic injections of the retrograde tracer Fluorogold were placed in the paraventricular nucleus, and the anterograde tracer PHA-L in the ipsilateral central or medial amygdaloid nuclei. Single and double-label immunohistochemistry were used to detect tracers. Single label anterograde and retrograde tracing suggest limited evidence for direct connections between the central or medial amygdala and the paraventricular nucleus. In general, scattered PHA-L-positive terminals were seen in autonomic subdivisions of the paraventricular nucleus (lateral parvocellular, dorsal parvocellular and ventral medial parvocellular subnuclei) following central or medial amygdaloid nucleus injection. Double-label studies indicate that central and medial amygdaloid nucleus efferents contact paraventricular nucleus-projecting cells in several forebrain nuclei. In the case of central nucleus injections, PHA-L positive fibers occasionally contacted Fluorogold-labeled neurons in the anteromedial, ventromedial and preoptic subnuclei of the bed nucleus of the stria terminalis. Overall, such contacts were quite rare, and did not occur in the bed nucleus of the stria terminalis regions showing greatest innervation by the central amygdaloid nucleus. In contrast, medial amygdala injections resulted in a significantly greater overlap of PHA-L labeling and Fluorogold-labeled neurons, with axosomatic appositions observed in medial divisions of the bed nucleus of the stria terminalis, anterior hypothalamic area and preoptic area. The results provide anatomical evidence that a substantial proportion of amygdaloid connections with hypophysiotrophic paraventricular nucleus neurons are likely multisynaptic, relaying in different subregions of the bed nucleus of the stria terminalis and hypothalamus.     

Self-stimulation in 7- and 10-day-old rats.

It has been shown that the infant rat exhibits learned behaviors characteristic of the adult. With a modified self-stimulation paradigm, the present study explored whether 7- and 10-day-old Long-Evans rat pups could learn a discriminated operant to obtain direct electrical stimulation in neural sites that support self-stimulation in adults. By nudging 1 of 2 response manipulanda, at 2 ages (7 and 10 days) and temperatures (22 and 35°C), Ss self-stimulated with electrodes implanted in a variety of forebrain sites, including the prefrontal cortex, bed nucleus of the stria terminalis, medial nucleus of the amygdala, and the medial forebrain bundle. The only temperature-sensitive site might be the nucleus accumbens, which was positive only at the higher temperature in 10-day-olds. Results indicate that several forebrain sites demonstrate rewarding properties of stimulation in the preweanling rat pup. (40 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Co-infusion with a TrkB-Fc receptor body carrier enhances BDNF distribution in the adult rat brain

Intraspecific confrontation between male rats represents a biologically relevant form of social stress. C-fos expression has been used to map the pattern of neural activation following either a single (acute) or repeated (10 times) exposure of an intruder male to a larger male in the latter's home cage. These conditions induce high levels of aggressive interaction. Sixty minutes after a single defeat, there was intense c-fos expression (quantified using image analysis) in restricted areas of the basal forebrain (including lateral septum, bed nucleus of stria terminalis, lateral preoptic area, lateral hypothalamic area, paraventricular nucleus, and medial and central amygdala) as well as in the autonomic and monoaminergic nuclei of the brainstem (central grey, dorsal and median raphe, locus coeruleus and nucleus of the solitary tract). After the tenth defeat, this pattern was modified despite persistently high levels of aggression. Some areas in the forebrain (bed nucleus of stria terminalis, paraventricular nucleus and medial amygdala) continued to express increased c-fos; others (the septum, lateral hypothalamic area, lateral preoptic area and central amygdala) no longer expressed c-fos. The brainstem response was equally varied: the central grey and the raphe nuclei continued to respond after repeated defeat, whereas the solitary nucleus and locus coeruleus did not. On the other hand, there was no change in the behaviour of intruder rats after repeated defeat. This study shows the pattern of adaptation at a cellular level in the basal forebrain and brainstem to repeated defeat. As in our previous studies of repeated restraint, modulation in the expression of c-fos following repeated stress is highly regionally specific, suggesting that differential neural processing is involved in adaptation to social stress.     

Moving beyond fear: lessons learned through a longitudinal review of the literature regarding health care providers and the care of people with HIV/AIDS

Exposure to hostile conditions initiates the secretion of several hormones, including corticosterone/cortisol, catecholamines, prolactin, oxytocin, and renin, as part of the survival mechanism. Such conditions are often referred to as "stressors" and can be divided into three categories: external conditions resulting in pain or discomfort, internal homeostatic disturbances, and learned or associative responses to the perception of impending endangerment, pain, or discomfort ("psychological stress"). The hormones released in response to stressors often are referred to as "stress hormones" and their secretion is regulated by neural circuits impinging on hypothalamic neurons that are the final output toward the pituitary gland and the kidneys. This review discusses the forebrain circuits that mediate the neuroendocrine responses to stressors and emphasizes those neuroendocrine systems that have previously received little attention as stress-sensitive hormones: renin, oxytocin, and prolactin. Anxiolytic drugs of the benzodiazepine class and other drugs that affect catecholamine, GABAA, histamine, and serotonin receptors alter the neuroendocrine stress response. The effects of these drugs are discussed in relation to their effects on forebrain neural circuits that regulate stress hormone secretion. For psychological stressors such as conditioned fear, the neural circuits mediating neuroendocrine responses involve cortical activation of the basolateral amygdala, which in turn activates the central nucleus of the amygdala. The central amygdala then activates hypothalamic neurons directly, indirectly through the bed nucleus of the stria terminalis, and/or possibly via circuits involving brainstem serotonergic and catecholaminergic neurons. The renin response to psychological stress, in contrast to those of ACTH and prolactin, is not mediated by the bed nucleus of the stria terminalis and is not suppressed by benzodiazepine anxiolytics. Stressors that challenge cardiovascular homeostasis, such as hemorrhage, trigger a pattern of neuroendocrine responses that is similar to that observed in response to psychological stressors. These neuroendocrine responses are initiated by afferent signals from cardiovascular receptors which synapse in the medulla oblongata and are relayed either directly or indirectly to hypothalamic neurons controlling ACTH, prolactin, and oxytocin release. In contrast, forebrain pathways may not be essential for the renin response to hemorrhage. Thus current evidence indicates that although a diverse group of stressors initiate similar increases in ACTH, renin, prolactin, and oxytocin, the specific neural circuits and neurotransmitter systems involved in these responses differ for each neuroendocrine system and stressor category.     

Ascending projections from the area postrema and the nucleus of the solitary tract of Suncus murinus: anterograde tracing study using Phaseolus vulgaris leucoagglutinin

Suncus murinus (suncus) is a new experimental animal model for research on the mechanisms underlying emesis. In the present study, we examined the ascending projections from the area postrema (AP) and the nucleus of the solitary tract (NTS) in suncus based on anterograde transport of phaseolus vulgaris leucoagglutinin. The AP projected heavily to the dorsal vagal complex, especially in the commissural and medial subnuclei of the NTS, and the dorsal motor nucleus of the vagus. Some ascending fibers from the AP projected bilaterally to the parabrachial nucleus (Pb), but no labeling was observed rostral to this area. In contrast, the NTS had extensive projections as far as the basal forebrain. The NTS projections were observed in the AP, ventrolateral reticular formation including the nucleus ambiguus, A5 noradrenergic area, locus coeruleus, Pb, and central gray matter of the midbrain. At the level of the diencephalon, the NTS projections were seen in the dorsomedial, lateral, paraventricular, periventricular, supraoptic, retrochiasmatic and arcuate nuclei of the hypothalamus, in addition to the paraventricular nucleus of the thalamus. Terminal fields within the basal forebrain were also shown to include the medial preoptic area, the bed nucleus of the stria terminalis, the substantia innominata and the ventral pallidum. The results indicated that the neurological relationship between the chemo- and/or barosensitive systems including the trigger of the emetic response and the general viscerosensory and/or -motor systems may exist also in the suncus.     

Thirst and sodium appetite after colloid treatment in rats with septal lesions.

Previous experiments in which angiotensin II (AII) and mineralocorticoids were administered to rats have suggested that these hormones play a natural role in mediating thirst and sodium appetite. This hypothesis was examined by making use of 20 male Sprague-Dawley rats with septal lesions, which have an apparent sensitivity to the central effects of AII, and by studying their behavioral response to sc treatment with 5 ml of a 30% polyethylene glycol solution, which produces hypovolemia and thereby stimulates the secretions of renin and aldosterone. The induced thirst and sodium appetite both were markedly enhanced in the brain-damaged Ss. However, water intake was not increased when the hypovolemia was moderate, and sodium appetite was augmented only when Ss had been sodium deprived, a procedure known to potentiate aldosterone secretion. Findings support suggestions that while AII normally contributes little to thirst, it may help to mediate sodium appetite in rats when aldosterone is abundant. The 2 drives were not elicited uniformly; those Ss that drank the most water after colloid treatment consumed the least saline. While septal lesions may sensitize the rat's brain to the sodium-appetite-eliciting effects of AII as well as to its dipsogenic effects, sodium appetite may emerge only if the induced thirst is not too pronounced. (16 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Glutamatergic transmission in the nucleus of the solitary tract modulates memory through influences on amygdala noradrenergic systems.

The authors examined whether glutamate release from the vagus nerve onto the nucleus of the solitary tract (NTS) is one mechanism by which the vagus influences memory and neural activity in limbic structures. Rats trained to drink from a spout were given a footshock (0.35 mA) on Day 5 after approaching the spout. Phosphate-buffered saline or 5.0, 50.0, or 100.0 nmol/0.5 μl glutamate was then infused into the NTS. Glutamate (5.0 or 50.0 nmol) significantly enhanced memory on the retention test. In Experiment 2, this effect was attenuated by blocking noradrenergic receptors in the amygdala with propranolol (0.3 μg/0.5 μl). Experiment 3 used in vivo microdialysis to determine whether footshock plus glutamate (50.0 nmol) alters noradrenergic output in the amygdala. These treatments caused a significant and long-lasting increase in amygdala noradrenergic concentrations. The results indicate that glutamate may be one transmitter that conveys the effects of vagal activation on brain systems that process memory. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Construction and expression of a modular gene encoding bacteriophage T7 RNA polymerase

Tachykinins inhibit salt appetite when applied intracranially in a number of brain regions and may function as endogenous inhibitors of sodium intake. To test the hypothesis that induced increases in salt appetite might involve disinhibition via a reduction in endogenous tachykinin expression, we used a semi-quantitative in situ hybridization analysis to investigate changes in brain areas expressing preprotachykinin-A (PPT-A) and preprotachykinin-B (PPT-B) mRNAs of rats after 1 day of sodium depletion (1d Na dep). PPT-A mRNA levels were detected in neurons of the olfactory tubercle (Tu), the nucleus of the olfactory tubercle (LOT), the dorsal and ventral caudate-putamen (d-CPu and v-CPu), the bed nucleus of the stria terminalis (BNST), the medial preoptic area (mPOA), the habenula (Hb) and the postero-dorsal part of the amygdala (MePD). PPT-B mRNA levels were measured in fundus striati (FStr), d-CPu, v-CPu, BNST, mPOA, dorsomedial hypothalamic nucleus (DMD), arcuate nucleus (Arc), central amygdaloid nucleus (CeL), basolateral amygdaloid nucleus (BLV), LOT, Hb and basal nucleus of Meynert (B). 1d Na dep reduced by 33-61% the mean number of PPT-A grains/cell in Tu, LOT, d-CPu, BNST, mPOA, Hb and MePD compared to control animals. Levels of PPT-B mRNA were not reduced as much by 1d Na dep, although statistically significant reductions of 26, 34 and 17% were found in v-CPu, BNST and B, respectively. These findings, therefore, support the hypothesis that endogenous tachykinins exert an inhibitory influence over sodium appetite.     

Salt appetite and lesions of the ventral part of the ventral median preoptic nucleus.

Angiotensin receptors in the most ventral part of the ventral median preoptic nucleus (VVMnPO) or organum vasculosum laminae terminalis appear to be important for salt appetite to angiotensin in rats. If so, then small lesions of this region should reduce salt appetite that is dependent on angiotensin. In separate experiments, the lesion greatly reduced salt appetite after treatments with chronic oral captopril or sodium depletion. On the other hand, the VVMnPO lesion actually enhanced salt appetite to deoxycorticosterone acetate. The lesion did not affect water intake to water deprivation, combined food-water deprivation, isoproterenol, or hypertonic saline, and basal plasma osmolality and sodium values were normal. These experiments suggest that VVMnPO lesions selectively affect angiotensin-induced salt appetite without producing the gross hydrational deficits that occur with larger lesions of the ventral forebrain. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Behavioural, autonomic and endocrine responses associated with C-fos expression in the forebrain and brainstem after intracerebroventricular infusions of endothelins

Endothelins are a range of peptides (endothelin-1, endothelin-2, and endothelin-3) well known to act peripherally as powerful cardiovascular-regulating agents. Recently, they have been shown to be localized in CSN, where they may act as central neurotransmitters. A variety of putative roles has been ascribed to them in the CNS. To identify those regions of the brain capable of responding to these peptides, the expression of c-fos (an immediate-early gene), has been used to map patterns of activation following intracerebroventricular (i.c.v.) infusions of endothelins in Lister-hooded rats. This has been correlated with changes in heart rate, core temperature and plasma corticosterone levels. Endothelin-3 i.c.v. (50 pmol) decreased both heart rate and core temperature (both recorded by telemetry). This effect lasted for about 30-45 min. Endothelin-1 (10 pmol) or endothelin-3 (50 pmol) i.c.v. induced c-fos expression in the specific regions in the forebrain and brainstem. Strong expression was found in the septum, bed nucleus of the stria terminalis, parvicellular paraventricular nucleus, the central nucleus of the amygdala, dorsal motor nucleus of the vagus and solitary nucleus. There was less marked c-fos expression in other areas of the basal forebrain, such as the organum vasculosum of the lamina terminals, median preoptic nucleus, supraoptic nucleus and the magnocellular. There are two classes of endothelin receptor (A and B). An endothelin-A receptor antagonist, BQ-123, abolished c-fos expression in all structures in the forebrain and brainstem following endothelin-1 infusions. However, an endothelin-B agonist (TetraAla endothelin-1) did not induce discernible c-fos expression in the forebrain or brainstem. These results suggest that the endothelin-A receptor is responsible for endothelin-dependent c-fos induction in the brain. Interactions between endothelins and angiotensin II were also studied. The pattern of c-fos induced by endothelin-3 and angiotensin II was different (particularly in the anteroventral region of the third ventricle). Furthermore, prior infusions of endothelin-3 interfered with the expression of c-fos induced by subsequent angiotensin II, and also suppressed the latter's dipsogenic effect. These results show that endothelin-3 and angiotensin II interact at both behavioural and cellular levels, and that endothelins may play significant roles in the central control of fluid balance and autonomic activity.     

Neuroanatomical patterns of fos-like immunoreactivity induced by a palatable meal and meal-paired environment in saline- and naltrexone-treated rats

Opioid antagonists block the positive hedonic response to food taste and are potent inhibitors of palatability-driven feeding. However, the specific brain regions within which opioid peptide secretion contributes to the maintenance of palatability-driven feeding have not been clearly established. In the present study, c-Fos immunohistochemistry was used to identify regions rostral to the hindbrain that display cellular activation in response to a palatable meal and the meal-paired environment. Further, it was determined whether any of the cellular responses could be prevented by pretreating animals with naltrexone. Twenty brain regions known to be involved in gustation, appetite and reward functions were examined. Ingestion of the palatable meal (3.0 g of 30% shortening, 20% sucrose and 50% powdered Purina rat chow) increased Fos-like immunoreactivity (FLI) in lateral hypothalamus (LH), ventral tegmentum (VTA) and medial preoptic area (MPOA), and decreased FLI in the habenula (Hab). The meal-paired environment increased FLI in the VTA and nucleus accumbens shell (NAC shell). Naltrexone (1.0 mg/kg, i.p.) did not block consumption of the small meal but did prevent all of the distinctive increases in FLI induced by the meal and meal-paired environment. Since naltrexone, alone, increased FLI in VTA, NAC shell, central amygdala (ceA) and laterodorsal bed nucleus of the stria terminalis (BSTLD), the blunting of ingestion reward by naltrexone may result from direct or transsynaptic activating effects on opponent neuronal activity within this highly interconnected set of structures that mediate and modulate reward.     

Patterns of induction of the immediate-early genes c-fos and egr-1 in the female rat brain following differential amounts of mating stimulation

Vaginocervical stimulation received either during mating or by artificial mechanical means has been shown to induce FOS expression in medial amygdala, preoptic area, hypothalamus, and midbrain of female rats. While mating-induced increases in FOS-like immunoreactivity (FOS-IR) have been shown to require intromissive stimulation from males, the pattern of FOS-IR in animals receiving numbers of intromissions across a range relevant to the induction of the prolactin surges of early pregnancy has not been explored. Experiment 1 examined brain FOS-IR following 15 mounts without intromission or 5, 10, or 15 intromissions in ovariectomized females treated with estrogen and progesterone; these treatments are known to be less than or more than sufficient to trigger prolactin surges in cycling females. FOS was expressed in a graded fashion in the medial amygdala with respect to the numbers of intromissions received and in an all-or-nothing manner in preoptic area, bed nucleus of the stria terminalis, and ventromedial nucleus of the hypothalamus. In experiment 2, 15 intromissions induced expression of another immediate-early gene, egr-1, in each of these same areas as well as in a second division of the bed nucleus of the stria terminalis and in the paraventricular nucleus of the hypothalamus. These studies demonstrate that mating is differentially effective in inducing FOS expression in responsive brain areas and point to the medial amygdala as a site in which summation of intromissive stimulation may occur. Furthermore, the induction of EGR-1 may be a more sensitive marker for mating-induced neural activation in these areas than is FOS.     

Involvement of Central Amygdalar and Bed Nucleus of the Stria Terminalis Corticotropin-Releasing Factor in Behavioral Responses to Social Defeat.

The authors investigated whether corticotropin-releasing factor (CRF) within the central nucleus of the amygdala (CeA) and bed nucleus of the stria terminalis (BNST) is a critical component of the neural circuitry mediating conditioned defeat. In this model, hamsters that have experienced social defeat subsequently display only submissive-defensive agonistic behavior instead of territorial aggression. Conditioned defeat was significantly reduced following infusion of the CRF receptor antagonist D-Phe CRF(12-41) into the BNST but not into the CeA. In another experiment, hamsters given unilateral lesions of the CeA and infusions of D-Phe CRF(12-41) into the contralateral BNST displayed significantly less submissive behavior than did controls. These data suggest that CRF acts within a neural circuit that includes the amygdala and the BNST to modulate agonistic behavior following social defeat. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Mutual interactions between HIV-1 and cytokines in adherent cells during acute infection

Intracerebroventricular (i.c.v.) infusions of angiotensin II (AII) reliably induced c-fos expression in the supraoptic (SON) and paraventricular (PVN) nuclei, as well as other areas of the basal forebrain including the OVLT, subfornical organ (SFO), and bed nucleus (BNST). Double-labelling showed that AII-induced c-fos was observed in both vasopressin (AVP-) and oxytocin (OXY)-containing neurons of the SON and PVN in male rats. Allowing rats to drink water after AII infusions suppressed c-fos expression both AVP- and OXY-stained magnocellular neurons. Intragastric infusions of water were also effective, showing that oro-pharyngeal stimuli were not critical. Maximal suppression occurred in rats in whom water had been infused intragastrically about 5 min before i.c.v. AII infusions, suggesting that changes in osmolarity were responsible. i.c.v. AII also induced c-fos expression in a number of brainstem structures, including the solitary nucleus (NTS), lateral parabrachial nucleus (LPBN), locus coeruleus (LC), and the area postrema (AP). These results indicate that AVP and OXY-containing neurons in the magnocellular parts of the SON and PVN alter their immediate-early gene response to AII after water intake, and that this does not depend upon oro-pharyngeal factors. Furthermore, AII can induce c-fos expression in a number of brainstem nuclei associated with autonomic function, and these do not respond to water intake.     

Ethanol-induced changes in plasma proteins, angiotensin II, and salt appetite in rats.

Sodium depletion in rats elicits a sodium appetite that results from a cerebral action of angiotensin II (ANG II) and aldosterone. Alcohol also activates the renin-angiotensin system, but the mechanism is poorly understood and not related to sodium excretion. In this study, 2.5 g/kg intraperitoneal/ly (ip) ethanol produced a 20% decline in plasma volume and plasma protein concentration 1–2 hrs and elicited salt appetite beginning in 3–4 hrs. Blockade of ANG II synthesis in the brain and periphery with the angiotensin-converting enzyme inhibitor captopril eliminated the thirst and salt appetite. Peripheral captopril alone enhanced fluid intake, which indicated that alcohol elevated renin secretion. Ethanol-induced suppression of hepatic plasma protein secretion and the consequent fall in plasma colloid osmotic pressure apparently resulted in hypovolemia and renin secretion, which then produced thirst and salt appetite through an action of ANG II on the brain. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Perseveration in two aphasic patients

In the present study a comparison was made between the distribution of Fos immunoreactivity in the brain of female and male rats following successive elements of sexual behavior. The distribution of Fos immunoreactivity following either mounting, eight intromissions or one or two ejaculations was compared with that in control animals. In both females, Fos immunoreactivity was induced in the medial preoptic nucleus, posteromedial part of the bed nucleus of the stria terminalis, posterodorsal part of the medial amygdala, and the parvicellular part of the subparafascicular thalamic nucleus. In addition, Fos immunoreactivity in females was induced in the ventrolateral part and the most caudoventral part of the ventromedial nucleus of the hypothalamus and in the premammillary nucleus. Differences between females and males were detected in the phases of sexual activity that resulted in Fos immunoreactivity in these brain areas, allowing more insight in the nature of the sensory and hormonal stimuli leading to the induction of Fos immunoreactivity. The posteromedial bed nucleus of the stria terminalis appears to be involved in chemosensory investigation, while specific distinct subregions are only activated following ejaculation. In addition, the parvicellular subparafascicular nucleus and the lateral part of the posterodorsal medial amygdala appear to be involved in the integration of viscero-sensory input. The neural circuitries underlying sexual behavior in males and females appear to be similar in terms of integration of sensory information. In males the medial preoptic nucleus may be regarded as the brain area where the integration of sensory and hormonal stimulation leads to the onset of male sexual behavior, while in females the ventrolateral part of the ventromedial hypothalamic nucleus appears to have this function. In addition, Fos immunoreactivity was distributed in distinct clusters in subregions with various brain areas in males and females. This was observed especially in the posteromedial bed nucleus of the stria terminalis and posterodorsal medial amygdala, but also in the parvicellular subparafascicular nucleus, ventromedial hypothalamic nucleus and ventral premammillary nucleus. It appears that relatively small subunits within these nuclei seem to be concerned with the integration of sensory and hormonal information and may play a critical role in sexual behavior.