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At least 1,531 records · Page 85Linked to original sources
PubMed1992

Alpha 1-adrenergic agonists act on the ventromedial hypothalamus to cause neuronal excitation and lordosis facilitation: electrophysiological and behavioral evidence.

To see if activation of central alpha 1-adrenergic receptors can cause facilitation of lordosis in rats, the behavioral effects of centrally administered alpha 1-agonists, methoxamine (MA) and phenylephrine (PhE), and related agents were studied. In ovariectomized rats treated with estrogen, infusion of MA, PhE, or a beta-agonist isoproterenol, into the lateral ventricle, or bilateral infusions of MA or PhE into the ventromedial hypothalamus (VMH) facilitated lordosis. Conversely, intra-VMH infusion of the alpha 1-antagonist prazosin (PZ) inhibited lordosis. Intra-VMH infusion of isoproterenol or an alpha 2-agonist clonidine, had no effect. Neither was the intra-VMH infusion of MA effective if: (i) the rats were not primed with estrogen; (ii) the tips of the cannulae were outside the VMH; or (iii) it was preceded by an intra-VMH infusion of the alpha 1b-antagonist, chloroethylclonidine (CEC). These results not only verify implications from recent studies that alpha 1-receptors in the hypothalamus are important for lordosis facilitation, but further show that the adrenergic facilitatory effect are: (i) mediated specifically by alpha 1b-subtype of the alpha 1-receptor, (ii) estrogen-dependent, and (iii) site-specific to VMH. To investigate neural mechanisms potentially underlying the lordosis-facilitating effect of alpha 1-activation, the actions of MA and PhE on the electrical activity of single neurons of the ventromedial nucleus of the hypothalamus (VMN) in vitro were studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1993

Glucagon injected in the lateral hypothalamus stimulates sympathetic activity and suppresses monoamine metabolism.

Glucagon injected in the lateral hypothalamus stimulates sympathetic activity and suppresses monamine metabolism. The central hypothesis underlying this study is that there is a reciprocal relationship between food intake and sympathetic activity to IBAT. This hypothesis was tested by using intrahypothalamic microinjections of glucagon, a peptide that has been reported to decrease food intake. Sympathetic nerve activity to interscapular brown adipose tissue (IBAT) was measured as electrophysiological discharges of sympathetic nerves to IBAT. The microinjection of glucagon into the lateral hypothalamus (LH) increased sympathetic nerve activity by +103.8 +/- 35.0% (mean +/- S.E.M.) from pre-injection basal level by 30 min after injection. There was a gradual return to baseline. Micro-injection of glucagon into the LH depressed food intake. Monoamine metabolism was measured by using a microdialysis probe attached to a guide cannula for microinjection of glucagon into the LH. After microinjection of glucagon, the dialysates were collected over 30 min intervals and assayed for norepinephrine (NE), serotonin (5-HT), dopamine (DA) and their metabolites (3-methoxy-4-hydroxyphenylglycol (MHPG); 5-hydroxyindole-3-acetic acid (5-HIAA); and 3,4-dihydroxyphenylacetic acid (DOPAC). Glucagon suppressed both NE and MHPG concentrations in the lateral hypothalamus (LH), and the concentration of DOPAC was also decreased. There was no change of 5-HT concentration but 5-HIAA levels were reduced by glucagon treatment. These data show that glucagon injected in the LH stimulates sympathetic activity and suggest that this may have occurred by suppression of norepinephrine, dopamine and serotonin turnover in the LH of freely moving rats. These data support the hypothesis of a reciprocal relationship between food intake and sympathetic activity.

Adipose Tissue, Brown↗
PubMed1987

Somatosensorimotor function of the superior colliculus, somatosensory cortex, and lateral hypothalamus in the rat.

The role of the superior colliculus in multimodal sensory function is unsettled, in large part because a clear distinction between the somatosensory effects and the postural/motor effects of damage to the deep layers of the superior colliculus has not been obtained. Unilateral lesions of the entire superior colliculus impair orienting of the head and eyes to tactile, visual, and auditory stimuli presented on the side of the body contralateral to the lesion; however, even in the absence of sensory stimulation animals with such a lesion tend to circle ipsiversively and fail to make contralateral head movements. To determine whether or not unilateral damage to the superior colliculus produces a somatosensory asymmetry independently of head movement/circling biases, a neurological test was used in which lateral head or trunk movements were not required. Small pieces of adhesive-backed paper were attached to each forelimb and the latencies to contact and remove the stimuli were recorded. A battery of standard neurological tests was administered as well. The entire superior colliculus was removed unilaterally, and for comparison, the sensorimotor cortex or lateral hypothalamus were damaged in additional groups. Lesions of the superior colliculus produced the expected deficit in contralateral orienting and ipsilateral circling/postural biases, but failed to produce a somatosensory asymmetry in the head movement-independent sensorimotor test. In contrast, both sensorimotor cortex and lateral hypothalamus lesions produced a severe asymmetry in the head-movement-independent sensorimotor test. We conclude that the superior colliculus is involved in the control of lateral head movements and that its role in somatosensory function is fundamentally different from that of the sensorimotor cortex or lateral hypothalamus regions.

Animals↗
PubMed1992

Abstinence from U-50,488H, a kappa-opiate receptor agonist, decreases the binding of [3H]DPAT to 5-HT1A receptors in the hypothalamus of the rat.

The effect of trans-(+/-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl) cyclohexyl]-benzene-acetamide methane sulfonate (U-50,488H), a kappa-opiate agonist-induced tolerance and abstinence on 5-HT1A receptors was determined in regions of the brain and spinal cord of the rat. The administration of U-50,488H (25 mg/kg, i.p., twice daily) to male Sprague-Dawley rats for 4 days resulted in the development of almost complete tolerance to its analgesic and hypothermic effects. On day 5, the animals were divided into tolerant and abstinent groups and sacrificed. The brain and spinal cord were excised from all groups of rats and the brain was dissected into 6 regions, namely, amygdala, hypothalamus, striatum, midbrain, pons+medulla and cortex. The 5-HT1A receptors were characterized by using [3H]8-hydroxy-2-(di-n-propylamino)tetralin ([3H]DPAT) as the ligand. The binding constants (Bmax and Kd values) of [3H]DPAT in regions of the brain and spinal cord of rats tolerant to U-50,488H and vehicle did not differ. However, the Bmax value of [3H]DPAT in the hypothalamus of U-50,488H-abstinent rats was decreased but the Kd value did not change. In the other regions of the brain and spinal cord of U-50,488H-abstinent rats, the Bmax and Kd values of [3H]DPAT were unaffected. Subcutaneous administration of DPAT produced hypothermic response in vehicle- and U-50,488H-treated rats. The intensity of this effect was more marked in U-50,488H-abstinent group. It is concluded that 5-HT1A receptors are down-regulated in the hypothalamus of U-50,488H-abstinent rats but the hypothermic response to 5-HT1A agonist is intensified.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1982

Iontophoretic injections of kainic acid into the rat lateral hypothalamus: effects on ingestive behavior.

Iontophoretic injections of kainic acid into the dorsolateral hypothalamus of rats resulted in localized, partial depletions of neurons from the area without significant damage to adjacent areas of the diencephalon, including the zona incerta, dorsomedial hypothalamus and anterior as well as posterior regions of the hypothalamus that have been reported to be severely affected by mechanical injections of KA into the LH. Distant KA-sensitive structures such as the hippocampus and temporal lobe also showed no discernible neuronal loss or glial proliferation. The neuronal loss within the LH was far less severe after iontophoretic injections than after mechanical injections of KA. Our KA treated animals nonetheless displayed transient aphagia and adipsia, followed by variable periods of hypophagia and hypodipsia. After recovery of essentially normal ad lib feeding, the KA-treated rats failed to eat in response to a glucoprivic challenge (2-deoxy-D-glucose) but consumed normal quantities of water during periods of food deprivation. Their drinking response to hypertonic saline was somewhat reduced during the first hour after the treatment but normal at 6 as well as 24 hours. Unilateral KA injections produced only transient changes in ad lib food intake.

Animals↗
PubMed1985

Estrogen action in anterior and ventromedial hypothalamus and the modulation of heterosexual behavior in female golden hamsters.

Changes in heterosexual patterns of agonistic, marking, and sexual behavior were examined in female hamsters over a three day period following implantation of either estrogen or cholesterol in the hypothalamus. Animals were habituated to large arenas that permit the display of a wide range of behavior. Estrogen implants located in the ventromedial (VMH) but not the anterior (AH) portion of the hypothalamus were effective in facilitating the occurrence of vaginal marking, over a two day estrogen priming period. During this two day period, the exhibition of agonistic behavioral patterns declined significantly. Systemic administration of progesterone elicited sexual receptivity in 75% of the females in the VMH group, in contrast to only 25% in the AH group. Females with hypothalamic implants of cholesterol remained unreceptive following progesterone injections. The results provide important information on the estrogen sites of action at the hypothalamus in mediating heterosexual interactions.

Agonistic Behavior↗
PubMed1987

Asymmetry in responsiveness of the hypothalamus of the female rat to estradiol.

Asymmetry of function is an increasingly general principle of neuroanatomy, and right-left asymmetry has been observed in some neuroendocrine functions. We report that the right side of the hypothalamus of female rats is more responsive to estradiol than the left side of the hypothalamus for the induction of sexual receptivity. These results are consistent with previous suggestions that the left side of the hypothalamus is more sensitive to the defemininizing actions of neonatal hormones.

Animals↗
PubMed1991

Ventromedial hypothalamus vs. lateral hypothalamic D2 satiety receptors in the body weight increase induced by systemic sulpiride.

Two experiments were conducted in order to see if dopamine satiety receptors in the lateral hypothalamus or satiety mechanisms in the ventromedial hypothalamus were involved in the hyperphagia and body weight increase induced by systemic sulpiride. In the first experiment, it was shown that systemic sulpiride (20 mg/kg) does not block the anorexia caused by intraperifornical injections of amphetamine. In the second experiment, sulpiride (20 mg/kg during 18 days) did not produce an additional increase in body weight in previously VMH-lesioned female rats. This last fact cannot be explained by a ceiling effect since insulin (5 U/day during 7 days) increased body weight in the same VMH rats in which sulpiride was not effective. These results do not support the hypothesis that systemic sulpiride reaches the perifornical dopamine D2 receptors to disinhibit feeding, but suggest instead an involvement of the ventromedial hypothalamus. This last suggestion is more in agreement with the hypothesis that sulpiride alters feeding and body weight gain through the induction of a functional gonadectomy.

Amphetamine↗
PubMed1992

NMDA lesions of lateral hypothalamus enhance the acquisition of schedule-induced polydipsia.

Schedule-induced polydipsia (SIP) is affected by damage to various limbic structures that have connections with the lateral hypothalamus. The present experiment sought to determine whether or not SIP could be induced in rats bearing NMDA-induced lesions of the lateral hypothalamus. Following surgery, lesioned rats lost weight and were hypophagic and hypodipsic. Drinking, in response to systemic injection of hypertonic saline, was impaired in lesioned rats. Prior to testing for SIP, all rats were placed on a food-restriction regime to maintain body weight at 85% of normal. There was no statistically significant difference in mean body weight between lesioned and control groups before deprivation began, though lesioned rats were hypodipsic in their home cages. The lateral hypothalamic-lesioned rats acquired SIP significantly more rapidly than controls over the first six sessions, but over four following sessions no differences were present. The enhanced acquisition of SIP by lateral hypothalamic-lesioned rats cannot be accounted for by postoperative recovery of body weight or by hypodipsia in the home cage, neither of which correlated with SIP. It is suggested that the lateral hypothalamus has a role in cueing appropriate and inhibiting inappropriate behavior in conditions of motivational excitement. SIP is suggested to have two CNS components--one excitatory and one inhibitory.

Animals↗
PubMed1987

Norepinephrine release from PVN and lateral hypothalamus during perfusion with 2-DG or insulin in the sated and fasted rat.

Both insulin and 2-deoxy-D-glucose (2-DG) when given systemically to the rat modify the activity of noradrenergic systems in different regions of the animal's hypothalamus. The purpose of the present investigation was to ascertain whether the nutritional status of the animal would serve to influence the pattern of efflux of norepinephrine (NE) from sites in the hypothalamus perfused with either 2-DG or insulin. Permanent guide cannulae were first implanted stereotaxically above the paraventricular nucleus (PVN) or lateral hypothalamus (LH). Following recovery from surgery, each rat was either satiated with food or deprived of food for 20-22 hr with water always freely available. Then 0.1 microCi of [3H]-NE was micro-injected into the intended site of perfusion in a volume of 1.0 microliter. After 15 min had elapsed, the site was perfused repeatedly with an artificial CSF at a rate of 20 microliters/min. At the mid-point of successive 5.0 min perfusions, either 10 micrograms/microliter 2-DG or 4.0 mU/microliters porcine insulin was incorporated into the CSF perfusate. Thereafter, an additional set of 3-4 samples of perfusate was collected. When perfused in the PVN of the satiated rat, 2-DG significantly enhanced the efflux of [3H]-NE, whereas in the fasted animal insulin tended to suppress the output of the catecholamine. Conversely, at sites of perfusion in the LH, insulin evoked the release of [3H]-NE when the rat was fasted, whereas 2-DG tended to induce mixed effects on the release of [3H]-NE under both sated and fasted conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Effects of ibotenic acid lesion in the basal forebrain on electrical self-stimulation in the middle part of the lateral hypothalamus.

The aim of the present study was to analyse the involvement of neurons located in some basal forebrain areas in electrical self-stimulation elicited from the middle part of the lateral hypothalamus. The anterior hypothalamic region was unilaterally lesioned by local injection of ibotenic acid. Ten to 20 days later 4 electrodes were implanted bilaterally, two at the lesion level and two in the middle lateral hypothalamus. A small but significant self-stimulation deficit was observed in the lesioned area, while self-stimulation on the contralateral side was normal. At the middle lateral hypothalamic level, no deficit was observed when stimulation was applied either ipsilaterally or contralaterally to the anterior lesioned side. In most cases the lesion destroyed the dorsolateral part of the lateral preoptic area, the ventral pallidum-substantia innominata complex and the lateral part of the bed nucleus of the stria terminalis. Given the fact that these regions are known to project massively to the middle lateral hypothalamic area, our data suggest that descending influences originating in the damaged regions are not involved in self-stimulation elicited from the middle hypothalamus.

Animals↗
PubMed1985

Cholecystokinin-immunoreactive innervation of the ventromedial hypothalamus in the rat: possible substrate for autonomic regulation of feeding.

Cholecystokinin octapeptide (CCK) injected into the medial hypothalamus of the rat has been reported to suppress feeding. In this species, the superior lateral parabrachial subnucleus, which predominantly innervates the ventromedial nucleus of the hypothalamus, is composed primarily of CCK-immunoreactive neurons. Combined retrograde tracing using fluorescent dyes and immunofluorescence for CCK confirms that 80-90% of the neurons in the superior lateral parabrachial nucleus which innervate the ventromedial nucleus of the hypothalamus are CCK-positive. This pathway may underlie autonomic regulation of feeding behavior.

Animals↗
PubMed1989

Modulation by corticotropin-releasing factor of monoamine metabolism in the lateral hypothalamus.

Corticotropin-releasing factor (CRF) was injected into the lateral hypothalamus of conscious unrestrained rats and the local concentration of monoamines in the vicinity of the microinjection monitored by microdialysis. The concentration of norepinephrine and MHPG in the dialysis fluid from the lateral hypothalamic areas of rats fasted for 24 h was nearly 4 times higher than in fed rats. Following the injection of 2 micrograms of CRF into the lateral hypothalamus of fasted rats there was a rapid decline in levels of both norepinephrine and 3-methoxy-4-hydroxyphenylglycol (MHPG) to the level in fed rats after 60-90 min. The changes in MHPG and norepinephrine in the fed rats were not significant There was no difference in serotonin concentration between fasted and fed animals, although the mean value for 5-hydroxyindoleacetic acid (5-HIAA) was slightly increased. Following the injection of CRF, there was a fall in serotonin in the fed rats but not in the fasted animals. There was a fall in the concentration of 5-HIAA in both the fasted and fed rats so that at 30, 60 and 90 min their concentrations were not significantly different. The concentration of DOPAC in the lateral hypothalamus was twice as high in the fasted as in the fed rats. Following injection of CRF there was a rapid decline in DOPAC concentrations in the fasted rats and a small decline in the fed rats. By the end of 30 min after the injection of CRF, concentrations of DOPAC were similar in fed and fasted rats.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

Modulation by catecholamine of hypothalamus-pituitary-adrenocortical (HPA) axis activity in morphine-tolerance and withdrawal.

1. Hypothalamic noradrenaline (NA), dopamine (DA) and plasma corticosterone concentrations were determined after acute morphine administration to both naive and morphine-tolerant rats and during naloxone-induced withdrawal. 2. Acutely administered morphine (30 mg/kg) significantly increased the plasma level of corticosterone and reduced the NA and DA content in the hypothalamus. Naloxone (1 mg/kg), administered before morphine, blocked the effect of the opiate on both plasma corticosterone and hypothalamic NA concentration. 3. In chronically morphine-treated rats, a challenge dose of morphine (30 mg/kg) neither modified the plasma corticosterone level nor the NA concentration, while DA content was significantly enhanced. 4. After naloxone-induced withdrawal, the hypothalamic content of NA was significantly reduced, simultaneously with an increase in plasma corticosterone, while DA content remained unchanged. 5. These results suggest that the hypothalamic noradrenergic neurons are mainly mainly implicated in the effect of acute morphine on the hypothalamus-pituitary-adrenocortical (HPA) axis and in the tolerance development to this effect. The results also suggest that a hyperactivity of noradrenergic pathways in the hypothalamus would be one of the physiologically relevant mechanisms mediating the neuroendocrine opiate withdrawal at the HPA level.

Animals↗
PubMed1984

Axon collaterals of supraoptic neurones: anatomical and electrophysiological evidence for their existence in the lateral hypothalamus.

The magnocellular neurones of the supraoptic nucleus which synthesize and secrete vasopressin and oxytocin have been commonly regarded as simple "output" neurones in that they receive an input, generate an action potential and in turn release hormone from their terminals in the posterior pituitary. Three lines of evidence are presented which suggest that rat supraoptic nucleus neurons also have axon collaterals which terminate in the hypothalamus close to the nucleus. Small injections of horseradish peroxidase were made directly into the nucleus in hypothalamic slices, allowing visualization of the axons of supraoptic neurones. Collaterals of these axons could be observed in regions both dorsal and dorsolateral to the supraoptic nucleus. In a separate series of experiments, sections of perfusion-fixed hypothalamus were stained for vasopressin and oxytocin using specific antisera. Peptide-containing collaterals of both types were observed near the supraoptic nucleus, in a region similar to that seen after horseradish peroxidase injections. Finally, electrophysiological studies were carried out on hypothalamic slices containing the supraoptic nucleus. A small concentric bipolar stimulating electrode was placed directly into the nucleus and activity of lateral hypothalamic neurones within 0.1-1 mm of the nucleus was recorded. Of 68 neurones studied, 52 were excited by supraoptic stimulation via a synaptic pathway that could be blocked by Ca2+ -free solutions containing 18 mM Mg2+. These studies suggest that supraoptic neurones communicate via axon collaterals with other neurones in the lateral hypothalamus, in addition to their previously well characterised functional role in neurosecretion.

Animals↗
PubMed1991

Lesions of the dopaminergic nigrostriatal pathway alter preprosomatostatin messenger RNA levels in the striatum, the entopeduncular nucleus and the lateral hypothalamus of the rat.

The distribution and level of labeling for the messenger RNA encoding preprosomatostatin was studied in the striatum and entopeduncular nucleus of rats with and without a selective destruction of the dopaminergic nigrostriatal pathway. 6-Hydroxydopamine was injected unilaterally in the substantia nigra and the animals were killed 2 or 3 weeks after the lesion. Preprosomatostatin messenger RNA was visualized with a 35S-labeled RNA or DNA probe in frontal cryostat-cut sections by in situ hybridization histochemistry. The number of labeled cells as well as the intensity of labeling overlying each cell were measured on radioautograms developed before saturation of the emulsion. In rats with a 6-hydroxydopamine lesion, the number of labeled cells and the intensity of labeling over each cell were decreased in the striatum ipsilateral to the lesion compared to the contralateral side and to both striata of control rats. In the same sections, the number of cells in the cerebral cortex was lower in the ipsilateral side of the lesion but the difference was only significant in the frontoparietal cortex. In contrast, a massive increase (+300%) in the number of labeled cells and in the intensity of labeling per cell was observed in the entopeduncular nucleus and the adjacent lateral hypothalamus on the side ipsilateral to the lesion when compared to the contralateral side and to control rats. The results suggest that dopamine exerts opposite effects on somatostatin gene expression in neurons of the striatum and the entopeduncular nucleus/lateral hypothalamus, effects which are likely to be of importance for the control of basal ganglia output activity. In addition, the dramatic changes observed in the somatostatinergic neurons of the lateral hypothalamus, an area involved in the control of food and water intake, may be related to some aspects of the symptomatology of Parkinson's disease.

Animals↗
PubMed1991

The regulation of feeding and drinking in rats with lesions of the lateral hypothalamus made by N-methyl-D-aspartate.

Rats bearing excitotoxic lesions of the lateral hypothalamus are hypodipsic and hypophagic, but responses to 24 h food or water deprivation are normal, as are responses to different taste stimuli. The most striking deficit present in lateral hypothalamic-lesioned rats is an inability to respond as controls to dehydrating, dipsogenic or glucoprivic challenges. The present experiments examined the ability of rats bearing bilateral N-methyl-D-aspartate-induced lesions of the lateral hypothalamus to recognize and respond to changes in their internal environments. All of the lesioned rats tested showed mild to moderate hypophagia and hypodipsia, and none responded properly by drinking over 1 h after i.p. injection of hypertonic saline. However, the addition of glucose to the water supply promoted an increase in drinking and a decrease in lab chow consumption to maintain a constant energy intake; the addition of salt to the diet promoted an increase in drinking and no change in eating; 24 h water deprivation induced the same amount of drinking in lateral hypothalamic-lesioned rats as in controls; and injection i.p. of water (but not physiological saline) before drinking water was returned to rats which were 24 h water deprived suppressed drinking. These data suggest that lateral hypothalamic-lesioned rats are in receipt of normal information from their peripheries, and that they can adjust their behaviour over a period of days or minutes to changes in the internal milieu. The most consistent deficit is in responding actively and rapidly to challenging stimuli; the nature of this and the mechanisms which might produce it are discussed. We suggest that the consequences of excitotoxic lesion are better explained by disruption of input to the cortex from the lateral hypothalamus rather than by interference with metabolic processes.

Adaptation, Physiological↗
PubMed1987

Projections between the hypothalamus and the dorsal vagal complex in the cat: an HRP and autoradiographic study.

The hypothalamus is known to be intimately involved in the control of autonomic function. This study provides detailed information about pathways between the hypothalamus and the dorsal vagal complex in cat. Injection of horseradish peroxidase into the dorsomedial medulla produced retrograde neuronal labeling in the paraventricular nucleus of the hypothalamus. Injection of 3H-leucine into the paraventricular nucleus produced dense anterograde labeling in the dorsal motor nucleus of the vagus, and lighter labeling in the nucleus of the tractus solitarius, particularly in its medial subnucleus. The subnucleus gelatinous was virtually free of label, except in its medial and lateral portions. Anterograde labeling was distributed bilaterally, with an ipsilateral predominance. Injection of horseradish peroxidase into the area of the paraventricular nucleus produced retrograde neuronal labeling bilaterally in the nucleus of the tractus solitarius and the reticular formation ventrolateral to the dorsal vagal complex. anterograde terminal labeling overlapped the distribution of retrogradely labeled neurons. These findings are compared to those in rat, and discussed in relation to their functional implications.

Animals↗