[Serotonergic control of feeding behavior via the lateral hypothalamic area analysis using in-vivo voltammetry].
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Results for “Hypothalamic Area, Lateral”
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[Reparative changes in the neurons of the lateral hypothalamic area of the brain in food deprivation].
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Animals↗
Electrolyte excretion in adrenalectomized rats submitted to cholinergic stimulation of the lateral hypothalamic area (LHA).
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Adrenalectomy↗
[The effect of calcitrin and corticotropin on pulmonary surfactant and engorgement in rats during activation of the lateral hypothalamic area].
The level of phospholipids, cholesterol, lipase activity in bronchoalveolar washes and lungs' blood capacity were studied in rats. An action exerted upon the hypothalamus led to a decrease in the surfactant lipids and the blood capacity of lungs. Possible peptidergic mechanisms of this are discussed.
Adrenocorticotropic Hormone↗
Brainstem projections from the lateral hypothalamic area in the rat, as studied with autoradiography.
Descending projections from the lateral hypothalamic area to the brainstem were studied, using [3H]-amino acid autoradiography, in the rat. Two main ipsilateral paths were reorganized. One is the periventricular fiber system projecting to the midbrain central gray. The other is a fiber system which eventually descends the central tegmental field, projecting strongly to the dorsal raphe nucleus, medial and lateral parabrachial nuclei, nucleus reticularis parvocellularis, solitary nuclei and dorsal motor nucleus of the vagus nerve. Sparse projections were observed to the nuclei raphe magnus, obscurus and pallidus, group B3 (or the ventrolateral subpial group) and spinal trigeminal nucleus.
Animals↗
Convergence of gastric vagal and cerebellar fastigial nuclear inputs on glycemia-sensitive neurons of lateral hypothalamic area in the rat.
Gastric vagal and cerebellar fastigial nuclear afferents have been implicated in the regulation of food intake by their communication with lateral hypothalamic area (LHA), which is generally referred to be the feeding center. This study was designed to examine the possible convergence of the inputs from the gastric vagal trunks and cerebellar fastigial nucleus (FN) on the LHA neurons. Among recorded 191 LHA neurons, 99 (51.8%) responded to the stimulation of the gastric vagal trunks, of which 55 (55.6%) also responded to the cerebellar FN stimulation. Of 62 LHA neurons that responded to the gastric vagal stimulation, 43 (69.4%) showed an inhibitory response to the intravenous glucose application indicating they were glycemia-sensitive neurons. When the gastric vagal trunks and cerebellar FN were stimulated simultaneously, a summation of the responses usually could be seen in the recorded LHA neurons (16/20, 80%). Moreover, of 45 LHA neurons that responded to both of the gastric vagal trunks and FN stimuli, 30 (66.7%) were identified to be glycemia-sensitive neurons. These results demonstrated that gastric vagal afferents could reach glycemia-sensitive neurons of the LHA, and that the inputs from cerebellar FN and gastric vagal trunks could converge onto glycemia-sensitive neurons in the LHA. According to the facts that gastric vagal inputs and blood glucose level may transmit meal-related visceral signals and FN may forward the somatic information to the LHA, we suggest that an integration of the somatic-visceral response related to the food intake may take place in the LHA following the gastric vagal and cerebellar FN afferent inputs and the integration may play an important role in the short-term regulation of feeding behavior.
Animals↗
[Effect of er'bao granule on integration of ingestion behavior-related information by neurons in lateral hypothalamic area of anorexia rats].
OBJECTIVE: To confirm the effect of Er'bao granule (EBG) on the sensitivity to peripheral afferent signal of neurons in lateral hypothalamic area (LHA) to illustrate the central mechanism of EBG in promoting ingestion behavior. METHODS: The anorexia rat model was established by feeding special prepared forage for one week, and all the model rats were administrated with EBG by gavage for 3 weeks. The spontaneous discharge of LHA neurons was recorded using electro-physiological extracellular recording method, and its response to electrical stimulus on gastric vagus nerve and intravenous injection of glucose were observed and compared among the normal, model and treated groups. RESULTS: As compared with the normal group, among the LHA neurons responding to afferent gastric vagal impulse, the proportion of glycemia-sensitive neurons in the model group was significantly decreased (P <0.01), but insignificant difference was shown in comparison between the treated group and the normal group. CONCLUSION: EBG play a role in regulating the sensitivity of LHA neurons to peripheral afferent signal and thus to influence the multi-afferent information integration of ingestion central neurons.
Afferent Pathways↗
[Effect of electro-acupuncture of zusanli on unit discharges in the lateral hypothalamic area induced by stomach distension].
Previous studies in our laboratory have shown that some unit discharges of the neurons in Feeding Centre of the lateral hypothalamic area (LHA) may be inhibited by distending stomach. The present study was performed to observe the effect of electro-acupuncture of "Zusanli" point on the discharge-inhibitory reaction induced by distending stomach in rats. Among 52 unit discharges observed, 36 (69.2%) showed that electro-acupuncturing "Zusanli" point abolished the inhibitory reaction induced by distending stomach. The durations of the effect range from 5 to 15 minutes. These results indicate that the somatic input from "Zusanli" plant may influence the reactivity of Feeding Centre of LHA to the activity of stomach.
Acupuncture Points↗
Enhancement of optokinetic responses by lateral hypothalamic areas associated with attack in cats.
Stimulation of lateral hypothalamic sites associated with predatory attack and known to modify trigeminal reflex systems enhanced efficiency of visual following over a wide range of target velocities. Furthermore, lateral hypothalamic stimulation reversed reflex habituation seen after continuous and after repeated optokinetic stimulation. These findings support the hypothesis that the lateral hypothalamus directs behavioral responses relevant to orienting to and capturing prey, at least in part, by regulation of reflex mechanisms in different sensory modalities. Possible neural substrates for the observed effects are discussed.
Animals↗
Glucagon release after stimulation of the lateral hypothalamic area in rats: predominant beta-adrenergic transmission and involvement of endorphin pathways.
Catheterization of the portal vein and stereotaxic implantation of electrodes in the lateral hypothalamic area (LHA) were performed in normal rats after thiopental anesthesia. Immunoreactive glucagon (IRG) and insulin (IRI), glucose, catecholamines, and beta-endorphin were monitored in portal and peripheral plasma, before and during electrical stimulation of the LHA. The influences on glucose and hormone concentrations of propranolol, phentolamine, atropine, and naloxone infusions were also investigated in similar rats. A basal portoperipheral concentration gradient was found for IRG, IRI, and catecholamines, but not for beta-endorphin. The LHA stimulation induced a significant rise in portal catecholamine, IRG, and glucose concentrations; IRI remained unchanged; the portoperipheral catecholamine gradient was augmented. These alterations were not observed after bilateral splanchnicectomy. Propranolol infusion abolished the LHA-dependent IRG and glucose rises. Naloxone reduced the IRG rise significantly. Phentolamine and atropine did not modify the LHA-induced reactions. These results suggest that the glucagon release which follows LHA electrical stimulation depends mainly on beta-adrenergic transmission by the splanchnic nerves. Opioid peptide receptors may modulate this effect.
Animals↗
Opposing roles of the nucleus accumbens and anterior lateral hypothalamic area in the control of sexual behaviour in the male rat.
Opposing roles have been implicated for the nucleus accumbens (NAc) and anterior portion of the lateral hypothalamic area (aLHA) in the regulation of sexual behaviour in male rats based on in vivo neurochemical correlates. The present study provides functional evidence supporting this hypothesis by examining the effects of lesions to these structures on copulation, noncontact erection and receptive female preference. Sexually naïve male Long-Evans rats received either bilateral 1.0- micro L injections of NMDA (10 micro g/ micro L/side) or vehicle (shams) into either the aLHA or the NAc. During repeated tests of copulation most of the sham-lesioned males, but few of the aLHA-lesioned and NAc-lesioned males, copulated to ejaculation. Most of the NAc-lesioned males also failed to intromit, whereas the majority of the aLHA-lesioned males intromitted repeatedly. During exposure to an inaccessible receptive female behind a wire-mesh screen, aLHA-lesioned males displayed facilitation of noncontact erections, whereas NAc-lesioned males displayed impaired noncontact erections. Conversely, during simultaneous exposure to inaccessible receptive and nonreceptive females in different compartments, all males spent more time in the proximity of the receptive female. These findings indicate that the aLHA plays an inhibitory role in the regulation of sexual arousal and an excitatory role in the regulation of ejaculation. Conversely, the NAc plays an excitatory role in the regulation in sexual arousal.
Animals↗
Participation of opiate pathways in the lateral hypothalamic area in the control of renal electrolyte and water excretion.
Injection of Met-enkephalin (0.05, 0.25 and 0.50 micrograms in 1 microliter) solutions into the lateral hypothalamic area (LHA) of unrestrained and unanesthetized rats caused a significant decrease of sodium (0.39 +/- 0.13 to 0.07 +/- 0.01, P less than 0.05) and potassium (0.61 +/- 0.17 to 0.21 +/- 0.04, P less than 0.05) excretion. When the blocking agent naloxone (0.20 micrograms in 1 microliter) was injected alone, a significant increase of sodium (0.34 +/- 0.04 to 0.96 +/- 0.28, P less than 0.05) and potassium (0.76 +/- 0.13 to 1.72 +/- 0.30, P less than 0.05) excretion was observed. However, a dose-response relationship was not observed. However, when in another experiment naloxone was injected before Met-enkephalin into the same area, reversal of the effect of naloxone occurred, with decreased sodium and potassium excretion. We conclude that the enkephalinergic pathway of the LHA when stimulated with Met-enkephalin plays an inhibitory role in the control of sodium and potassium excretion.
Animals↗
The presence of creatine kinase (CK)-immunoreactive neurons in the zona incerta and lateral hypothalamic area of the mouse brain.
Immunohistochemical studies of mouse brain using antibody to creatine kinase (CK) revealed a distinctive group of positive neurons in zona incerta and lateral hypothalamic area. These CK-immunoreactive neurons showed an intense, granular staining pattern, while other positive neurons distributed in other brain areas showed a weak, diffuse pattern.
Animals↗
Type II glucocorticoid receptor involvement in habituated activation of lateral hypothalamic area orexin-A-immunopositive neurons during recurring insulin-induced hypoglycemia.
Neurons that synthesize the potent orexigenic neuropeptide, orexin-A (ORX-A) are confined to the lateral hypothalamic area (LHA) and adjacent structures, and project throughout the central neuroaxis to structures that govern central nervous system responses to energy imbalance. Insulin-induced hypoglycemia (IIH) upregulates prepro-orexin mRNA and Fos immunostaining of LHA ORX-A neurons. These neurons apparently become desensitized to this metabolic challenge, since both responses are diminished by recurrent insulin-induced hypoglycemia (RIIH). Recent studies implicate central type II glucocorticoid receptors (GR) in RIIH-associated glucose counterregulatory collapse and decline in Fos labeling of central metabolic loci, including the LHA. The present studies evaluated the role of GR in patterns of LHA ORX-A neuronal transcriptional activation during RIIH. Groups of adult male rats were injected subcutaneously with one or four doses of the intermediate-acting insulin, Humulin NPH, on as many days, or with diluent alone. Rats injected with four doses of insulin were pretreated by intracerebroventricular (icv) administration of the selective GR antagonist, CP-472555, or the vehicle, propylene glycol, prior to insulin administration on days 1-3. All animals were sacrificed by transcardial perfusion 2h after injections on day 4. Processing of LHA tissue sections for dual-immunoperoxidase staining of ORX-A- and Fos-immunoreactivity (-ir) showed that colabeling of ORX-A neurons for Fos was increased by a single injection of NPH, whereas this genomic response was diminished by RIIH. Icv administration of CP-472555 during antecedent hypoglycemia prevented RIIH-associated reductions in Fos expression by these neurons. Antagonist treatment of diluent-injected controls did not alter mean numbers of ORX-A- plus Fos-ir neurons. Total numbers of ORX-A-immunopositive neurons were not different among treatment groups. These data demonstrate that precedent central GR blockade prevents adaptation of LHA ORX-A neuronal reactivity to RIIH. These results provide unique pharmacological evidence that hypoglycemic hypercorticosteronemia diminishes activation of this neurotransmitter phenotype in this critical metabolic structure to subsequent hypoglycemia via central GR-dependent mechanisms.
Animals↗
Sleep-waking discharge of neurons in the posterior lateral hypothalamic area of cats.
Damage to the posterior hypothalamic area produces a syndrome of EEG synchrony and behavioral somnolence. Cells of a recently described projection system within the posterior lateral hypothalamic area (PLHa) are potential candidates for mediating this area's influences on EEG and behavioral arousal. We examined PLHa neuronal activity during sleep and wakefulness in freely moving cats, identifying projection neurons by antidromic activation from stimulation sites in the external capsule, anterior cingulate bundle, or mesencephalic reticular formation. Orthodromic response evoked from these sites were also investigated. Twenty-two cells were found to send axons outside the PLHa; 9 with ascending projections and 13 with descending projections. Projection cells were found to discharge phasically in relation to waking movements. Most seemed to be related to complex head movements, although specific movement correlates were difficult to ascertain. Discharge rates during periods of waking immobility were similar to those occurring during slow-wave sleep. Rates during phasic REM sleep were generally similar to peak waking rates. Cells with ascending and descending projections displayed similar discharge profiles, although the former had somewhat higher rates in all conditions. Seventy-four cells were orthodromically driven from external capsule or anterior cingulate bundle. Responses evoked from these two sites were similar; an initial brief period of excitation, followed by a sustained (mean greater than 100 msec) episode of discharge suppression. Twenty-four cells exhibited orthodromic excitation from the mesencephalic reticular formation, but the duration of the subsequent discharge suppression was comparatively brief (mean less than 30 msec). With few exceptions, the discharge correlates of orthodromically driven cells were identical to those described above for identified projection neurons. These results do not support a role for neurons within the PLHa in the control of tonic EEG arousal. They are consistent with a possible involvement in either motor function, or phasic movement-related aspects of EEG activation.
Action Potentials↗
Estrogen attenuates the drinking response induced by activation of angiotensinergic pathways from the lateral hypothalamic area to the subfornical organ in female rats.
The present study was carried out to investigate whether estrogen modulates the drinking response induced by activation of angiotensinergic neural pathways from the lateral hypothalamic area (LHA) to the subfornical organ (SFO) in the female rats. Microinjection of ANG II (10(-10) M, 0.2 microl) into the LHA caused drinking in 17 out of 26 ovariectomized (OVX) female rats that were treated with propylene glycol (PG) vehicle and in 18 out of 28 OVX female rats that were treated with estrogen benzoate (EB). In both groups, previous injections of the ANG II antagonist saralasin (Sar, 10(-10) M, 0.2 microl) into the SFO significantly attenuated the water intake caused by the ANG II injection, suggesting that the ANG II-induced drinking response may be mediated by the angiotensinergic LHA projections to the SFO. Injections of ANG II (10(-10) M, 0.2 microl) into the SFO elicited drinking in all the animals that demonstrated the drinking response to ANG II injected into the LHA. The amount of water intake caused by either the injection of ANG II into the LHA or the SFO was significantly greater in the PG-treated than in the EB-treated animals. These results suggest that the circulating estrogen may act to attenuate the dipsogenic response induced by activation of the angiotensinergic pathways from the LHA to the SFO.
Angiotensin II↗
Modulation of natural killer cell activity affected by electroacupuncture through lateral hypothalamic area in rats.
Electroacupuncture (EA) has been reported to modulate natural killer cell (NK cell) activities. Also it is well known that hypothalamus directly mediates the effects of EA on analgesia. Especially lateral hypothalamic area (LHA) is related to splenic NK cell activities. In order to investigate the relationship between hypothalamus and effects of EA on NK cell activity, lesions have been made bilaterally at LHA of Spraque-Dawley rats. Subsequently, NK cell cytotoxities of normal and lesioned rats were measured with (51)Cr release immunoassay after EA stimulation for 2 and 14 days. NK cell activity of EA group was significantly higher than sham group. In addition, lesions abolished effects of EA on NK cell activity. These results strongly suggest that LHA is closely related to increase of NK cell activity induced by EA.
Animals↗
Renal water handling evaluated by lithium clearance following adrenergic and cholinergic stimulation of the lateral hypothalamic area.
Male Wistar rats weighing 230-300 g were used to characterize the participation of adrenergic and cholinergic receptors of the lateral hypothalamic area (LHA) in the control of renal water excretion. Since stimulation of adrenergic or cholinergic receptors has no effect on glomerular filtration rate, the antidiuresis and significant delay in urinary flow observed after lateral hypothalamic stimulation with carbachol (CCh) (0.036 +/- 0.005 to 0.019 +/- 0.003 microliters min-1 100 g body weight-1) and noradrenaline (Nad) (0.024 +/- 0.005 to 0.025 +/- 0.004 microliters min-1 100 g body weight-1) are secondary to an increase in distal tubular fluid reabsorption (DFR). Data are reported as means +/- SEM for ten rats in each group. Tubular water handling measured by lithium clearance demonstrated that LHA simulation with CCh (2.8 nmol in 1 microliter) and Nad (30.0 nmol in 1 microliter) leads to a significant reduction in proximal water reabsorption (CCh, 93.3 +/- 2.6 to 85.4 +/- 1.4%; Nad, 92.7 +/- 0.9 to 88.6 +/- 1.3%), with a simultaneous and significant increase in fluid reabsorption along the post-proximal nephron segments when compared to control (CNa) (CCh, 6.7 +/- 0.7 to 14.5 +/- 1.1%; Nad, 8.2 +/- 0.8 to 11.4 +/- 1.6%). These effects are blocked by muscarinic (atropine, 5 nmol in 1 microliter) and alpha-1 adrenoceptors (prazosin, 4 nmol in 1 microliter) antagonists. The results indicate the effective participation of the post-proximal nephron in the antidiuresis occurring after cholinergic and adrenergic LHA stimulation.
Animals↗