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1.
Article in Chinese | WPRIM | ID: wpr-877651

ABSTRACT

OBJECTIVE@#To observe the effect of electroacupuncture (EA) preconditioning at heart meridian acupoints on the contents of dopamine (DA) and 5-hydroxytryptamine (5-HT) in lateral hypothalamus area (LHA) and cerebellar fastigial nucleus (FN) in the rats with acute myocardial ischemia-reperfusion injury (MIRI), and explore the role and mechanism of LHA and FN in the effect of EA at heart meridian acupoints against acute MIRI.@*METHODS@#Sixty SD rats were randomly divided into a sham-operation group, a model group, an EA heart meridian group and an EA lung meridian group, 12 rats in each group, as well as an LHA plus heart meridian group (damage of bilateral LHA) and an FN plus heart meridian group (damage of bilateral FN), 6 rats in each one. Three days after nucleus destruction, EA was applied to "Shenmen" (HT 7) and "Tongli" (HT 5) in the EA heart meridian group, the LHA plus heart meridian group and the FN plus heart meridian group and EA was applied to "Taiyuan" (LU 9) and "Lieque" (LU 7) in the EA lung meridian group, with 1 V in stimulating voltage and 2 Hz in frequency, lasting 20 minutes each time, once a day, for consecutively 7 days before model replication. Except in the sham-operation group, MIRI rat models were duplicated by ligation of the left anterior descending branch of the coronary artery in the rest groups. Using Power lab physiological recorder, ST segment displacement value was recorded before modeling, 30 min after ligation and 120 min after reperfusion separately. The high performance liquid chromatography-electrochemical detection and analysis system was adopted to determine the contents of DA and 5-HT in LHA and FN dialysate after rat modeling in each group.@*RESULTS@#In comparison of ST segment displacement value 30 min after ligation and 120 min after reperfusion among groups, the value in the model group was higher than that in the sham-operation group (@*CONCLUSION@#EA preconditioning at heart meridian acupoints can effectively alleviate myocardial injury in acute MIRI rats, during which, DA and 5-HT in LHA and FN may be the important material basis.


Subject(s)
Acupuncture Points , Animals , Cerebellar Nuclei , Dopamine , Electroacupuncture , Hypothalamic Area, Lateral , Myocardial Ischemia , Myocardial Reperfusion Injury/therapy , Rats , Rats, Sprague-Dawley , Serotonin
2.
Experimental Neurobiology ; : 307-317, 2016.
Article in English | WPRIM | ID: wpr-172189

ABSTRACT

Chronic stress induces changes in neuronal functions in specific brain regions regulating sociability and mood-related behaviors. Recently we reported that stress-induced persistent upregulation of the neuropeptides orexin and melanin-concentrating hormone (MCH) in the basolateral amygdala (BLA) and the resulting activation of orexin receptors or MCH receptors within the BLA produced deficits in sociability and mood-related behaviors. In the present study, we investigated the neural targets that were innervated by BLA neurons containing orexin receptors or MCH receptors. The viral vector system AAV2-CaMKII-ChR2-eYFP was injected into the BLA to trace the axonal tracts of BLA neurons. This axon labeling analysis led us to identify the prelimbic and infralimbic cortices, nucleus accumbens (NAc), dorsal striatum, paraventricular nucleus (PVN), interstitial nucleus of the posterior limb of the anterior commissure, habenula, CA3 pyramidal neurons, central amygdala, and ventral hippocampus as the neuroanatomical sites receiving synaptic inputs of BLA neurons. Focusing on these regions, we then carried out stimulus-dependent c-Fos induction analysis after activating orexin receptors or MCH receptors of BLA neurons. Stereotaxic injection of an orexin receptor agonist or an MCH receptor agonist in the BLA induced c-Fos expression in the NAc, PVN, central amygdala, ventral hippocampus, lateral habenula and lateral hypothalamus, which are all potentially important for depression-related behaviors. Among these neural correlates, the NAc, PVN and central amygdala were strongly activated by stimulation of orexin receptors or MCH receptors in the BLA, whereas other BLA targets were differentially and weakly activated. These results identify a functional connectivity of BLA neurons regulated by orexin and MCH receptor systems in sociability and mood-related behaviors.


Subject(s)
Axons , Basolateral Nuclear Complex , Brain , Central Amygdaloid Nucleus , Depression , Extremities , Habenula , Hippocampus , Hypothalamic Area, Lateral , Neurons , Neuropeptides , Nucleus Accumbens , Orexin Receptors , Paraventricular Hypothalamic Nucleus , Pyramidal Cells , Up-Regulation
3.
Experimental Neurobiology ; : 163-173, 2016.
Article in English | WPRIM | ID: wpr-78639

ABSTRACT

Chronic stress induces anxiety disorders, whereas physical exercise is believed to help people with clinical anxiety. In the present study, we investigated the mechanisms underlying stress-induced anxiety and its counteraction by exercise using an established animal model of anxiety. Mice treated with restraint for 2 h daily for 14 days exhibited anxiety-like behaviors, including social and nonsocial behavioral symptoms, and these behavioral impairments lasted for more than 12 weeks after the stress treatment was removed. Despite these lasting behavioral changes, wheel-running exercise treatment for 1 h daily from post-stress days 1 - 21 counteracted anxiety-like behaviors, and these anxiolytic effects of exercise persisted for more than 2 months, suggesting that anxiolytic effects of exercise stably induced. Repeated restraint treatment up-regulated the expression of the neuropeptide, melanin-concentrating hormone (MCH), in the lateral hypothalamus, hippocampus, and basolateral amygdala, the brain regions important for emotional behaviors. In an in vitro study, treatment of HT22 hippocampal cells with glucocorticoid increased MCH expression, suggesting that MCH upregulation can be initially triggered by the stress hormone, corticosterone. In contrast, post-stress treatment with wheel-running exercise reduced the stress-induced increase in MCH expression to control levels in the lateral hypothalamus, hippocampus and basolateral amygdala. Administration of an MCH receptor antagonist (SNAP94847) to stress-treated mice was therapeutic against stress-induced anxiety-like behaviors. These results suggest that repeated stress produces long-lasting anxiety-like behaviors and upregulates MCH in the brain, while exercise counteracts stress-induced MCH expression and persisting anxiety-like behaviors.


Subject(s)
Animals , Anti-Anxiety Agents , Anxiety , Anxiety Disorders , Basolateral Nuclear Complex , Behavioral Symptoms , Brain , Corticosterone , Exercise , Hippocampus , Hypothalamic Area, Lateral , In Vitro Techniques , Mice , Models, Animal , Neuropeptides , Up-Regulation
4.
Article in English | WPRIM | ID: wpr-149835

ABSTRACT

Dexmedetomidine (DEX), a highly selective alpha2-adrenergic receptor agonist, is the newest agent introduced for sedation in intensive care unit (ICU). The sedation strategy for critically ill patients has stressed light sedation with daily awakening and assessment for neurologic, cognitive, and respiratory functions, since Society of Critical Care Medicine (SCCM) guidelines were presented in 2002. The traditional GABAergic agents, including benzodiazepines and propofol, have some limitations for safe sedatives in this setting, due to an unfavorable pharmacokinetic profile and to detrimental adverse effects (such as lorazepam associated propylene glycol intoxication and propofol infusion syndrome). DEX produces it's sedative, analgesic and cardiovascular effects through alpha2 receptors on the locus ceruleus (LC). Activities of LC, the tuberomammillary nucleus (TMN) are depressed and activity of the ventrolateral preoptic nucleus (VLPO) is increased during DEX sedation, which is similar in features to normal non-REM (NREM) sleep. At the same time, perifornical orexinergic activity is maintained, which might be associated with attention. This mechanism of action produces a normal sleep-like, cooperative sedation. The characteristic feature of sedation, together with a concomitant opioid sparing effect, may decrease the length of time spent on a ventilator, length of stay in ICU, and prevalence and duration of delirium, as the evidence shown from several comparative studies. In addition, DEX has an excellent safety profile. In conclusion, DEX is considered as a promising agent optimized for sedation in ICU.


Subject(s)
Alkenes , Benzodiazepines , Critical Care , Critical Illness , Delirium , Dexmedetomidine , GABA Agents , Humans , Hypnotics and Sedatives , Hypothalamic Area, Lateral , Intensive Care Units , Length of Stay , Light , Locus Coeruleus , Lorazepam , Prevalence , Propofol , Propylene Glycol , Ventilators, Mechanical
5.
Acta Pharmaceutica Sinica ; (12): 247-252, 2011.
Article in Chinese | WPRIM | ID: wpr-348969

ABSTRACT

Histaminergic neurons solely originate from the tuberomammillary nucleus (TMN) in the posterior hypothalamus and send widespread projections to the whole brain. Experiments in rats show that histamine release in the central nervous system is positively correlated with wakefulness and the histamine released is 4 times higher during wake episodes than during sleep episodes. Endogeneous prostaglandin E2 and orexin activate histaminergic neurons in the TMN to release histamine and promote wakefulness. Conversely, prostaglandin D2 and adenosine inhibit histamine release by increasing GABA release in the TMN to induce sleep. This paper reviews the effects and mechanisms of action of the histaminergic system on sleep-wake regulation, and briefly discusses the possibility of developing novel sedative-hypnotics and wakefulness-promoting drugs related to the histaminergic system.


Subject(s)
Adenosine , Physiology , Animals , Dinoprostone , Physiology , Histamine , Metabolism , Physiology , Hypothalamic Area, Lateral , Physiology , Intracellular Signaling Peptides and Proteins , Physiology , Neurons , Physiology , Neuropeptides , Physiology , Orexins , Prostaglandin D2 , Physiology , Sleep , Physiology , Wakefulness , Physiology , gamma-Aminobutyric Acid , Metabolism
6.
Rev. méd. hondur ; 78(4): 188-190, oct.-dic. 2010. graf, tab
Article in Spanish | LILACS | ID: lil-644932

ABSTRACT

Introducción. Se ha sugerido la relación entre trastornos neuropsíquicos así como de las crisis epilépticas con la localización de túberes corticales en el Complejo Esclerosis Tuberosa (CET). El objetivo del estudio fue determinar esta relación en una muestra de pacientes evaluados en el período 1995-2005 en la Consulta Externa del Servicio de Neurología Pediátrica del Hospital Infantil de México “Federico Gómez”. Presentación de casos. Se evaluó dicha comorbilidad en 46 pacientes que cumplieron los criterios para el completo CET y se estudió la correlación entre epilepsia y los trastornos del comportamiento y lenguaje durante el último año en relación con el número de túberes corticales. El 52% de los pacientes presentaron conducta normal, 19.6% presentó agresividad, 15.2 % rasgos autistas y 13% trastornos de lenguaje. El 78% presentaba epilepsia de varios tipos. Conclusión. Aunque hubo una tendencia en la relación, no hubo significancia estadística entre los trastornos de conducta y el número de túberes (p= 0.31), ni entre la ocurrencia de epilepsia y los trastornos de la conducta y lenguaje (p= 0.96). Se requiere de una muestra más grande para evaluar mejor esta comorbilidad; sin embargo, es recomendable en la práctica clínica, la vigilancia por trastornos de conducta y lenguaje en pacientes con más de un túber cerebral...


Subject(s)
Humans , Male , Female , Child , Epilepsy/complications , Tuberous Sclerosis/diagnosis , Mental Disorders/psychology , Hypothalamic Area, Lateral , Language Development Disorders/psychology
7.
Acta Physiologica Sinica ; (6): 451-457, 2009.
Article in Chinese | WPRIM | ID: wpr-302428

ABSTRACT

In the present study, rat model of gastric ischemia-reperfusion (GI-R) injury was established by clamping the celiac artery for 30 min followed by 1 h of reperfusion. Subsequently, the regulatory effect of electrical stimulation of cerebellar fastigial nucleus (FN) on GI-R injury and its neural mechanisms were investigated in Sprague-Dawley rats. The results are as follows. Electrical stimulation of the cerebellar FN not only obviously attenuated the GI-R injury in an intensity-dependent manner, but also decreased the apoptosis rate of gastric mucosal cells. Chemical lesion of FN eliminated the protective effect of electrical stimulation of FN on GI-R injury. Electrical stimulation of cerebellar FN decreased both the frequency and amplitude of the discharges of greater splanchnic nerve, but it could not change the discharge of greater splanchnic nerve following the lesion of the lateral hypothalamic area (LHA). After bilateral section of the greater splanchnic nerves, electrical stimulation of the FN also attenuated the GI-R injury. Chemical lesion of the LHA reversed the protective effect of electrical stimulation of FN on GI-R injury. Electrical stimulation of FN increased the activity of superoxide dismutase (SOD), but decreased the content of malondialdehyde (MDA) in gastric mucosa under GI-R. These results indicate that the cerebellar FN may regulate GI-R injury. Therefore, the cerebellar FN is an important brain site protecting the stomach against GI-R. The LHA and greater splanchnic nerves participate in the regulatory effects of cerebellar FN stimulation on GI-R injury. In addition, antioxidation may also be involved in the protection mechanism of cerebellar FN stimulation.


Subject(s)
Animals , Apoptosis , Cerebellar Nuclei , Physiology , Electric Stimulation , Gastric Mucosa , Cell Biology , Metabolism , Hypothalamic Area, Lateral , Malondialdehyde , Metabolism , Rats , Rats, Sprague-Dawley , Reperfusion Injury , Superoxide Dismutase , Metabolism
8.
Article in English | WPRIM | ID: wpr-727515

ABSTRACT

Signal transducer and activator of transcription 4 (STAT4), a STAT family member, mediates interleukin 12 (IL12) signal transduction. IL12 is known to be related to calorie-restricted status. In the central nervous system, IL12 also enhances the production of nitric oxide (NO), which regulates food intake. In this study, the expression of neuronal NO synthase (Nos1), which is also related to food intake, was investigated in the hypothalamic areas of Stat4 knockout (KO) mice using nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry, a marker for neurons expressing Nos1 enzyme. Western blots were also performed to evaluate Nos1 and Fos expression. Wild-type Balb/c (WT group, n=10 male) and Stat4 KO mice (Stat4 KO group, n=8 male) were used. The body weight and daily food intake in the WT group were 22.4+/-0.3 and 4.4 g per day, while those in the Stat4 KO group were 18.7+/-0.4 and 1.8 g per day, respectively. Stat4 mice had lower body weight and food intake than Balb/c mice. Optical intensities of NADPH-d-positive neurons in the paraventricular nucleus (PVN) and lateral hypothalamic area (LHA) of the Stat4 KO group were significantly higher than those of the WT group. Western blotting analysis revealed that the hypothalamic Nos1 and Fos expression of the Stat4 KO group was up-regulated, compared to that in the WT group. These results suggest that Stat4 may be related to the regulation of food intake and expression of Nos1 in the hypothalamus.


Subject(s)
Animals , Blotting, Western , Body Weight , Central Nervous System , Eating , Humans , Hypothalamic Area, Lateral , Hypothalamus , Interleukin-12 , Mice , Mice, Knockout , NAD , Neurons , Nitric Oxide , Nitric Oxide Synthase , Paraventricular Hypothalamic Nucleus , Signal Transduction , STAT4 Transcription Factor
9.
Article in Korean | WPRIM | ID: wpr-198854

ABSTRACT

A current hypothesis of sleep-wake regulation proposes that the sleep process starts with the activation of sleep-promoting neurons located in the preoptic area of the anterior hypothalamus. This activation leads to the inhibition of wake-promoting neurons located in the posterior hypothalamus, basal forebrain, and mesopontine tegmentum, which, in turn removes inhibition from the sleep-promoting structures(i.e., disinhibition) to initiate the sleep process. Mutual inhibition between these wake- and sleep-promoting neurons results in switching properties that define discrete wakeful and sleep states with sharp transitions between them. Wake-promoting nuclei include the orexinergic lateral hypothalamic/perifornical area, the histaminergic tuberomammillary nucleus, the cholinergic pedunculopontine tegmental nucleus, the noradrenergic locus coeruleus, the 5-hydroxytryptaminergic raphe nuclei, and possibly the dopaminergic ventral tegmental area. The major sleep-promoting nucleus is the GABAergic ventrolateral preoptic nucleus of the hypothalamus. The regulation of sleep is classically viewed as the dual interaction of circadian(SCN-based) and homeostatic processes, and the propensity to be asleep or awake at any given time is a consequence of a sleep debt and its interaction with signals from the SCN circadian clock. To better understand the mechanisms of sleep and wakefulness, the focus of pharmacotherapy is on targeting specific therapies to the particular defect in sleep-wake regulation.


Subject(s)
Circadian Clocks , Circadian Rhythm , Drug Therapy , Hypothalamic Area, Lateral , Hypothalamus , Hypothalamus, Anterior , Hypothalamus, Posterior , Locus Coeruleus , Neuroanatomy , Neurons , Pedunculopontine Tegmental Nucleus , Preoptic Area , Prosencephalon , Raphe Nuclei , Sleep Wake Disorders , Ventral Tegmental Area , Wakefulness
10.
Article in Chinese | WPRIM | ID: wpr-269848

ABSTRACT

<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>


Subject(s)
Afferent Pathways , Animals , Anorexia , Drug Therapy , Drugs, Chinese Herbal , Pharmacology , Therapeutic Uses , Electrophysiology , Feeding Behavior , Hypothalamic Area, Lateral , Neurons , Physiology , Phytotherapy , Random Allocation , Rats , Rats, Sprague-Dawley , Vagus Nerve
11.
Article in English | WPRIM | ID: wpr-79785

ABSTRACT

This study was aimed to investigate the changes of orexin-A (OXA) and neuropeptide Y (NPY) expression in the hypothalamus of the fasted and high-fat diet fed rats. For the experiments, the male Sprague-Dawley (SD) rats were used as the model of high-fat diet-induced obesity. The mean loss of body weight (MLBW) did not show the linear pattern during the fasting; from 24 h to 84 h of fastings, the MLBW was not significantly changed. The numbers of OXA-immunoreactive (IR) neurons were decreased at 84 h of fasting compared with those in other five fasting subgroups. The NPY immunoreactivities in the arcuate nucleus (ARC) and the suprachiasmatic nucleus (SCN) observed at 84 h of fasting were higher than that observed at 24 h of fasting. The number of OXA-IR neurons of the LHA (lateral hypothalamic area) in the high-fat (HF) diet fed group was more increased than that of the same area in the normal-fat (NF) diet fed group. The NPY immunoreactivities of the ARC and the SCN were higher in HF group than those observed in the same areas of NF group. Based on these results, it is noteworthy that the decrease of the body weight during the fast was not proportionate to the time-course, implicating a possible adaptation of the body for survival against starvation. The HF diet might activate the OXA and the NPY in the LHA to enhance food intake.


Subject(s)
Adaptation, Physiological/physiology , Animals , Arcuate Nucleus of Hypothalamus/metabolism , Dietary Fats , Eating , Fasting/physiology , Hypothalamic Area, Lateral/metabolism , Hypothalamus/metabolism , Immunohistochemistry/veterinary , Intracellular Signaling Peptides and Proteins/metabolism , Male , Neuropeptide Y/metabolism , Neuropeptides/metabolism , Obesity , Rats , Rats, Sprague-Dawley/physiology , Suprachiasmatic Nucleus/metabolism
12.
Article in Korean | WPRIM | ID: wpr-137186

ABSTRACT

Brain natriuretic peptide (BNP) is a neuropeptide, isolated from porcine brain that is homologous with atriopeptin. Magnocellular neurosecretory cells located in the paraventricular nucleus and supraoptic nucleus synthesize and secrete neurohormones. The purpose of this study was to investigate distribution of BNP immunoreactivity throughout the rat hypothalamus from the day of birth to 30 days and adult using immunoperoxidase and immunofluorescent staining. The first BNP immunoreactive neurons appeared in the paraventricular and supraoptic nucleus at P10. In adult, BNP immunoreactivity was widely distributed throughout regions of the hypothalamus including dorsomedial hypothalamic nucleus, ventromedial hypothalamic nucleus, arcuate nucleus and internal layer of median eminence. The intensity of BNP immunoreactivity was weak in almost all hypothalamic nuclei except the paraventricular and supraoptic nuclei. BNP immunoreactivity was first observed in the lateral hypothalamic area at P15. In retrochiasmatic supraoptic nucleus, BNP immunoreactivity was first observed at P20 and remarkably distributed in adult. In the present study, distinct localization of BNP immunoreactivity was in the hypothalamic cell bodies and fibers. Although the role of BNP in the brain is yet to be determined, these results indicate that BNP in the neurons of hypothalamus play important role in the regulation of a variety of neurosecretory functions as a neuromodulator during postnatal development of the hypothalamus.


Subject(s)
Adult , Animals , Arcuate Nucleus of Hypothalamus , Brain , Dorsomedial Hypothalamic Nucleus , Humans , Hypothalamic Area, Lateral , Hypothalamus , Immunohistochemistry , Median Eminence , Natriuretic Peptide, Brain , Neurons , Neuropeptides , Neurotransmitter Agents , Paraventricular Hypothalamic Nucleus , Parturition , Rats , Supraoptic Nucleus , Ventromedial Hypothalamic Nucleus
13.
Article in Korean | WPRIM | ID: wpr-137183

ABSTRACT

Brain natriuretic peptide (BNP) is a neuropeptide, isolated from porcine brain that is homologous with atriopeptin. Magnocellular neurosecretory cells located in the paraventricular nucleus and supraoptic nucleus synthesize and secrete neurohormones. The purpose of this study was to investigate distribution of BNP immunoreactivity throughout the rat hypothalamus from the day of birth to 30 days and adult using immunoperoxidase and immunofluorescent staining. The first BNP immunoreactive neurons appeared in the paraventricular and supraoptic nucleus at P10. In adult, BNP immunoreactivity was widely distributed throughout regions of the hypothalamus including dorsomedial hypothalamic nucleus, ventromedial hypothalamic nucleus, arcuate nucleus and internal layer of median eminence. The intensity of BNP immunoreactivity was weak in almost all hypothalamic nuclei except the paraventricular and supraoptic nuclei. BNP immunoreactivity was first observed in the lateral hypothalamic area at P15. In retrochiasmatic supraoptic nucleus, BNP immunoreactivity was first observed at P20 and remarkably distributed in adult. In the present study, distinct localization of BNP immunoreactivity was in the hypothalamic cell bodies and fibers. Although the role of BNP in the brain is yet to be determined, these results indicate that BNP in the neurons of hypothalamus play important role in the regulation of a variety of neurosecretory functions as a neuromodulator during postnatal development of the hypothalamus.


Subject(s)
Adult , Animals , Arcuate Nucleus of Hypothalamus , Brain , Dorsomedial Hypothalamic Nucleus , Humans , Hypothalamic Area, Lateral , Hypothalamus , Immunohistochemistry , Median Eminence , Natriuretic Peptide, Brain , Neurons , Neuropeptides , Neurotransmitter Agents , Paraventricular Hypothalamic Nucleus , Parturition , Rats , Supraoptic Nucleus , Ventromedial Hypothalamic Nucleus
14.
Article in Korean | WPRIM | ID: wpr-644814

ABSTRACT

The hippocampus is known as involved in learning and memory functions and the entorhinal cortex plays a crucial role as a gateway connecting the several areas and hippocampal formation. Entorhinal cortex lesions have been employed in numerous studies as the Alzheimer's disease model. The purpose of this study were to identify the CNS hip-pocampal and cholinergic pathway and to investigate the morphological changes of the hippocampal cholinergic inner-vations by using the Pseudorabies virus injection into the hippocampus after entorhinal cortex lesions. The pseudorabies virus and double labelled neurons (ChAT and PRV) were distributed at several different nuclei including agranular insular cortex, bed nucleus of stria terminalis, central amygdala, globus pallidus, lateral segment, lateral hypothalamic area, laterodorsal tegmental nucleus, medial septal nucleus, mesencephalic reticular nucleus, periaqueductal gray matter and substantia innominata The morphological changes were observed in the hippocampal cholinergic innervation after entorhinal cortex lesions. These data suggested that the hippocampal cholinergic innervation showed morphological changes throughout the whole brain areas after entorhinal cortex lesion.


Subject(s)
Alzheimer Disease , Amygdala , Animals , Brain , Entorhinal Cortex , Globus Pallidus , Herpesvirus 1, Suid , Hippocampus , Hypothalamic Area, Lateral , Learning , Memory , Neurons , Periaqueductal Gray , Rats , Septal Nuclei , Substantia Innominata
15.
Acta Physiologica Sinica ; (6): 417-421, 2002.
Article in Chinese | WPRIM | ID: wpr-318975

ABSTRACT

The effects of administration of motilin into the lateral hypothalamic area (LHA) on gastric antrum motility in conscious rats and on gastric distention (GD) sensitive neurons in dorsal vagal complex (DVC) in anesthetized rats were studied. Microinjection of motilin (0.37 nmol/0.5 microl) into the LHA increased the gastric antrum motility index by 76.29 +/- 4.09% (P<0.01). In 60 GD sensitive neurons, firing rate increased in 39 neurons (65%) and decreased in 21 neurons (35%), which were classified as GD-excitatory and GD-inhibitory neurons, respectively. Firing rate by 7.17 +/- 7.89% within 1.5 min in 15 of 24 GD-excitatory neurons, and firing rate increased by 44.35 +/- 7.89% in 12 of 14 GD-inhibitory neurons after motilin microinjection into the LHA. The results suggest that exogenous motilin in LHA plays a role in the regulation of gastric antrum motility possibly via the vagal pathway from LHA-DVC to the stomach.


Subject(s)
Animals , Hypothalamic Area, Lateral , Microinjections , Motilin , Pharmacology , Neurons , Physiology , Pyloric Antrum , Physiology , Rats , Rats, Wistar , Vagus Nerve , Physiology
16.
Acta Physiologica Sinica ; (6): 435-440, 2002.
Article in Chinese | WPRIM | ID: wpr-318971

ABSTRACT

The effects of electrical and chemical stimulation and electrolytic lesion of lateral hypothalamic area (LHA) on gastric ischemia-reperfusion injury (GI-RI) were investigated in rats whose celiac arteries were clamped for 30 min and reperfused for 60 min by removal of the clamp. The results are as follows. (1) Electrical stimulation of LHA could aggravate GI-RI in an intensity-dependent manner by using 0.2, 0.4 or 0.6 mA current respectively. Microinjection of L-glutamic acid into LHA resulted in a similar effect to that of electrical stimulation of LHA on GI-RI. After electrolytic lesion of bilateral LHA, the area of gastric mucosal injury induced by gastric ischemia-reperfusion (GI-R) was smaller than that by electrical stimulation of LHA plus GI-R. (2) Dorsal vagal complex (DVC) lesion or vagotomy could eliminate the effect of electrical stimulation of LHA on GI-RI. (3) Electrical stimulation of LHA increased the content of malondialdehyde (MDA) but decreased the activity of superoxide dismutase (SOD) of ischemia-reperfusion (I-R) gastric mucosa. (4) Electrical stimulation of LHA plus gastric I-R increased gastric juice volume and total acid output, but there were no significant changes in acidity, pepsin activity and gastric barrier mucus. These results indicate that the LHA is an area in the CNS exerting aggravate effects on GI-RI. The DVC and vagus may be involved in the regulative effects of LHA on GI-RI. These effects are associated with increases in gastric mucosal MDA content, gastric juice volume, and total acid output, and a decrease in SOD activity.Acidity, pepsin activity and gastric barrier mucus do not seem to play an important role.


Subject(s)
Animals , Electric Stimulation , Gastric Mucosa , Metabolism , Pathology , Hypothalamic Area, Lateral , Metabolism , Male , Malondialdehyde , Metabolism , Rats , Rats, Sprague-Dawley , Reperfusion Injury , Metabolism , Pathology , Superoxide Dismutase , Metabolism
17.
Article in Korean | WPRIM | ID: wpr-19040

ABSTRACT

BACKGROUND: Several studies have reported that cholecystokinin (CCK), a short-term meal related satiety signal, and leptin, long-term signal for controlling feeding behaviour and body weight, act synergistically to inhibit food intake. However the mechanism and neuroanatomical basis for this response remain unclear. To clarify the neuronal mechanisms underlying the synergistic interaction between leptin and CCK, we examined the neuron activated by single or combined injection of leptin and CCK in fasted rats using immunohistochemistry for Fos. The expression of Fos can be used to trace neuronal activation pathways. METHODS: The rats were divided into 4 groups; Tris solution-saline, Tris solution-CCK, leptin-saline, leptin-CCK. Rats were received a single intracerebroventricular injection of either 3mul Tris solution or 3microgram leptin, and a single intraperitoneal injection of either 2mul saline or 2microgram/kg sulfated CCK-8. The changes of the Fos expression were investigated in the paraventricular nucleus (Pa), retrochiasmatic area (RCh), lateral hypothalamic nucleus (LH), central nucleus of amygdala(Ce), supraoptic nucleus (SO), arcuate nucleus (Arc), ventromedial hypothalamic nucleus(VMH),dorsomedial hypothalamic nucleus (DM), ventral premammillary nucleus (PMV), superior lateral subdivision of parabrachial nucleus (LPBS), external lateral subdivision of parabrachial nucleus (LPBE), supragenual nucleus (SGe), area postrema (AP), medial area (SolM) and commissural area (SolC) of nucleus of the solitary tract nuclei. RESULTS: CCK increased the Fos expression in the Pa, RCh, LH, Ce, SO, Arc, VMH, DM, PMV, LPBS, LPBE and SolM. Leptin increased the Fos expression in the Pa, RCh, LH, SO, Arc, VMH, DM, PMV, LPBS, LPBE, SGe, AP and SolM. Injections of leptin and CCK significantly enhanced the Fos expression in the Pa, RCh, VMH, DM, LPBS, and SolM compared with those induced by leptin or CCK alone. CONCLUSION: Our results suggest that the Pa, RCh, VMH, DM, LPBS and SolM may be essential sites mediating the synergistic effect of leptin and CCK to regulate food intake.


Subject(s)
Animals , Arcuate Nucleus of Hypothalamus , Area Postrema , Body Weight , Brain , Cholecystokinin , Eating , Hypothalamic Area, Lateral , Immunohistochemistry , Injections, Intraperitoneal , Leptin , Meals , Negotiating , Neurons , Paraventricular Hypothalamic Nucleus , Rats , Sincalide , Solitary Nucleus , Supraoptic Nucleus
18.
Korean Journal of Anatomy ; : 141-154, 2001.
Article in Korean | WPRIM | ID: wpr-648904

ABSTRACT

This experimental studies was to investigate the location of PNS and CNS labeled neurons following injection of 2% WGA-HRP and pseudorabies virus (PRV), beta-galactosidase inserted Bartha strain, into the epididymis of rats. After survival times 4~5 days following injection of 2% WGA-HRP and PRV-Ba-Gal, the rats were perfused, and their brain, spinal cord, sympathetic ganglia and spinal ganglia were frozen sectioned (30 mm). These sections were stained by HRP histochemical and beta-galactosidase histochemical staining methods, and observed with light microscope. The results were as follows : 1. The WGA-HRP labeled sympathetic ganglia projecting to the epididymis were observed in pelvic ganglion and L1-6 lumbar sympathetic ganglia. 2. The WGA-HRP labeled spinal ganglia projecting to the epididymis were observed in L1-6 spinal ganglia. 3. The beta-galactosidase labeled neurons projecting to the epididymis were observed in lamina VII of cervical segments. In thoracic segments, beta-galactosidase labeled neurons were observed in dorsomedial part of lamina I, II and III. Dense labeled neurons were observed in intermediolateral n. and dorsal commissural n.. In lumbar segment, labeled neurons were observed in lamina III, IV, V, dorsal commisural n. and superficial dorsal horn. 4. In the medulla oblongata, beta-galactosidase labeled neurons projecting to the epididymis were observed in the trigeminal spinal n., A1 noradrenalin cells/C1 adrenalin cells/caudoventrolateral reticular n., rostroventrolateral reticular n., area postrema, n. tractus solitarius, raphe obscurus n., raphe pallidus n., raphe magnus n., parapyra-midal n., lateral reticular n. and lateral paragigantocellular reticular n.. 5. In the pons, labeled neurons were observed in Kolliker-Fuse n., locus coeruleus, subcoeruleus n. and A5 noradrenalin cells. 6. In midbrain, labeled neurons were observed in periaqueductal gray substance, retrorubral n., substantia nigra and dorsal raphe n.. 7. In the diencephalon, labeled neurons were observed in paraventricular hypothalamic n., lateral hypothalamic nucleus., medial preoptic n. and retrochiasmatic n.. These results suggest that WGA-HRP labeled neurons of the spinal cord projecting to the rat epididymis might be the first-order neurons related to the viscero-somatic sensory and sympathetic postganglionic neurons, and beta-galactosidase labeled neurons of the brain and spinal cord may be the second and third-order neurons response to the movement of vascular smooth muscle in epididymis. These beta-galactosidase labeled neurons may be central autonomic center related to the integration and modulation of reflex control linked to the sensory and motor system monitoring the internal environment. These observations provide evidence for previously unknown projections from epididymis to spinal cord and brain which may be play an important neuroanatomical basic evidence in the regulation of epididymal function.


Subject(s)
Animals , Area Postrema , beta-Galactosidase , Brain , Diencephalon , Epididymis , Ganglia, Spinal , Ganglia, Sympathetic , Ganglion Cysts , Herpesvirus 1, Suid , Horns , Hypothalamic Area, Lateral , Locus Coeruleus , Male , Medulla Oblongata , Mesencephalon , Muscle, Smooth, Vascular , Neural Pathways , Neurons , Periaqueductal Gray , Pons , Pseudorabies , Rats , Reflex , Spinal Cord , Substantia Nigra , Wheat Germ Agglutinin-Horseradish Peroxidase Conjugate
19.
Indian J Physiol Pharmacol ; 1999 Jul; 43(3): 323-31
Article in English | IMSEAR | ID: sea-108301

ABSTRACT

The hypothalamo-limbic system has been implicated in recognizing the affective significance of pain and elicitation of related emotional responses. Several evidences from different studies support a role of these areas in endogenous analgesic mechanisms for pain modulation as elucidated by different pain tests in more than one animal model. In the above context, the aim of this study was to investigate the relative effectiveness of the pain modulatory action of hypothalamic and limbic structures in rat using similar stimulation parameters, and studying the effect on tooth pulp stimulation evoked jaw opening reflex (TP-JOR). To achieve the objective, unilateral stimulation of hypothalamic (lateral = LH; ventromedial = VMN; anterior = AH) and limbic areas (amygdala = AMYG; hippocampus = HIPP) was done on the TP-JOR test. A significant reduction in the amplitude of EMG recorded from the digastric muscle (dEMG) as a result of tooth-pulp stimulation was observed on stimulation of LH, VMN, AMYG and HIPP but not from AH. Also, the magnitude of this effect was almost similar from these areas. The results suggest that these areas (except AH) have an antinociceptive role in tooth-pulp stimulation evoked pain response.


Subject(s)
Amygdala/physiology , Animals , Dental Pulp/physiology , Electric Stimulation , Electromyography , Hippocampus/physiology , Hypothalamic Area, Lateral/physiology , Hypothalamus/physiology , Limbic System/physiology , Male , Nociceptors/physiology , Pain Measurement , Rats , Rats, Wistar , Reflex/physiology , Ventromedial Hypothalamic Nucleus/physiology
20.
Article in Korean | WPRIM | ID: wpr-150969

ABSTRACT

The localization and number of oxytocin- and vasopressin-immunoreactive neurons (OXY-IR & VP-IR) and their fibers in the hypothalamic areas (supraoptic nucleus, paraventricular nucleus, lateral hypothalamic area and median eminence) of the hypophysectomized rat were compared with normal rats at 6 months of survival after surgery at the light microscopic level. The number of VP-IR neurons was markedly decreased in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) in the hypophysectomized rats as compared to normal rats. Moreover, The number of VP-IR fibers was decresed in the SON, PVN, lateral hypothalamic area (LHA) and median eminence in the hypophysectomized rats. The number of OXY-IR neurons and thier fibers were also decreased in the SON and PVN in the hypophysectomized rats. The present results demonstrate that hypophysectomy induces a significant decrease in the number of OXY- and VPIR neurons and fibers within hypothalamic areas (SON, PVN, and LHA at 6 months of post-hypophysectomy) are decreased.


Subject(s)
Animals , Hypophysectomy , Hypothalamic Area, Lateral , Immunohistochemistry , Median Eminence , Neurons , Oxytocin , Paraventricular Hypothalamic Nucleus , Rats , Supraoptic Nucleus , Vasopressins
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