Corticosterone is known to modulate GABAergic synaptic transmission in the hypothalamic paraventricular nucleus. However, the underlying receptor mechanisms are largely unknown. In the anterior hypothalamic area (AHA), the sympathoinhibitory center that project GABAergic neurons onto the PVN, we examined the expression of glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) of GABAergic neurons using intact GAD65-eGFP transgenic mice, and the effects of corticosterone on the burst firing using adrenalectomized transgenic mice. GR or MR immunoreactivity was detected from the subpopulations of GABAergic neurons in the AHA. The AHA GABAergic neurons expressed mRNA of GR (42%), MR (38%) or both (8%). In addition, in brain slices incubated with corticosterone together with RU486 (MR-dominant group), the proportion of neurons showing a burst firing pattern was significantly higher than those in the slices incubated with vehicle, corticosterone, or corticosterone with spironolactone (GR-dominant group; 64 vs. 11~14%, p<0.01 by chi2-test). Taken together, the results show that the corticosteroid receptors are expressed on the GABAergic neurons in the AHA, and can mediate the corticosteroid-induced plasticity in the firing pattern of these neurons. This study newly provides the experimental evidence for the direct glucocorticoid modulation of GABAergic neurons in the AHA in the vicinity of the PVN.
Animals ; Anterior Hypothalamic Nucleus ; Brain ; Corticosterone ; Fires ; GABAergic Neurons ; Mice ; Mice, Transgenic ; Mifepristone ; Neurons ; Paraventricular Hypothalamic Nucleus ; Plastics ; Receptors, Glucocorticoid ; Receptors, Mineralocorticoid ; Receptors, Steroid ; RNA, Messenger ; Spironolactone ; Synaptic Transmission

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.
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

This experimental studies was to investigate the location of CNS labeled neurons following injection of pseudorabies virus (PRV), Bartha strain, into the rat thymus. After survival times of 96~120 hours following injection of PRV, the rats were perfused, and their spinal cord and brain were frozen sectioned(30micrometer). These sections were stained by PRV immunohistochemical staining method, and observed with light microscope The results were as follows: 1. The PRV labeled spinal cord segments projecting to the rat thymus were founded in cervical and thoracic segments. Densely labeled areas of each spinal cord segment were founded in lamina V, VII, X, intermediolateral nucleus and dorsal nucleus. 2. In the rhombencephalon, PRV labeled neurons projecting to the thymus were founded in the A1 noradrenalin cells/C1 adrenalin cells/caudoventrolateral reticular nucleus, rostroventro-lateral reticular nucleus, medullary reticular nucleus, area postrema, nucleus solitary tract, nucleus raphe obscurus, nucleus raphe pallidus, nucleus raphe magnus, gigantocellular reticular nucleus, lateral paragigantocellular nucleus and spinal trigeminal nucleus. 3. In the mesencephalon, PRV labeled neurons were founded in parabrachial nucleus, Kolliker-Fuse nucleus, central gray matter, substantia nigra, nucleus dorsal raphe, A8 dopamin cells of retrorubral field, Edinger-Westphal nucleus, locus coeruleus, subcoeruleus nucleus and A5 noradrenalin cells. 4. In the prosencephalon, PRV labeled neurons were founded in reuniens thalamic nucleus, paraventricular thalamic nucleus, precommissural nucleus, paraventricular hypothalamic nucleus, anterior hypothalamic nucleus, lateral hypothalamic nucleus, preoptic hypothalamic nucleus, retrochiasmatic area, arcuate nucleus, dorsomedial hypothalamic nucleus and ventromedial hypothalamic nucleus. These results suggest that PRV labeled neurons of the spinal cord projecting to the rat thymus might be the neurons related to the viscero-somatic sensory and sympathetic preganglionic neurons, and PRV labeled neurons of the brain may be the neurons response to the movement of smooth muscle in blood vessels. These PRV labeled neurons may be central autonomic center related to the integration and modulation of reflex control linked to the sensory system monitoring the internal environment. These observations provide evidence for previously unknown projections from spinal cord and brain to the thymus which may be play an important role in the regulation of thymic function.
Animals ; Anterior Hypothalamic Nucleus ; Arcuate Nucleus ; Area Postrema ; Blood Vessels ; Brain ; Dorsomedial Hypothalamic Nucleus ; Herpesvirus 1, Suid* ; Hypothalamic Area, Lateral ; Immunohistochemistry ; Locus Coeruleus ; Mesencephalon ; Midline Thalamic Nuclei ; Muscle, Smooth ; Neurons* ; Paraventricular Hypothalamic Nucleus ; Prosencephalon ; Pseudorabies* ; Rats* ; Reflex ; Rhombencephalon ; Spinal Cord ; Substantia Nigra ; Thymus Gland* ; Trigeminal Nucleus, Spinal ; Ventromedial Hypothalamic Nucleus

Widespread brain-derived neurotrophic factor (BDNF) mRNA and protein expression has been detected in the brain. Despite substantial overlap between BDNF mRNA and protein expression, there is general anatomical regions, where there is discordance of these expression. We performed, therefore, immunohistochemistry after colchicine treatment into the ventricle to evaluate the possible presence of BDNF-immunoreactive (IR) in the regions where BDNF mRNA was expressed, but not BDNF-IR. The results obtained were as follows; There was substantial increase in the number of BDNF-IR neurons in the anterior olfactory nucleus, the piriform cortex, the cerebral cortex, the claustrum, the stratum pyramidale of the CA2 and the CA3, the granule cell layer of the dentate gyrus, the basolateral amygdaloid nucleus, the lateral geniculate nucleus, the anteromedial thalamic nucleus, the anterodorsal thalamic nucleus, the paraventricular thalamic nucleus, the paraventricular hypothalamic nucleus and the ventromedial hypothalamus nucleus, compared to the same brain area of non-colchicine treated rat. We detected many new BDNF-IR neurons in the stratum pyramidale of the CA1, A1, A2, A4-A10 cell groups, C1-C3 cell groups, the raphe magnus nucleus, the lateral paragigantocellular nucleus and the spinal vestibular nucleus. The results show that the localization of BDNF-IR neurons after colchicine treatment is consistant with that of BDNF mRNA containing neurons in the brain.
Animals ; Anterior Thalamic Nuclei ; Basal Ganglia ; Brain* ; Brain-Derived Neurotrophic Factor ; Cerebral Cortex ; Colchicine* ; Dentate Gyrus ; Hypothalamus ; Immunohistochemistry ; Midline Thalamic Nuclei ; Neurons* ; Paraventricular Hypothalamic Nucleus ; Rats* ; RNA, Messenger

The presence and coexistence of nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-diaphorase) with tyrosine hydroxylase (TH) was investigated by combining NADPH-diaphorase histochemistry with TH immunohistochemistry in hypothalamic nuclei of the rat. TH-immunoreactive and NADPH-diaphorase positive neurons were found in the medial preoptic area and medial preoptic nucleus, anterior hypothalamic area, dorsomedial hypothalamic nucleus, paraventricular nucleus, supraoptic nucleus and posterior hypothalamic area, respectively. TH and NADPH-diaphorase did not coexist in the anterior hypothalamic area, dorsomedial hypothalamic nucleus, medial preoptic area and posterior hypothalamic area. A considerable portion (30~50%) of the NADPH-diaphorase positive neurons in the supraoptic nucleus colocalized TH. In the medial preoptic area and paraventricular nucleus, some (5~15%) of TH-immunoreactive neurons also contained NADPH-diaphorase activity. NADPH-diaphorase is known to be an indicator of the enzyme nitric oxide synthase; these results therefore suggest that nitric oxide may play an important role in the regulation of the activity of the hypothalamic dopaminergic system of the rat.
Animals ; Anterior Hypothalamic Nucleus ; Dorsomedial Hypothalamic Nucleus ; Hypothalamus ; Immunohistochemistry ; NAD* ; Neurons* ; Niacinamide* ; Nitric Oxide ; Nitric Oxide Synthase ; Paraventricular Hypothalamic Nucleus ; Preoptic Area ; Rats* ; Supraoptic Nucleus ; Tyrosine 3-Monooxygenase* ; Tyrosine*

The distributions and morphological characteristics of neurons displaying immunoreactivity to the catecholamine synthetic enzymes, tyrosine hydroxylase[TH], dopamine-beta-hydroxylase[DBH], and phenyletha-nolamine-N-methyltransferase[PNMT] were examined in the adjacent sections of the diencephalon of the striped field mouse [Apodemus agrarius coreae].Only TH-, and no DBH- or PNMT-immunoreactive neurons were found in the diencephalon. In the preoptic area, TH-immunoreactive neurons were found in the anterior preoptic nucleus of Loo[APN], periventricular preoptic nucleus, medial preoptic nucleus, lateral preoptic nucleus and suprachiasmatic nucleus. In the hypothalamus, TH-immunoreactive neurons were found in theparaventricular hypothalamic nucleus, periventricular gray, retrochiasmatic area,anterior hypothalamic nucleus of anterior hypothalamic area and retrochiasmatic region of the hypothalamus. In the rostral tuberal region of the hypothalamus, TH-immunoreactive neurons were found in the paraventricular nucleus, periventricular gray and arcuate nucleus. In the midtuberal region of the hypothalamus, TH-immunoreactive neurons were found in the paraventricular nucleus, dorsomedial hypothalamic nucleus, zona incerta and arcuate nucleus. In the caudal tuberal region of the hypothalamus, dorsal hypothalamic nucleus, posterior hypothalamic complex and arcuate nucleus.
Animals ; Anterior Hypothalamic Nucleus ; Arcuate Nucleus ; Diencephalon* ; Dopaminergic Neurons* ; Dorsomedial Hypothalamic Nucleus ; Hypothalamus ; Immunohistochemistry ; Mice ; Neurons ; Paraventricular Hypothalamic Nucleus ; Preoptic Area ; Subthalamus ; Suprachiasmatic Nucleus ; Tyrosine

Plasma levels of growth hormone(GH), luteinizing hormone(LH) and cortisol were determined by radioimmunoassay following radiofrequency(RF) stimulation or coagulation of various nuclei in thalamus and hypothalamus. RF stimulation or coagulation of many nuclei in thalamus and hypothalamus consisted of pulvinar and dorsomedial nucleus in thalamus and anterior and posterior hypothalamic nuclei in hypothalamus. Anterior thalamic stimulation resulted in highly significant increase of plasma LH, GH, cortisol and TH levels. However thalamic stimulation resulted no change in the level of various plasma hormones. Hypothalamic lesion produced significantly decreased plasma LH, GH and cortisol levels. Plasma cortisol and LH levels were highest 2 hours after stimulation while GH levels did not increased until 6 hours and TH until 72 hours respectively after stimulation. The significant difference in latency for beginning of hormone secretion suggests that GH, cortisol and LH may be controlled by several separate neuronal networks. Plasma GH and cortisol levels were lowest 72 hrs after coagulation of the anterior hypothalamic area, while GH, cortisol and LH levels did not change following stimulation or coagulation of posterior hypothalamic nucleus and thalamic nucldi. It was also noted that the anterior hypothalamic stimulation or coagulation caused increased or decreased in GH, cortisol, and LH than that observed from stimulation or coagulation of other hypothalamic and thalamic nuclei respectively.
Anterior Hypothalamic Nucleus ; Hydrocortisone ; Hypothalamus* ; Lutein ; Mediodorsal Thalamic Nucleus ; Neurons ; Plasma ; Pulvinar ; Radioimmunoassay ; Thalamic Nuclei ; Thalamus*