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At least 19 recordsLinked to original sources

PubMed2003

Actions of neuropeptide Y and growth hormone secretagogues in the arcuate nucleus and ventromedial hypothalamic nucleus.

Systemic or central administration of growth-hormone secretagogues (GHS) induces dense Fos expression in the arcuate nucleus but little or no Fos expression in the ventromedial hypothalamic nucleus, although both sites show intense expression of mRNA for the GHS receptor. Here, we recorded the electrical activity of single neurons from the arcuate nucleus and from the ventromedial hypothalamic nucleus in a rat hypothalamic slice preparation, and compared responses of these two populations to GHS. At both sites, the predominant neuronal response to GHS was a long-lasting excitation, indicating that GHS receptors at both sites are functional and similarly coupled to electrical excitation. We also tested neurons at both sites for their responses to neuropeptide Y and to somatostatin; at both sites the predominant response to each of these peptides was inhibitory. The arcuate cells that are activated by GHS include neuropeptide Y cells and growth hormone-releasing hormone cells. It seems possible that neuropeptide Y released in the ventromedial hypothalamus from the terminals of arcuate neurons counteracts the activation of ventromedial hypothalamic neurons by GHS in vivo, or that somatostatin released following liberation of growth hormone may do so.

Animals↗

PubMed2005

Use of laser-capture microdissection for the identification of marker genes for the ventromedial hypothalamic nucleus.

The ventromedial hypothalamic nucleus (VMH) plays an important role in the control of feeding and energy homeostasis. In contrast to other hypothalamic nuclei that are also known to regulate energy balance, there is a paucity of nucleus-specific marker genes for the VMH, limiting the application of molecular approaches for analyzing VMH information processing, function, and circuitry. Here, we report the use of laser-capture microdissection to isolate a set of cDNAs that are enriched in the VMH relative to two adjacent hypothalamic nuclei, the arcuate and dorsomedial hypothalamus. The relative expression levels of nine of the 12 most robustly expressed VMH-enriched genes were confirmed by real-time PCR analysis using separate RNAs from these three nuclei. Three of these VMH-enriched genes were further characterized by in situ hybridization histochemistry, including pituitary adenylate cyclase activating polypeptide, cerebellin 1, and an expressed sequence tag named LBH2. Finally, to test whether some of these genes were coordinately regulated, we monitored their expression in steroidogenic factor 1 (SF-1) knock-out mice. SF-1 is a transcription factor that controls the development of the VMH. The RNA levels for four of these genes were reduced in these knock-out animals, further suggesting that they are direct or indirect targets of this orphan nuclear receptor. The VMH-enriched genes identified here provide a basis for a functional analysis of VMH neuronal subpopulations via the use of bacterial artificial chromosome transgenics and related technologies. These results also demonstrate the utility of laser-capture microdissection coupled with microarray technology to identify nucleus-specific transcriptional networks.

Animals↗

PubMed1985

An enkephalinergic projection from the hypothalamic paraventricular nucleus to the hypothalamic ventromedial nucleus of the rat: an experimental immunohistochemical study.

The distribution and origins of enkephalin-like immunoreactive (ENK-IR) fibers in the nucleus ventromedialis hypothalami (vm) of the rat were examined using immunohistochemistry. A dense plexus was evenly distributed in the vm with no regional differences. A group of ENK-IR neurons was concentrated in the ventrolateral portion of the vm. The destruction of the hypothalamic paraventricular nucleus (pv) which contained numerous ENK-IR neurons, resulted in a marked decrease in ENK-IR fibers in the vm on the operated side. In addition, the destruction of the magnocellular portion of the pv, while leaving most of parvocellular portion intact, failed to substantially decrease the ENK-IR fibers in the vm, suggesting that these fibers originate from ENK-IR neurons located in the parvocellular portion of the pv. The present study further showed that the axons of these neurons first proceeded laterally to the perifornical area, next ran ventrolaterally to the ventrolateral portion of the anterior hypothalamic nucleus and finally turned medially to the vm.

Animals↗

PubMed1991

Endogenous opioid-immunoreactive neurons of the ventromedial hypothalamic nucleus concentrate estrogen in male and female rats.

Estrogen stimulates expression of proenkephalin mRNA in neurons of the hypothalamic ventromedial nucleus, and evidence is accumulating that synaptic release of one of the peptide end products, met-enkephalin, influences events that regulate reproductive behavior. To address the question of whether estrogen acts directly on neurons that synthesize met-enkephalin or indirectly through a separate neuronal population, we combined estrogen autoradiography with endogenous opioid peptide (EOP) immunohistochemistry. In agreement with previous studies, the ventrolateral subdivision of the hypothalamic ventromedial nucleus was densely packed with EOP-immunoreactive cells. In males, 48% of the estrogen-concentrating cells of the ventrolateral subdivision of the hypothalamic ventromedial nucleus contained EOP, and, in females, 27% of the estrogen-concentrating cells contained EOP. These findings indicate that estrogen acts directly on neurons that express EOP and suggest a mechanism that underlies sexually differentiated reproductive behavior.

Animals↗

PubMed1996

Functional analysis of opioid receptor subtypes in the ventromedial hypothalamic nucleus of the rat.

Effects of [Met5]enkephalin and agonists selective for mu-, delta- and kappa-opioid receptors were tested in vitro on neurons of the hypothalamic ventromedial nucleus of ovariectomized, estrogen-primed rats. Brain slices were perfused with artificial cerebrospinal fluid and opioid drugs were applied by bolus injection into the perfusion line. Single unit activity was recorded extracellularly. The majority of ventromedial hypothalamic nucleus neurons tested exhibited marked inhibitory responses to [Met5]enkephalin. The inhibition was blocked by naloxone, by the selective delta-opioid receptor antagonist naltrindole and, to a lesser extent, by the mu-opioid receptor antagonist beta-funaltrexamine. The kappa-opioid receptor antagonist nor-binalmorphimine had virtually no effect on [Met5]enkephalin inhibition. Agonists selective for delta-([D-Pen2,D-Pen5]enkephalin, DPDPE) and for mu-([D-Ala2,MePhe4,Gly-ol5]enkephalin, DAGO) opioid receptors also potently inhibited the ventromedial hypothalamic nucleus neurons while the kappa-opioid receptors agonist U50,488 only produced a small inhibition in a smaller number of units. These results provide functional evidence that [Met5]enkephalin, a potential opioid transmitter in the ventromedial hypothalamic nucleus, can exert an inhibitory effect by acting on delta-and mu-opioid receptors.

Action Potentials↗

PubMed1988

Partial compensation of sexual receptivity deficits in female rats with bilateral lesions of the hypothalamic ventromedial nucleus by transplants of fetal mediobasal hypothalamic tissue.

Bilateral aspiration as well as bilateral electrolytic lesions of the hypothalamic ventromedial nucleus (VMN) in ovariectomized, adult female rats treated with testosterone or estrogen resulted in a long-lasting decrease of sexual receptivity. Fetal mediobasal hypothalamic (MBH) tissue was grafted successfully to the site of VMN lesions. The following presuppositions for a sufficient rate of long-term survival of the grafts could be defined: (1) careful lesioning and minimalizing of damage to the surrounding tissues, (2) high vitality of the donor fetuses, (3) delay of transplantation after lesioning, and (4) testosterone treatment of the recipient animals at an early stage of graft development. In rats with surviving MBH grafts the receptivity deficits resulting from bilateral aspiration of the VMN were compensated partially.

Animals↗

PubMed1987

Electrophysiological characteristic of the ventromedial hypothalamic nucleus and lateral hypothalamic area in normally fed and 24 hour food deprived conscious sheep.

We registered telemetrically the spontaneous electrical activity of the hypothalamic ventromedial nucleus (VMH) and the lateral hypothalamic area (LH) in conscious adult sheep-male, with implanted electrodes,-in a state of normal feeding or after 24 hour food deprivation. The frequency of electrical activity, the amplitude of electrical activity and the frequency by Fourier analysis were evaluated. The frequency of electrical activity was found to be approximately the same in the VMH and LH with mean values +/- S.E.M. 11.5 +/- 0.5 Hz in feed sheep. The amplitude of electrical activity in the VMH was higher compared with the LH, with mean absolute values +/- S.E.M. 41.5 +/- 2.7 microV in the VMH and 35.5 +/- 3.2 microV in the LH. The Fourier analysis showed that from the total amount of harmonic frequencies-the first one i.e. the basic frequency represented 48-56%, the rest are higher frequencies. In sheep after 24 hour food deprivation the frequency of electrical activity decreased on 9.4-9.6 Hz in average in both regions under study and the absolute values of the amplitude of electrical activity increased. The mean absolute value +/- S.E.M. was 115 +/- 5.2 microV in the VMH and 101.2 +/- 3.0 microV in the LH. Along with theses changes we found by Fourier analysis that in the total amount of harmonic frequencies the basic frequency decreased by 6% due to the greater amount of higher harmonic frequencies.

Animals↗

PubMed1982

Morphological study on the central subdivision of the rat hypothalamic ventromedial nucleus.

Central subdivision of the rat hypothalamic ventromedial nucleus (VMN) was examined with the transmission electron microscope. This portion of VMN consists of densely packed neuronal somata which are characterized by a large pale nucleus with a prominent nucleolus, with clear cytoplasm containing many free ribosomes and randomly distributed fragments of rough endoplasmic reticulum, with small mitochondria and homogeneous lysosomes, with well developed Golgi complex surrounded by a few clear and largely 2-3 dense-core vesicles of 90-110 nm in size and with nucleotid bodies. Besides neuronal somata and their processes also astrocytes, oligodendrocytes and microglial cells and their processes are often seen in this portion of VMN. In the neuropil axo-somatic and axo-dendritici synapses, capillaries, myelinated nerve fibers, nerve profiles filled with dense-core vesicles and distal parts of ependymal tanycytic processes are usually found in the central subdivision of VMN.

Animals↗

PubMed1986

Projections of oestrogen-sensitive neurones from the ventromedial hypothalamic nucleus of the female rat.

Stimulation of the mesencephalic central grey matter caused antidromic activation of 199 neurones in the hypothalamic ventromedial nucleus of forty-six urethane-anaesthetized female rats, of which twenty-two (ten ovariectomized and twelve ovariectomized and oestrogen treated) had the lateral projection of the nucleus disrupted by a small parasagittal knife-cut. The remaining twenty-four rats (ten ovariectomized and fourteen ovariectomized and oestrogen treated) had a cut in the frontal plane to interrupt caudal projection of the nucleus. In eight animals with the lateral knife-cut, eighteen cells were antidromically activated from the central grey matter as well as from the dorsal longitudinal fascicle. Collision between the potentials activated from these two sites revealed that seventeen of them descended to the central grey matter by way of the periventricular system, one cell having a bifurcated axon to these sites. Likewise, eleven cells in another group of eight animals with the posterior cut were found to project to the central grey matter via the perifornical region. Pre-treatment with oestrogen significantly lowered the activation thresholds and absolute refractory periods of neurones antidromically stimulated from the central grey in ovariectomized animals bearing posterior but not lateral knife-cuts. These results suggest that the ventromedial hypothalamic neurones responsible for oestrogen-dependent autonomic and behavioural functions project to the central grey via a lateral rather than a posterior pathway.

Action Potentials↗

PubMed1983

Modification by hypothalamic lesions of the release of growth hormone (GH) following stimulation of the ventromedial hypothalamic nucleus in the rat.

This study was designed to clarify the localization(s) of hypothalamic area(s) concerned with the regulation of growth hormone (GH) release evoked by electrical stimulation of the hypothalamic ventromedial nucleus (VMH) of rats. Bipolar concentric stimulating electrodes were implanted in the bilateral VMH or dorsal premammillary nucleus and the jugular vein was cannulated for blood sampling one week prior to the experiments. At the same time lesions of the anterior periventricular nucleus or dorsal premammillary nucleus were performed with an anodal current. The rats were pretreated with alpha-methyl-p-tyrosine to prevent spontaneous GH bursts. As previously reported, stimulation of the VMH for 10 min appeared to suppress GH release during the period of stimulation but within 10 min after termination of stimulation plasma GH had risen from a resting level of 19.3 +/- 2.3 ng/ml plasma, to 275.3 +/- 62.3 ng/ml. The apparent suppression of GH release during the VMH stimulation was abolished in the anterior periventricular nucleus-lesioned rats. In these rats, GH release occurred during the VMH stimulation and plasma GH increased to 905.4 ng/ml by 10 min, at which time the stimulus was terminated. On the other hand, the VMH stimulation completely failed to raise plasma GH levels in rats with dorsal premammillary nucleus lesions either during or after VMH stimulation. Although lesions of the dorsal premammillary nucleus blocked the delayed VMH-induced rise, stimulation of the dorsal premammillary nucleus itself caused no change in the plasma GH level.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2003

Ultrastructure of the ventromedial hypothalamic nucleus in fasted and refed young and old rats.

Many hypothalamic nuclei are involved in the regulation of food intake and energy homeostasis. An ultrastructural investigation of the hypothalamic ventromedial nucleus (VMN), a hypothetical "satiety centre" was performed to explore the morphological basis of altered feeding behaviour of old rats in an experimental model of fasting/refeeding. Young (5 months old, n=12) and old (24 months old, n=12) male Wistar rats were fasted for 48 hours, then refed for 24 hours and sampled thereafter. Brain tissue was fixed by perfusion, histological and ultrathin sections were obtained by routine methods. Although food intake was similar in control young and old rats, during refeeding old animals consumed less chow than young ones. The EM analysis of VMN neurones of old control rats revealed, besides typical age-related residual bodies, deep indentations of the nuclear envelope and the presence of long, undulating rough endoplasmic reticulum cisternae in the cell periphery. In both young and old rats fasting for 48 hours led to the expansion of Golgi complexes and increased folds of the nuclear envelope, which is suggestive of enhanced cellular activity of the VMN neurones. These fasting-induced alterations were sustained in the VMN neurones of refed rats in both age groups. The results showed that the VMN neurones of old control rats differ at the ultrastructural level from young ones. However, starvation and subsequent refeeding cause similar alterations in the hypothalamic neurones of "satiety centre" of both young and old rats.

Age Factors↗

PubMed2004

Physiological and molecular characteristics of rat hypothalamic ventromedial nucleus glucosensing neurons.

To evaluate potential mechanisms for neuronal glucosensing, fura-2 Ca(2+) imaging and single-cell RT-PCR were carried out in dissociated ventromedial hypothalamic nucleus (VMN) neurons. Glucose-excited (GE) neurons increased and glucose-inhibited (GI) neurons decreased intracellular Ca(2+) ([Ca(2+)](i)) oscillations as glucose increased from 0.5 to 2.5 mmol/l. The Kir6.2 subunit mRNA of the ATP-sensitive K(+) channel was expressed in 42% of GE and GI neurons, but only 15% of nonglucosensing (NG) neurons. Glucokinase (GK), the putative glucosensing gatekeeper, was expressed in 64% of GE, 43% of GI, but only 8% of NG neurons and the GK inhibitor alloxan altered [Ca(2+)](i) oscillations in approximately 75% of GK-expressing GE and GI neurons. Insulin receptor and GLUT4 mRNAs were coexpressed in 75% of GE, 60% of GI, and 40% of NG neurons, although there were no statistically significant intergroup differences. Hexokinase-I, GLUT3, and lactate dehydrogenase-A and -B were ubiquitous, whereas GLUT2, monocarboxylate transporters-1 and -2, and leptin receptor and GAD mRNAs were expressed less frequently and without apparent relationship to glucosensing capacity. Thus, although GK may mediate glucosensing in up to 60% of VMN neurons, other regulatory mechanisms are likely to control glucosensing in the remaining ones.

Animals↗

PubMed2006

Acute estradiol application increases inward and decreases outward whole-cell currents of neurons in rat hypothalamic ventromedial nucleus.

Acute estradiol (E2) can potentiate the excitatory responses of hypothalamic ventromedial nucleus (VMN) neurons to neurotransmitters. To investigate the mechanism(s) underlying the potentiation, the whole-cell patch voltage clamp technique was used to study VMN neurons in hypothalamic slices prepared from female juvenile (3-5 weeks) rats. A voltage step and/or ramp was applied every 5 min to evoke whole-cell currents before, during and after a treatment with E2 (10 nM), corticosterone (10 nM) or vehicle for up to 20 min. Acute E2 increased inward currents in 38% of neurons tested. Their average peak inward current amplitudes started to increase within 5 min and reached the maximum of 163% of pretreatment level (Pre) at 20 min of treatment before recovering toward Pre. These increases are significantly greater than the Pre and corresponding vehicle controls and non-responsive neurons. Outward currents were decreased significantly by E2 in 27% of E2-treated cells, down to 60% of Pre levels. E2 also appeared to affect the kinetics of the inward and outward currents of estrogen-responsive neurons. Whenever observed, the effects of acute E2 were reversible after a 5- to 10-min washing. Probability analysis indicates that E2 affected the inward and the outward currents independently. The E2 effects are specific in that they were not produced by similar treatment with vehicle or corticosterone. Pharmacological characterizations using ion replacement and channel blockers showed that the inward currents were mediated practically all by Na(+) and the outward currents mainly by K(+). Thus, acute E2 can enhance inward Na(+) and attenuate outward K(+) currents. Since both effects will lead to an increase in neuronal excitability, they may explain our previous observation that E2 potentiates the excitation of VMN neurons.

Animals↗

PubMed1977

[Frequency-voltage dependence in the region of the ventromedial hypothalamic nucleus and the lateral hypothalamus of rats fed various diets].

Adult rats (males) of the Wistar species and of SPF origin were studied for the dependence of frequency on the electric potential on EEG records of the region of the hypothalamic ventromedial nucleus and lateral hypothalamus of animals fed high-protein and high-fat diets. Similar values of control animals were used for comparison. Each group comprised seven animals. In the control animals, constantly fed the basic diet, the values of the frequency-voltage dependence remained unchanged. In the animals fed high-protein diet frequency increased with rising voltage whereas in those fed high-fat diet frequency declined with increasing voltage in both body regions under study.

Action Potentials↗

PubMed1984

Are the amygdaloid projections to the hypothalamic ventromedial nucleus involved in estrous rhythm regulation in the female rat?

The aim of this investigation was to determine whether the corticomedial amygdaloid nucleus (CMA) and its projections to the hypothalamic ventromedial nucleus (VMN) were involved in the regulation of estrous rhythm by the VMN in the rat. It is known (Carrer et al., 1973-1974) that partial VMN lesions caused the occurrence of either 5-day or alternate 4- or 5-day cycles in about 50% of 4-day cyclic female rats and that large lesions induced cycle prolongation in most of the operated animals while hypothalamic dorsomedial nucleus (DMN) lesions left estrous rhythm unmodified. CMA lesions in 4-day cyclic female rats caused the occurrence of either 5-day or alternate cycles with sequence of 4, 5, 4 days, more frequently than in their sham operated counterparts (15/20 vs 3/20). Stria terminalis (ST) lesions placed at its emergence from the CMA or at its horizontal course over the internal capsule induced a higher proportion (10/14 and 9/16, respectively) of females to display changes in cycle duration than did sham operated and unoperated controls as well (10/32 and 7/29, respectively). Combined partial VMN and ST lesions resulted in a 24 hours cycle prolongation or alternate 4- and 5-day cycles in a greater number of females than in those bearing small VMN lesions only (15/18 vs 22/40). A noticeable proportion of CMA, ST and ST + small VMN lesioned females offered more or less prolonged diestrous periods immediately following surgery before resuming estrous cyclicity. It was suggested that the CMA neurons which project fibers to the VMN via the ST are implicated in estrous rhythm regulation in the rat.

Afferent Pathways↗

PubMed1994

Brown adipose tissue thermogenesis evoked by medial preoptic stimulation is mediated via the ventromedial hypothalamic nucleus.

Experiments were designed to determine if a functional ventromedial hypothalamic nucleus was required for the activation of brown adipose tissue thermogenesis evoked by medial preoptic stimulation. Male, urethane-anesthetized Long--Evans rats, maintained at 37 degrees C, had temperatures (thermistor probes for gastrocnemius, Tm; intrascapular brown adipose tissue, TIBAT; colonic, Tc; and tail, Tt), gastrocnemius electromyogram activity (via stainless steel recording electrodes), and systemic blood pressure and heart rate (via a femoral arterial catheter) measured before and after a series of unilateral medial preoptic electrical stimulations (monophasic 0.5-ms pulses of 300 microA at 50 Hz for 30 s). Measurements were made (i) after an initial control medial preoptic electrical stimulation, (ii) after medial preoptic stimulation was applied 1 min following an intracranial injection of 300 nL of sterile saline or buffered 2% Lidocaine into the ipsilateral posterior hypothalamic nucleus or the ipsilateral ventromedial hypothalamic nucleus, and (iii) after recovery medial preoptic stimulation 45 min after Lidocaine was injected into the ventromedial hypothalamic nucleus. TIBAT and blood pressure rose significantly (p < 0.05) above the corresponding prestimulation control values with all protocols, except when Lidocaine was injected into the ventro-medial hypothalamic nucleus prior to medial preoptic stimulation. Shivering (electromyogram) activity was not evoked following medial preoptic stimulation and Tm and Tt did not significantly change from the corresponding prestimulation values. A recovery medial preoptic stimulation 45 min after Lidocaine treatment of the ventromedial hypothalamic nucleus again evoked significant increases in TIBAT above the core temperature, similar to the rise in TIBAT seen after the first control medial preoptic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue, Brown↗

PubMed1997

Injections of nociceptin into nucleus accumbens shell or ventromedial hypothalamic nucleus increase food intake.

The novel opioid receptor ORL1 is widely distributed throughout the CNS of the rat, and is present in high densities in several brain regions known to participate in the control of food intake. We injected a recently identified endogenous agonist of this receptor, nociceptin, into two of these feeding-related areas. Microinjections of nociceptin (2.5-25 nmol) into either the ventromedial hypothalamic nucleus or the nucleus accumbens shell significantly increased food intake in rats. We believe this to be the first report of a specific effect of nociceptin on a motivated behavior.

Animals↗

PubMed2001

Convergence of pre- and postsynaptic influences on glucosensing neurons in the ventromedial hypothalamic nucleus.

Glucosensing neurons in the ventromedial hypothalamic nucleus (VMN) were studied using visually guided slice-patch recording techniques in brain slices from 14- to 21-day-old male Sprague-Dawley rats. Whole-cell current-clamp recordings were made as extracellular glucose levels were increased (from 2.5 to 5 or 10 mmol/l) or decreased (from 2.5 to 0.1 mmol/l). Using these physiological conditions to define glucosensing neurons, two subtypes of VMN glucosensing neurons were directly responsive to alterations in extracellular glucose levels. Another three subtypes were not directly glucose-sensing themselves, but rather were presynaptically modulated by changes in extracellular glucose. Of the VMN neurons, 14% were directly inhibited by decreases in extracellular glucose (glucose-excited [GE]), and 3% were directly excited by decreases in extracellular glucose (glucose-inhibited [GI]). An additional 14% were presynaptically excited by decreased glucose (PED neurons). The other two subtypes of glucosensing neurons were either presynaptically inhibited (PIR; 11%) or excited (PER; 8%) when extracellular glucose was raised to > 2.5 mmol/l. GE neurons sensed decreased glucose via an ATP-sensitive K(+) (K(ATP)) channel. The inhibitory effect of increased glucose on PIR neurons appears to be mediated by a presynaptic gamma-aminobutyric acid-ergic glucosensing neuron that probably originates outside the VMN. Finally, all types of glucosensing neurons were both fewer in number and showed abnormal responses to glucose in a rodent model of diet-induced obesity and type 2 diabetes.

Adenosine Triphosphate↗