Medial Basal Hypothalamic Area Research Articles

Effect of nicotine on the expression of leptin and forebrain leptin receptors in the rat

We have previously reported that chronic nicotine administration (4.0 mg/kg/day by i.p. injection over 14 days) up-regulates orexin/hypocretin and neuropeptide Y (NPY) mRNA expression and peptide levels within the hypothalamus. Since there exists a coregulation between these neuropeptides and the protein leptin, the present study was undertaken to determine whether nicotine has a regulatory effect on leptin signaling. Under the same experimental regimen used previously, we found that nicotine down-regulates plasma leptin concentration by 48.8% (P<0.001) and leptin RNA level by 11.4% and 12.4%, respectively, in the perirenal and epididymal white adipose tissue (PWAT, EWAT) compared to the saline controls. We also measured an approximately 20% decrease in white and brown adipose tissue (BAT) by weight in nicotine-treated animals relative to saline controls (P<0.05). On the other hand, we found that chronic nicotine administration increased the expression levels of OB-Rb mRNA by 12% and OB-R mRNA by 25% in the medial basal hypothalamus compared to control rats. Subsequent radioligand binding assays indicated that nicotine also significantly increased leptin binding in ventromedial hypothalamic area (VMA), medial basal hypothalamic area (MBA), arcuate nucleus/median eminence, paraventricular nuclei and piriform cortex. Taken together, our results revealed that nicotine is involved in the regulation of leptin signaling, suggesting that leptin and its receptor play a role in the anorectic effects of nicotine on food intake and body weight in rats.

Effect of nicotine on the expression of leptin and forebrain leptin receptors in the rat

We have previously reported that chronic nicotine administration (4.0 mg/kg/day by i.p. injection over 14 days) up-regulates orexin/hypocretin and neuropeptide Y (NPY) mRNA expression and peptide levels within the hypothalamus. Since there exists a coregulation between these neuropeptides and the protein leptin, the present study was undertaken to determine whether nicotine has a regulatory effect on leptin signaling. Under the same experimental regimen used previously, we found that nicotine down-regulates plasma leptin concentration by 48.8% ( P<0.001) and leptin RNA level by 11.4% and 12.4%, respectively, in the perirenal and epididymal white adipose tissue (PWAT, EWAT) compared to the saline controls. We also measured an approximately 20% decrease in white and brown adipose tissue (BAT) by weight in nicotine-treated animals relative to saline controls ( P<0.05). On the other hand, we found that chronic nicotine administration increased the expression levels of OB-Rb mRNA by 12% and OB-R mRNA by 25% in the medial basal hypothalamus compared to control rats. Subsequent radioligand binding assays indicated that nicotine also significantly increased leptin binding in ventromedial hypothalamic area (VMA), medial basal hypothalamic area (MBA), arcuate nucleus/median eminence, paraventricular nuclei and piriform cortex. Taken together, our results revealed that nicotine is involved in the regulation of leptin signaling, suggesting that leptin and its receptor play a role in the anorectic effects of nicotine on food intake and body weight in rats.

Estrogen receptor alpha expression in the medial preoptic area and the medial basal hypothalamus under different physiological conditions in cattle.

The distribution and morphology of immunoreactive estrogen receptor alpha (ERalpha)- containing cells were examined in the cattle brain. The brains were collected from two cows and a male calf. One of the cows was sacrificed one week after parturition. ERalpha expressions in the preoptic area of the rostral forebrain and the medial basal hypothalamic area were evaluated immunohistochemically using a mouse monoclonal antibody. In all animals, the signals that indicate ERalpha were detected in the medial preoptic area, the level of the organum vasculosum of the lamina terminalis and the bed nucleus of the stria terminalis. In the caudal hypothalamic region, they were detected in the arcuate nucleus, the periventricular and ventromedial hypothalamic nuclei. ERalpha-containing cells were characterized by a dense nuclear reaction product. In all the subjects examined, ERalpha signals were clearly detected in the cytoplasm as well. The density of ERalpha expression was different among the three cattle; the number of ERalpha containing cells in the postpartum cow was much lower than that in the other cow and the male calf. The present findings suggest that ERalpha expression in the forebrain is influenced by the reproductive status in the cattle.

Substance P and Luteinizing Hormone-Releasing Hormone Levels in the Brain of the Male Golden Hamster Are Both Altered by Castration and Testosterone Replacement

The effects of castration and testosterone (T) replacement on levels of substance P (SP) and luteinizing hormone-releasing hormone (LHRH) were assessed in discrete areas of the male hamster brain. The animals were either castrated, castrated and given a chronically low or high dose of T by Silastic implant, or sham-operated. Brain tissues and trunk blood were collected 3 weeks after surgery. Plasma T levels were maintained within the normal range by the implants but at significantly lower or higher levels than the mean for sham-operated males. Levels of SP and LHRH were quantified in the olfactory bulbs, rostral basal forebrain, anterior hypothalamic and preoptic area, medial basal hypothalamic area, medial basal hypothalamic area and median eminence, and brain stem. In general, castration and T replacement effected opposite changes in levels of SP and LHRH. In the medial basal hypothalamic area and median eminence SP levels were found to be inversely related to the chronic T levels, whereas the LHRH levels were directly correlated. In the anterior hypothalamic and preoptic area, castration reduced levels of SP. Conversely, castration elevated levels of LHRH in this area. This inverse dynamic relationship between changing peptide levels was also observed in the rostral basal forebrain but not in the olfactory bulbs. In most of these forebrain regions, the dose-response curves for the experimental groups could not incorporate the peptide levels in the sham-operated control group. SP levels in the brain stem showed a monotonic inverse relationship to circulating T levels which did include the control group values.(ABSTRACT TRUNCATED AT 250 WORDS)

Ontogenesis of immunoreactive tyrosine hydroxylase-containing neurons in rat hypothalamus

By employing anti-tyrosine hydroxylase (TH) serum, the ontogenesis of hypothalamic dopamine (DA) neurons was immunohistochemically examined with special attention to the medial basal hypothalamic area. DA neurons first appeared in the lateral hypothalamic walls on day 13.5 of gestation and in the anterior periventricular region and arcuate nucleus on day 15.5–16.5. In the arcuate nucleus, the appearance of the neurons was confined to the ventrolateral (VL) region, but extended to the periventricular region thereafter. About day 10 postnatally, the population of the arcuate DA neurons conjoins anterodorsally with the cell population in the anterior periventricular region. Concomitant with this, DA neurons in the VL region of the nucleus diminished in number and in stainability, becoming barely visible. Interestingly enough, the latter neurons reappeared after an anterolateral deafferentation of the medial basal hypothalamus. This did not occur in pregnant and lactating rats. Although most of the arcuate DA neurons were retarded by neonatal administration of monosodium glutamate, the immunoreactive fibers remained almost intact in the medial portion of the median eminence. It is concluded that in the periventricular-arcuate complex, DA neurons seem to play different roles relating with their ontogenetic heterogeneity.

THE EFFECTS OF ALCOHOL EXPOSURE &lt;italic&gt;IN UTERO&lt;/italic&gt; ON ACETYLCHOLINESTERASE, Na/K-ATPase AND Ca-ATPase ACTIVITIES IN SIX REGIONS OF RAT BRAIN

The neural membrane-bound enzymes, acetylcholinesterase, Na/K-ATPase and Ca-ATPase were examined in six brain areas in perinatal rats at 5, 15 and 25 days of age following alcohol exposure in utero. Female Wistar rats were mated with adult male Wistar rats and maintained on either a liquid diet containing ethanol (5% w/v) or on a control liquid diet for various periods during gestation and the perinatal period. These periods were: before and during gestation only (until birth of the offspring); before and during gestation and following birth; during only a period of gestation and continuing postnatally. Enzyme activity was determined by spectrophotometric methods in the following areas of the brain in each offspring: telencephalon, cerebellum, hippocampus, septal area, preoptic area, and medial basal hypothalamic area. Analysis of the data indicates that alcohol exposure in utero will heterogeneously decrease enzyme activity among the six brain areas when compared to enzyme activity in the same brain areas in animals which were not exposed to alcohol in utero. The activity of the three enzymes were most significantly reduced on day 5 of age, compared to levels in the control animals. Enzyme activity in each brain area was generally most significantly affected in animals exposed to alcohol both pre- and postnatally. The results indicate that fetal alcohol exposure reduces neuronal enzyme activity relative to the period of ethanol exposure in utero; the longer the period of time that alcohol was consumed by the mothers pre- and postnatally, the greater the effect of alcohol on the enzyme activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Endocrine Function in Female Rhesus Monkeys After Hypothalamic Disconnection

Fourteen adult female rhesus monkeys, 8 with regular menstrual cycles and 6 ovariectomized, were subjected to hypothalamic disconnection using a modified Halasz-type knife. Complete “islands” were produced in 5 animals. In 4 of these, the, “island” included the medial basal hypothalamus and the suprachiasmatic nucleus and its immediately adjacent preoptic area. None of the animals developed diabetes insipidus. The animals with complete “islands” doubled their body weights within 10 months. Four of these continued to show either spontaneous or estrogen-induced LH surges. An increase of serum estrogen-stimulated neurophysin concentrations accompanying the LH surge occurred in all animals. There was a loss in diurnal variation of cortisol in all monkeys. Basal prolactin levels were elevated in only one animal who had damage to the medial basal hypothalamic area. Although the prolactin response to TRH was not affected by the procedure, it was diminished in the ovariectomized animals. Growth hormone release af...

On the catecholamine innervation of the hypothalamus, with special reference to the median eminence

The CA innervation of the hypothalamus with special reference to the median eminence has been investigated by the use of fluorescence histochemical and isotope techniques in combination with deafferentation (circular hypothalamic islands according to Hala´sz) and 6-OH-DA experiments. Deafferentation produced an almost complete disappearance of CA nerve terminals in all parts of the hypothalamic island except those present in the external layer of the median eminence which were left largely intact. Incubation of brain slices from the median eminence together with the medial basal hypothalamic area in a high concentration of 6-OH-DA (10 −4 M) in vitro resulted in an almost complete blockage of 3H-NA formation from 3H-DA, whereas the uptake and retention of 3H-DA was unaffected. Such an incubation in 6-OH-DA also caused an almost complete disappearance of CA nerve terminals in the internal layer of the median eminence and the surrounding hypothalamic tissue, whereas the CA nerve terminals in the external layer of the median eminence displayed an unaffected fluorescence morphology. These results give further strong evidence for the view that CA nerve terminals in the external layer of the median eminence contain DA and originate from cell bodies present in the arcuate nucleus and the anterior periventricular hypothalamic nucleus, whereas the CA nerve terminals in the internal layer of the median eminence contain NA and have their origin in cell bodies present outside the hypothalamus. The incoming NA pathways to the hypothalamus are also described.