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PubMed1990

The distribution of lactogen receptors in the mammalian hypothalamus: an in vitro autoradiographic analysis of the rabbit and rat.

The hypothalamus contains a high concentration of lactogen receptors as detected with in vitro radioreceptor assay techniques. In an effort to define the location of the lactogen receptors relative to specific hypothalamic nuclei, an in vitro autoradiography technique was applied to frozen sections of rat and rabbit brains. Three lactogenic hormones, i.e. human growth hormone (hGH), ovine prolactin (oPRL), and rat prolactin (rPRL), were radiolabeled with iodine-125. Competition for observed binding sites was assessed with unlabeled hGH, oPRL, and bovine growth hormone (bGH). Analysis of the autoradiographs with a microcomputer-based densitometry system revealed that the rabbit hypothalamus contains specific lactogen binding sites within the supraoptic, paraventricular, suprachiasmatic, ventromedial, arcuate, and dorsomedial nuclei and the medial preoptic area. Unlabeled bGH was effective in competing for binding sites in all areas when hGH but not oPRL was used as the radiolabeled ligand, suggesting the presence of growth hormone receptors in the rabbit hypothalamus with a distribution similar to that of the lactogen binding sites. In contrast to the rabbit, no lactogen binding sites were detected in the rat hypothalamus regardless of the ligand used in the assay. All of the ligands were successful, however, in detecting lactogen receptors within the rat choroid plexus and liver. The results from the rabbits indicate that the influences of prolactin on hypothalamic activity are mediated via lactogen receptors that are widely distributed throughout the various pertinent hypothalamic nuclei. The broad distribution of lactogen receptors in the rabbit hypothalamus attests to the extensive influence of prolactin on hypothalamic regulatory systems. The results from the rat raise questions as to the nature of rat brain prolactin receptors in comparison to prolactin receptors in rat peripheral tissues.

Animals↗
PubMed1993

Neuronal histamine in the hypothalamus suppresses food intake in rats.

Using probes to manipulate hypothalamic neuronal histamine, we report here that changes in neuronal histamine modulate physiological feeding behavior in rats. Infusion of alpha-fluoromethylhistidine (FMH), a "suicide" inhibitor of histidine decarboxylase (HDC), into the third cerebroventricle induced feeding in the early light phase when the histamine synthesis was most accelerated. FMH at an optimum 2.24 mumol dose elicited feeding in 100% of rats. Treatment of FMH specifically and selectively decreased concentration of histamine without affecting concentrations of catecholamines in the hypothalamus. Immediately before the dark phase, when the histamine synthesis was normally lower, FMH infusion did not affect feeding-related parameters such as meal size, meal duration or latency to eat. Conversely, thioperamide, which facilitates both synthesis and release of neuronal histamine by blocking presynaptic autoinhibitory H3 receptors, significantly decreased food intake after infusion of a 100-nmol dose into the third cerebroventricle. The effect of thioperamide was abolished with i.p. injection of 26 mumol/kg chlorpheniramine, an H1antagonist. FMH at 224 nmol was microinfused bilaterally into the feeding-related nuclei in the hypothalamus. The ventromedial nucleus (VMH) and the paraventricular nucleus (PVN), but not the lateral hypothalamus, the dorsomedial hypothalamus or the preoptic anterior hypothalamus were identified as the active sites for the modulation. Neuronal histamine may convey suppressive signals of food intake through H1 receptors in the VMH and the PVN with diurnal fluctuation.

Animals↗
PubMed1977

3H-metaraminol releasing action of mescaline from rat hypothalamus in vitro.

The amine releasing action of mescaline was investigated in rat isolated hypothalamus labeled with 3H-metaraminol. Mescaline had no effect on the uptake of 3H-metaraminol but produced its release in a concentration-related manner. 4 x 10(-4) M mescaline, which produced submaximal effects was used for subsequent experiments. 3 x 10(-5) M cocaine had no effect on the 3H-metaraminol releasing action of mescaline. Mescaline was fully effective in Ca2+-free medium while 6 x 10(-2) M KCl was ineffective. 3 x 10(-7) M tetrodotoxin or 6 x 10(-5) M lidocaine partially blocked mescaline-induced release but substantially or completely blocked 3 x 10(-2) M KCl-induced release. Prior exposure of hypothalamus to 3 x 10(-4) M tyramine reduced the releasing action of mescaline. Thus, mescaline appears to release 3H-metaraminol both by Ca2+-independent (tyramine-like) and Ca2+-dependent (lidocaine-sensitive) mechanisms. 3 x 10(-4) M tyramine and 6 x 10(-2) M KCl released 14C from control hypothalamus labelled with 14C-mescaline, but not from reserpinized hypothalamus. The amounts of 14C recovered in 14C-mescaline labeled control and reserpinized hypothalamus at the end of 50 min of efflux were similar suggesting a poor retention of 14C-mescaline by storage particles.

Animals↗
PubMed1983

GABA-related enzymes in the hypothalamus of rats treated with estradiol.

The possibility that the activity of GABA-related enzymes in the hypothalamus, glutamic acid decarboxylase (GAD) and GABA-transaminase (GABA-T), may be modified by circulating prolactin levels was investigated in castrated female and male rats. Estradiol benzoate was chosen to induce an increase, while bromergocriptine was used to obtain a decrease of serum prolactin levels. Acute treatment with estradiol benzoate brought about 3 h later, a significant increase of serum prolactin, and a slight, non-significant increase of GAD activity in the hypothalamus. Chronic treatment with estradiol benzoate for 12 days induced significant increases in serum prolactin and GAD activity in the hypothalamus. Bromergocriptine significantly blocked this increase of GAD activity. Bromergocriptine-treated rats had significant increases of GABA-T activity in the hypothalamus. The results of this investigation support the possibility of the existence of a relationship between GABA-related enzymes in the hypothalamus and circulating prolactin levels.

4-Aminobutyrate Transaminase↗
PubMed1990

Pharmacological characterization of melatonin binding sites in Syrian hamster hypothalamus.

The radioligand [125I]iodomelatonin was used to study melatonin binding sites in Syrian hamster hypothalamus and hippocampus. Scatchard analysis revealed a single binding site with nanomolar affinity in hypothalamus (Kd = 1.8 +/- 0.3 nM, Bmax = 75 +/- 7 fmol/mg protein; n = 4) and hippocampus (Kd = 2.2 +/- 0.2 nM, Bmax = 49 +/- 5 fmol/mg protein; n = 4). The Kd value calculated from the association and dissociation rate constants in hypothalamus was (k-1/k1) = 2.4 nM. Regional studies revealed that the highest binding of [125I]iodomelatonin occurs in the hypothalamus. Only indoles structurally related to melatonin exhibited significant affinity at this site. Prazosin was found to be a potent inhibitor of [125I]iodomelatonin binding in all brain regions studied. The pharmacological profile of this binding site indicated it to be unique, since serotonergic, dopaminergic and adrenergic drugs (other than prazosin) did not have appreciable affinity for it. Although saturation studies revealed only one binding site, the low Hill coefficients obtained for several inhibitors suggest that [125I]iodomelatonin labels multiple sites (or affinity states) in the hypothalamus.

Animals↗
PubMed1984

Ontogeny of thymidine kinase and DNA in the hypothalamus and cerebral cortex of the rat: effects of neonatal estrogen.

Developmental patterns of activity for thymidine kinase and DNA content were determined for the hypothalamus and cerebral cortex of the female rat during the first 3 postnatal weeks. The DNA content and thymidine kinase activity for both brain structures were maximal at ages 1 and 3 days, respectively. Total DNA content for the hypothalamus significantly increased 21% between ages 1 and 21 days. Administration of 17 beta-estradiol benzoate (EB) during the sexually critical period of brain differentiation had no effect on thymidine kinase in either brain structure. However, a transient and highly significant decrease in DNA content occurred in the hypothalamus of the 2-day-old EB-treated rat. These data indicate that (a) DNA synthesis occurs in the postnatal hypothalamus, (b) DNA synthesis in the hypothalamus and cortex is not tightly coupled to the activity of thymidine kinase and, (c) the EB-induced decrease in hypothalamic DNA is not related to changes in thymidine kinase.

Aging↗
PubMed1985

Evidence that estradiol-2/4-hydroxylase activities in rat hypothalamus and hippocampus differ qualitatively and involve multiple forms of P-450: ontogenetic and inhibition studies.

Estradiol-2/4-hydroxylase activity was studied in hypothalamic and hippocampal microsomes of male and female Wistar rats between 22 and 75 days after birth. The activity exhibited substrate saturation (50-100 microM estradiol) required NADPH and was inhibited by carbon monoxide, alpha-naphthoflavone and metyrapone. With 30 microM estradiol, 50% inhibition required 50-70 microM alpha-naphthoflavone compared to 200 microM metyrapone. Metyrapone exhibited biphasic inhibition curves which did not differ significantly between hypothalamus and hippocampus, whereas alpha-naphthoflavone was a more potent inhibitor of the hippocampal enzyme than of the hypothalamic enzyme. The Km and Vmax of the hippocampal estradiol-2/4-hydroxylase were significantly greater than that of the hypothalamus in both sexes at all ages studied. In female rats the Km of the hypothalamic enzyme changed from 14 microM at 23 days of age, to 47 microM at 71 days, but remained constant at about 29 microM in males. The Km of the hippocampal enzyme showed no significant change with age in either sex. The present findings indicate that catechol estrogen formation in the brain is catalyzed by multiple forms of microsomal P-450. They also suggest that these enzyme activities in the rat hypothalamus and hippocampus differ qualitatively. Ontogenetic changes in the Km of estradiol-2/4-hydroxylases appeared to be limited to the female hypothalamus. This might reflect a specific biological requirement of the female hypothalamus during critical stages of sexual differentiation of the brain. The relatively high hippocampal activity might reflect the catalytic versatility of different P-450 isozymes and does not necessarily imply a physiologically meaningful role with respect to catechol estrogen biosynthesis in this particular brain area.

Aging↗
PubMed1986

Correlation between LH and estrogen receptor turnover in pituitary and hypothalamus of castrate rats following estrogen agonists and antagonists.

A series of studies was undertaken to correlate the short-term dynamics of LH secretion and depletion-replenishment patterns of estrogen receptors (ER) in hypothalamic and pituitary cytosols of ovariectomized rats. Animals castrated for 2 weeks were administered various test compounds and analyzed at 1, 3, 5, 10 and 15 h post-treatment. A single injection of 10 micrograms 17 beta-estradiol (E2) to ovariectomized rats elicited a rapid depletion of ER in both pituitary and hypothalamus and a dramatic, though delayed, fall in serum LH. ER replenishment occurred in both tissues through 15 h and LH recovered in a similar manner. When cycloheximide was administered along with E2, ER replenishment was completely inhibited in both tissues; serum LH fell and failed to recover. Actinomycin D injected with E2 blocked replenishment in pituitary but not hypothalamus; serum LH recovered in parallel with the hypothalamic ER pattern. 17 alpha-E2 elicited only slight changes in ER and LH was suppressed 10-20% through 15 h. CI-628 caused a near total depletion of pituitary ER with no subsequent replenishment, whereas hypothalamic ER content was virtually unaltered; serum LH was suppressed and later recovered. Orchidectomized rats given 5 micrograms E2 demonstrated a less complete ER depletion in hypothalamus, and an earlier replenishment than that seen in pituitary or hypothalamus of similarly treated ovariectomized females. Serum LH rebounded to 157% of control levels at 15 h. The results indicate that the acute feedback suppression of LH by exposure to estrogens correlates with binding to ER and nuclear translocation. Replenishment and/or retention of cytoplasmic ER in hypothalamus appears to be required for full resumption of LH secretion, following acute suppression.

Animals↗
PubMed1984

Muscarinic cholinoceptors and choline acetyltransferase activity in the hypothalamus of spontaneously hypertensive rats.

To study the role of central cholinergic mechanisms in hypertension, we have determined muscarinic receptors using [3H] (-)quinuclidinyl benzilate (QNB) and choline acetyltransferase (ChAT) activity in the brain regions of spontaneously hypertensive rats (SHR), stroke-prone SHR (SHRSP) and renal hypertensive rats. The number of muscarinic receptors was significantly (33-38 %) elevated in the hypothalamus of SHR and SHRSP at the ages of 16 and 24 weeks compared to that of Wistar-Kyoto rats (WKY). An increased density of muscarinic receptors was consistently observed in the prehypertensive (5 weeks) and developmental (10 weeks) stages of hypertension. In contrast, in the hypothalamus of rats with renal hypertension there was no muscarinic receptor alteration. The receptor alteration in the SHRSP hypothalamus was not abolished by a chronic hypotensive treatment which prevented the development of hypertension, suggesting that an enhancement of the muscarinic receptors in spontaneous hypertension does not occur secondarily to the elevation of blood pressure. The hypothalamus of SHR and SHRSP at the ages of 5 and 24 weeks showed significantly less activity of ChAT. These data demonstrate that there is a specific increase in muscarinic receptors and a decrease in cholinergic activity in the hypothalamus of SHR and SHRSP. Thus, the present study suggests an important role for hypothalamic cholinergic receptors in the pathogenesis of spontaneous hypertension.

Aging↗
PubMed1990

Changes in oxytocin and vasopressin content in posterior pituitary and hypothalamus following pantethine treatment.

Pantethine, a cysteamine precursor, depletes somatostatin in the cerebral cortex and hypothalamus and prolactin in the anterior pituitary and hypothalamus. This study investigated the effect of pantethine on oxytocin and arginine vasopressin content in the posterior pituitary and hypothalamus. Male Long-Evans rats were injected intraperitoneally with escalating doses of pantethine (i.e., 146.7 mg, 293.4 mg and 586.6 mg/100 gm body weight). Hormone content was determined by radioimmunoassay. Three hours after pantethine treatment, the oxytocin content in the posterior pituitary and the hypothalamus was markedly reduced with all doses of the drug. Vasopressin content in the posterior pituitary and hypothalamus was decreased but to a lesser extent than oxytocin and only with the highest dose of pantethine. Pantethine may act to reduce oxytocin and vasopressin content through intracellular conversion to cysteamine. The exact mechanism of action of pantethine on oxytocin and vasopressin remains to be elucidated.

Analysis of Variance↗
PubMed1985

Depletion of noradrenaline in the hypothalamus reduces the febrile responses induced by prostaglandin E2, thyrotropin-releasing hormone and beta-endorphin in rats.

The effects of pretreatment of rats with an intrahypothalamic injection of 6-hydroxydopamine on the thermal responses induced by intrahypothalamic injection of noradrenaline, prostaglandin E2, thyrotropin-releasing hormone or beta-endorphin were assessed. Administration of either noradrenaline (2-10 micrograms), prostaglandin E2 (10-40 ng), thyrotropin-releasing hormone (0.5-2.0 micrograms) or beta-endorphin (1-3 micrograms) into the preoptic anterior hypothalamus caused a dose-dependent rise in rectal temperature in conscious rats at an ambient temperature of 22 degrees C. In addition, it was found that three intrahypothalamic doses of 10 micrograms of 6-hydroxydopamine at intervals of 2 days caused a significant depletion of noradrenaline in the hypothalamus to 26.4% of control while the concentration of dopamine in the hypothalamus was not significantly reduced at 95.3% of control. Furthermore, the hyperthermic responses induced by prostaglandin E2, thyrotropin-releasing hormone, or beta-endorphin were greatly attenuated after selective depletion of noradrenaline in the hypothalamus in rats. However, selective depletion of noradrenaline did not affect the noradrenaline-induced hyperthermic responses. The data indicate that either prostaglandin E2, thyrotropin-releasing hormone or beta-endorphin may act through the endogenous release of noradrenaline from the hypothalamus to induce hyperthermic responses in rats.

Animals↗
PubMed1987

Adrenaline in the CNS: in vivo evidence for a functional pathway innervating the hypothalamus.

This article reviews the evidence, obtained from studies employing the technique of intracerebral dialysis, to monitor changes in extracellular adrenaline in the hypothalamus, that adrenaline is released from nerve endings in the hypothalamus and has a functional role. Studies using [3H] adrenaline to determine the specificity of uptake mechanisms for adrenaline indicate that labelled adrenaline is also taken up by noradrenergic nerve endings. This supports the need to develop techniques to monitor changes in endogenous release of adrenaline. In this study, it has been shown that inhibition of phenylethanolamine-N-methyltransferase selectively decreases tissue levels in the hypothalamus and in vivo release of adrenaline, while monoamine oxidase inhibition and antagonism of alpha 2-adrenoceptors increases the release of both adrenaline and noradrenaline. The "selective" noradrenergic neurotoxin DSP4 caused an initial increase in the release of both catecholamines, followed by a marked decrease in their release. Stimulation of the adrenaline-containing neurones in the rostral ventrolateral medulla (C1 region) increased the release of adrenaline in the posterior hypothalamus, but not that of noradrenaline, while also increasing mean arterial blood pressure. Pharmacological evidence indicates that B2-adrenoceptors in the hypothalamus and the spinal cord are involved in the rise in mean arterial pressure, as the response is reduced by a selective B2-antagonist (ICI 118551). The rise in mean arterial blood pressure during C1 stimulation is enhanced by the alpha 2-antagonist idazoxan, supporting observations that alpha 2-adrenoceptors are involved in the pre-synaptic regulation of release of adrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1988

Vasopressin receptor blockade in the anterior hypothalamus suppresses aggression in hamsters.

Although the anterior hypothalamus has been implicated in the control of aggression in various rodent species, little is known about the neurochemical mechanisms mediating this control. It has been established that flank marking, which occurs with high frequency during agonistic encounters in hamsters, is dependent upon vasopressin-sensitive neurons in the anterior hypothalamus. The present study was undertaken to determine whether intraspecific aggression in this species is similarly influenced by vasopressin in this area of the hypothalamus. Adult male hamsters, surgically implanted with guide cannulae aimed at the anterior hypothalamus, were microinjected with three different concentrations of the V1-receptor antagonist d(CH2)5Tyr(Me)AVP or a vehicle control of 0.9% NaCl. Sixty minutes after each microinjection a smaller male hamster was introduced into the home cage of the treated hamster. The resident hamsters showed a significant dose-dependent reduction in the number of biting attacks on the intruders over the 10 minute test period. The V1-receptor antagonist also caused a significant increase in the resident hamster's latencies to attack the intruder. However, the resident hamsters' total contact time with the intruder was unaffected by drug treatment suggesting that the reduction of aggression was not due to a generalized effect upon social behavior. The specificity of the drug treatment was further supported by the observation that it did not affect resident hamsters' sexual motivation or ability to mount a receptive female. These data suggest that vasopressin-sensitive neurons in the anterior hypothalamus are involved in the control of intraspecific aggression in male hamsters.

Aggression↗
PubMed1995

Hypoxia sensitive neurons in the caudal hypothalamus project to the periaqueductal gray.

Previous studies have demonstrated that the caudal hypothalamus modulates the respiratory responses to hypoxia and hypercapnia. In addition, many of the neurons in this area have a basal discharge related to the cardiac and/or respiratory cycles and are stimulated by hypoxia or hypercapnia. The purpose of the present study was to determine if these hypothalamic neurons project to a known cardiorespiratory area, the periaqueductal gray in the rat. In a first set of experiments, rhodamine-tagged microspheres were injected into the periaqueductal gray (PAG) to determine the areas of the caudal hypothalamus that project to the PAG. These studies revealed that the caudal hypothalamus sends strong ipsilateral and weak contralateral projections to the PAG. In a second set of experiments, single unit recordings were made from neurons in the caudal hypothalamus; the basal discharge of these neurons were examined with signal averaging techniques. Each neuron (n = 79) was tested for a response to inhalation of a hypoxic (10% O2) and a hypercapnic (5% CO2) gas. Antidromic activation techniques were then used to determine if neurons in the caudal hypothalamus send projections to or through the PAG. Nineteen percent (n = 15) of the hypothalamic neurons studied could be activated from the PAG; approximately 53% (n = 8) of these were excited by hypoxia and 27% (n = 4) by hypercapnia. Most of these neurons tested (42 of 64 neurons) had a basal discharge related temporally to the cardiac and/or respiratory cycles. These findings suggest that a caudal hypothalamic to periaqueductal gray projection is involved in the integrated response to hypoxia.

Animals↗
PubMed1976

Characterization of the androgen receptors in the hypothalamus, preoptic area and brain cortex of the rat.

The specific androgen receptors for testosterone (T) (1) and 5alpha-dihydrotestosterone (DHT) in the cytosol fraction of the hypothalamus, preoptic area and brain cortex of the rat have been characterized using electrophoresis and isoelectric focusing in polyacrylamide gels. After labeling of the cytosol fractions in vivo and in vitro we were able to demonstrate androgen-receptor complexes moving with an electrophoretic mobility (R(f) of 0.5 in 3.25% acrylamide gels containing 0.5% agarose and 10% glycerol. Polyacrylamide gel electrophoresis was used as a quantitative assay for androgen receptors in the tissues. The hypothalamus, preoptic area and brain cortex were found to possess a single class of high affinity binding sites for androgens and the dissociation constants (K(D) were estimated to be 3.4, 4.3 and 2.6 X 10 (-10M) respectively. The binding capacities were 3.7 (hypothalamus), 3.5 (preoptic area) and 1.8 X 10 (-15) (brain cortex) moles of high affinity binding sites per mg protein. Like other androgen-receptor complexes, the testosterone-receptor complexes of the hypothalamus, preoptic area and brain cortex were temperature labile, sulfhydryl dependent and revealed a very slow rate of dissociation at o degrees C (t1/2 greater than 36 hr). The receptors in all the tissues had an isoelectric point of 5.8. The steroid specificity of the cytoplasmic androgen receptors was tested in vitro by the competing efficiency of different unlabeled steroids for (3H)-testosterone binding. In the three tissues in investigation the following order of affinity was found: DHT greater than T greater than Cyproterone acetate greater than progesterone greater than androstenedione greater than 17beta-estradiol. Cortisol did not effect androgen binding significantly. Thus, the physiochemical characteristics of the cytoplasmic androgen receptors of the hypothalamus, preoptic area and brain cortex are very similar, if not identical, to those of the androgen receptors described in the anterior pituitary, ventral prostate, epididymis and testis.

Androgens↗
PubMedDate not supplied

Functional relationship of lateral hypothalamus and amygdala in control of eating.

Cannulas were stereotactically implanted in the lateral hypothalamus and the ipsilateral amygdaloid cortical nucleus of 7 male albino rats, Wistar strain. After functional checking of the accuracy of implants by adrenergic elicitation of increased food intake, the animals were injected with combinations of noradrenaline, phenoxybenzamine or tolazoline, or placebo under 6 treatment conditions, while food-and water satiated. The elicitation of increased food intake in the satiated rat by adrenergic stimulation of the lateral hypothalamus was confirmed, and it was further found that simultaneous adrenergic stimulation of the amygdaloid cortical nucleus augmented this increase. However, simultaneous anti-adrenergic blockade in the amygdaloid cortical nucleus reduced eating to control level. The lack of response of the amygdaloid cortical nucleus to adrenergic stimulation in the satiated rat, under simultaneous stimulation of the lateral hypothalamus with either placebo or an adrenergic blocker, was also demonstrated. It was concluded that the amygdaloid cortical nucleus has a modulatory influence on eating behavior, which is dependent on the level of activity in the lateral hypothalamus, and further that this modulatory influence is necessary to the behavioral output of the hypothalamic system. This is the same relationship between the hypothalamus and amygdala previously demonstrated in regard to drinking behavior and these results are seen as supporting the behavioral generality of the functional relationships reported.

Amygdala↗
PubMed1987

Electrical self-stimulation in the parabrachial area is depressed after ibotenic acid lesion of the lateral hypothalamus.

The involvement of lateral hypothalamic intrinsic neurons on electrical self-stimulation of the parabrachial area was analyzed. Rats were bilaterally implanted in the parabrachial area and with a guide cannula located above each lateral hypothalamus. They were subsequently tested for intracranial self-stimulation. Then, the lateral hypothalamus on one side of the brain was injected with ibotenic acid. The effect of the induced lesion was tested 8 days later on self-stimulation of the ipsilateral and contralateral parabrachial areas. The intrinsic neurons of the non-lesioned lateral hypothalamus were then destroyed with ibotenic acid. Self-stimulation was then tested 8, 12 and 30 days later. The unilateral lesion produced a significant decrease of self-stimulation using the electrode ipsilateral to the lesion, without any modification of the stimulation using the contralateral electrode. After bilateral lesion, self-stimulation was greatly reduced bilaterally. The results suggest that the main effect of the lesion was to increase the self-stimulation threshold. Given that the parabrachial area is a relay station for the gustatory inputs and that the intrinsic neurons of the lateral hypothalamus project back to the parabrachial area, the present results are tentatively interpreted as an indication that self-stimulation in this pontine area results from the activation of feedback loops between the lateral hypothalamus and the parabrachial area.

Animals↗
PubMed1994

Pituitary adenylate cyclase activating polypeptide (PACAP)-like immunoreactivity in human hypothalamus: co-localization with arginine vasopressin.

Pituitary adenylate cyclase activating polypeptide (PACAP) is a novel hypothalamic peptide consisting of 38 amino acids (PACAP1-38) with a potent stimulatory action on adenylate-cyclase in rat pituitary. The presence of PACAP-like immunoreactivity in human brain was studied by radioimmunoassay. Co-localization of PACAP with arginine vasopressin and oxytocin was investigated by immunocytochemistry in the human hypothalamus. Immunoreactive PACAP was detected in all regions of human brain (cortex, thalamus, hypothalamus, pons and hemisphere of cerebellum) with the highest levels found in the hypothalamus (8.5 +/- 1.9 pmol/g wet weight, n = 4, mean +/- S.E.M.). High performance liquid chromatography of the human hypothalamic extract showed that approximately 50% of the immunoreactive PACAP was eluted in the position of PACAP1-38. Immunocytochemical studies showed the presence of PACAP immunoreactive neurons in the paraventricular and supraoptic nuclei of human hypothalamus. PACAP co-localized with arginine vasopressin in magnocellular cells of these nuclei. These findings suggest that PACAP1-38 plays important physiological roles in the human hypothalamus.

Aged↗