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PubMed1990

Immunocytochemical colocalization of progestin receptors and beta-endorphin or enkephalin in the hypothalamus of female guinea pigs.

Double-label immunocytochemistry was used to determine whether estradiol-induced progestin receptors and either beta-endorphin or leucine-enkephalin are colocalized in female guinea pig brain. Ovariectomized, adult guinea pigs were implanted with capsules containing estradiol-17 beta to induce high levels of progestin receptors, and injected intracerebroventricularly with colchicine to improve visualization of the opiate peptides. Sections through the hypothalamus and preoptic area were processed for progestin receptor, followed by beta-endorphin or leucine-enkephalin immunocytochemistry. As reported previously, high concentrations of progestin receptor-immunoreactive (PR-IR) cells were found in the preoptic area (medial and periventricular portions, medial preoptic nucleus) and hypothalamus (anterior hypothalamic and arcuate nuclei, ventrolateral area). Many beta-endorphin-IR cells contained PR-IR in the arcuate nucleus and its surroundings (33%) and in the dorsomedial area of the hypothalamus (64%). Scattered enkephalin-IR cells were found in the septal nucleus, medial and lateral preoptic area, bed nucleus of the stria terminalis, and the arcuate nucleus. The ventromedial nucleus of the hypothalamus and dorsolateral magnocellular nucleus, respectively, contained moderate and heavy concentrations of enkephalin-IR cells. Although some of these areas also contained PR-IR, enkephalin-IR was colocalized consistently with PR-IR only in a small number of cells in the arcuate nucleus and ventromedial/ventrolateral area of the hypothalamus. These data, taken together with earlier observations that virtually all cells containing estradiol-induced PR-IR also contain estrogen receptor-IR, provide neuroanatomical evidence that hypothalamic actions of progesterone and estradiol may be mediated by beta-endorphin and/or enkephalin.

Animals↗
PubMed1994

Proposed pathways for vocal self-stimulation: met-enkephalinergic projections linking the midbrain vocal nucleus, auditory-responsive thalamic regions and neurosecretory hypothalamus.

In this study, we have investigated the neuroanatomical pathways that may underlie the influence of a female bird's vocal behavior upon her own reproductive endocrine response. We traced the ascending efferent projections of the midbrain vocal control nucleus, the intercollicularis (ICo), using an anterograde tracer, PHAL, delivered by iontophoretic application. We found labelled terminal fields in the anterior regions of the hypothalamus that contained luteinizing hormone releasing hormone- (LHRH) immunoreactive neurons. We injected into the LHRH-rich anterior medial hypothalamus (AM) the retrograde tracer, fluoro-gold, to verify the results of PHAL anterograde tracing and examine whether retrogradely labelled neurons in the ICo can be stained with met-enkephalin antiserum by the immunohistochemical method. Of the retrogradely labelled neurons in the medial division of ICo (mICo), between 5% and 15% were found to be met-enkephalin-immunoreactive positive perikarya. Our data suggest that axonal projections into the anterior medial hypothalamus may arise in part from enkephalin-immunoreactive neurons in the medial ICo. The mICo neurons distributed along the medial border of the midbrain auditory nucleus give rise to projections into the posterior medial hypothalamus (PMH) via synapses within the shell region of thalamic auditory nucleus, ovoidalis (Ov). We conclude that in the ring dove, the medial division of the vocal control nucleus, by virtue of its connection with the auditory thalamus and neurosecretory hypothalamus, is in a position to exert influence on endocrine response partly through enkephalinergic systems. Implications of similar connections in other species are discussed.

Animals↗
PubMed1998

Relationship between prolactin receptor mRNA in the anterior pituitary gland and hypothalamus and reproductive state in male and female bantams (Gallus domesticus).

The aim of this study was to test the hypothesis that prolactin may up- and down-regulate prolactin receptor gene expression in the anterior pituitary gland and hypothalamus respectively. Experiments were carried out in bantams (Gallus domesticus). Comparisons were made of concentrations of PRLR mRNA in the anterior pituitary gland and basal and preoptic hypothalamus in adult males and females held on long days (low vs high plasma prolactin); in 3-week-old juvenile male and females on short days (high vs low plasma prolactin); in 8-week-old juvenile male and females on short days (both low plasma prolactin); in adult laying, incubating, and out-of-lay (high, very high, and low plasma prolactin, respectively); in adult cockerels exposed to long or short days (high vs low prolactin); and in adult hens exposed to long or short days (high vs low prolactin). There was a sex difference in anterior pituitary and basal hypothalamic PRLR mRNA, with lower values in both tissues in females than in males. Compared with laying and out-of-lay hens, anterior pituitary and basal hypothalamic PRLR mRNA concentrations in incubating hens were increased and decreased, respectively. In adult birds of either sex held on long or short days, there was no difference in pituitary PRLR mRNA, while basal hypothalamic PRLR mRNA was lower on short days. PRLR mRNA in the preoptic hypothalamus was not affected by sex, reproductive state, or photoperiod. It is concluded that there is no consistent relationship between plasma prolactin, in the physiological range, and the concentration of PRLR mRNA in the anterior pituitary gland, basal hypothalamus, and preoptic hypothalamus.

Aging↗
PubMed1983

Serotonergic mechanisms in the hypothalamus mediate thermoregulatory responses in rats.

1. Either electrical stimulation of midbrain raphe nuclei or administration of 5-hydroxytryptamine (5-HT; serotonin) into the preoptic anterior hypothalamus caused hypothermia in conscious rats at ambient temperatures (Ta) of both 8 degrees C and 22 degrees C. The hypothermia was due to decreased metabolic heat production at Ta = 8 degrees C, while at Ta = 22 degrees C the hypothermia was due to both decreased metabolism and increased heat loss (cutaneous vasodilatation). However, at Ta = 30 degrees C, electrical stimulation of midbrain raphe or intrahypothalamic injection of 5-HT caused an insignificant change in the thermoregulatory responses. There was no changes in respiratory evaporative heat loss in response to these treatments at various Ta's. 2. Direct administration of the serotonergic receptor antagonists such as cyproheptadine and methysergide into the preoptic anterior hypothalamus caused hyperthermia in conscious rats at Ta's of 8 degrees C, 22 degrees C and 30 degrees C. The hyperthermia was due to increased metabolism and cutaneous vasoconstriction. 3. The hypothermia induced by intrahypothalamic administration of 5-HT was antagonized by pretreatment with an intrahypothalamic dose of either cyproheptadine or methysergide in rats at Ta = 22 degrees C. 4. Inhibition of 5-HT neuronal activity with administration of 5-HT into the midbrain raphe regions also caused hyperthermia, increased metabolism and cutaneous vasoconstriction in rats at Ta's of 8 degrees C, 22 degrees C and 30 degrees C. 5. These observations tend to suggest that the functional activity of serotonergic receptors in the preoptic anterior hypothalamus mediates thermoregulatory responses in the rat. Activation of serotonergic receptors in the hypothalamus decreases heat production and/or increases heat loss, while inhibition of serotonergic receptors in the hypothalamus increases heat production and/or decreases heat loss in the rat.

Animals↗
PubMed1992

Norepinephrine, dopamine, and 5-HT release from perfused hypothalamus of the rat during feeding induced by neuropeptide Y.

In the unrestrained rat, the hyperphagic-like ingestion of food evoked by the sustained elevation of neuropeptide-Y (NPY) in the hypothalamus was correlated with the release and turnover of monoaminergic transmitters in this structure. A single guide tube was implanted stereotaxically in the perifornical region of the hypothalamus for localized push-pull perfusion of an artificial CSF vehicle or NPY1-36 in a concentration of 10, 50, or 100 ng/1.0 microliters. After the rat was fully satiated, a site reactive to NPY was perfused repeatedly at a rate of 20 microliters/min for 6.0 min with an interval of 6.0-12 min elapsing between each perfusion. Samples of perfusate were analyzed by HPLC with coulometric detection for DA, HVA, DOPAC, NE, MHPG, 5-HT, and 5-HIAA. Although control perfusions were without effect on feeding or monoamine activity, NPY evoked mean cumulative intakes of food of 14 +/- 2.4, 25.6 +/- 3.0 and 26.5 +/- 3.2 g in response to 10, 50, or 100 ng/microliter concentrations of NPY, respectively, over the 4.0-5.0 hr test interval. HPLC analyses showed that during feeding the release of both NE and DA was enhanced significantly. The turnover of both catecholamines likewise increased significantly as reflected by the elevated levels of MHPG, DOPAC and HVA. However, neither the basal efflux of 5-HT nor its turnover, as reflected by the output of 5-HIAA, was affected during feeding induced by NPY perfused in the hypothalamus. These results suggest that a sustained elevation of NPY in the hypothalamus causes a perturbation in the basal activity of NE and DA which are both implicated in the neuronal mechanism regulating normal eating behavior. Thus, these catecholamine neurotransmitters are envisaged to comprise an intermediary step in the functional role played by NPY in the hypothalamus in integrating the control of energy metabolism and caloric intake.

Animals↗
PubMed1994

Hypothalamus involvement in the reticulo-rumen motor and behavioural disturbances induced by morphine in sheep.

Morphine (20 and 40 micrograms/kg) administered into the cerebral ventricle of conscious sheep caused significant inhibition of the mean frequency and the average amplitude of primary ruminal contractions by 45 min after injection. Between 90 and 120 min, morphine (40 micrograms) provoked a significant increase in the amplitude (p < 0.01). At both doses it caused strong psychomotor excitability that lasted for more than 140 min. Isolation of the hypothalamus prevented both the inhibitory effects of morphine on rumen motility and the drug-induced psychomotor excitability. Histopathological analysis of slices of the hypothalamus, pons and medulla indicated descending degenerative changes in the nervous pathways connecting the hypothalamus with lower structures in the brain. These results suggest either that hypothalamic isolation caused degeneration of inhibitory descending pathways that connect the hypothalamus with the gastric centres or that structures of importance for forestomach motility are not located within the gastric centres but elsewhere in the brain, for example in the hypothalamus.

Akathisia, Drug-Induced↗
PubMed1992

Effects of systemic carbidopa on dopamine synthesis in rat hypothalamus and striatum.

Significant concentrations of carbidopa (CD) were found in rat hypothalamus, striatum, and in striatal microdialysis efflux after intraperitoneal administration of the drug. Efflux levels peaked one hour after administration of 100 mg/kg at 0.37 micrograms/ml, or about 2% of serum levels. Concurrent CD levels in hypothalamus and striatum were about 2.5% and 1.5%, respectively, of corresponding serum levels. Levels of dopamine and its principal metabolites in striatal efflux were unaffected. The removal of the brain blood by saline perfusion decreased the striatal and hypothalamic CD concentrations only by 33% and 16%, respectively. In other rats receiving both CD and levodopa (LD), brain L-dopa, dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) levels after one hour tended to be proportionate to LD dose. When the LD dose remained constant, increasing the CD dose dose-dependently enhanced L-dopa levels in the hypothalamus and striatum. However dopamine levels did not increase but, in contrast, decreased dose-dependently (although significantly only in the hypothalamus). CD also caused dose-dependent decrease in striatal 3-O-methyldopa (3-OMD) and in striatal and hypothalamic homovanillic acid (HVA), when the LD dose was 50 mg/kg. We conclude that, at doses exceeding 50 mg/kg, sufficient quantities of CD enter the brain to inhibit dopamine formation, especially in the hypothalamus. Moreover, high doses of LD/CD, both of which are themselves catechols, can inhibit the O-methylation of brain catecholamines formed from the LD.

3,4-Dihydroxyphenylacetic Acid↗
PubMedDate not supplied

The role of the posterior hypothalamus in controlling the paradoxical phase of sleep.

Chronic experiments were performed on seven cats to study the effects of high-frequency electrical stimulation of the posterior hypothalamic area on the characteristics of paradoxical sleep; the excitability of this structure at different stages of paradoxical sleep was determined. These studies showed that at the stage showing ECoG desynchronization and phasic events (stage 1), the response threshold for behavioral arousal resulting from stimulation of posterior hypothalamus was 20-30% higher than at the stage characterized by alpha-like activity in the ECoG and the absence of phasic phenomena (stage 2). Transient stimulation of the posterior hypothalamus at stage 1, at a level which was subthreshold for arousal from this state, led to a transition to stage 2 or a reduction in phasic events in paradoxical sleep without altering the qualitative characteristics of phase 1. Stimulation of the posterior hypothalamus at a level subthreshold for arousal from stage 2 and applied continuously during paradoxical sleep led to a reduction in the duration of this stage by 25-50% and to an increase in the proportion of stage 2 in the structure of paradoxical sleep. These results provide evidence that the posterior hypothalamus is involved in the inhibitory control of the 'executive' mechanisms of paradoxical sleep responsible for the ECoG desynchronization and the phasic manifestations of this state. It is suggested that the functional activity of the posterior hypothalamus at stage 1 also increases at stage 2, thus evidently fulfilling a 'guard' function.

Animals↗
PubMed1990

The effects of histamine on the concentrations of immunoreactive thyrotropin-releasing hormone in the stomach and hypothalamus in rats.

The effects of histamine and its related compounds on the concentrations of immunoreactive thyrotropin-releasing hormone (ir-TRH) in the stomach, gastric juice and hypothalamus in rats were studied. Histamine, ranitidine or ethanolamine was injected intraperitoneally, and the rats were decapitated at various times after the injection. Ir-TRH concentrations in the stomach, gastric juice and hypothalamus were measured by a radioimmunoassay. Ir-TRH concentrations in the stomach decreased significantly after histamine injection and increased significantly after ranitidine injection in a dose-dependent manner, but did not change with ethanolamine. Ir-TRH concentrations in the gastric juice increased in a dose-dependent manner, peaking at 30 min after histamine injection, and its effect was blocked with ranitidine. Ir-TRH concentrations in the hypothalamus elevated significantly after histamine injection and reduced significantly after ranitidine injection, but did not change with ethanolamine. The effects of histamine on ir-TRH concentrations in the stomach and hypothalamus were significantly blocked with ranitidine, but not with ethanolamine. These findings suggest that histamine stimulates ir-TRH release from the stomach and inhibits ir-TRH release from the hypothalamus, and that these effects of histamine on ir-TRH release are mediated via an H2-receptor.

Animals↗
PubMed2002

Involvement of neuropeptide Y in glucose sensing in the dorsal hypothalamus of streptozotocin diabetic rats - in vitro and in vivo studies of transmitter release.

AIMS: Within the brain, subgroups of neurons respond differently to altered glucose concentrations. Identification of neuropeptide Y in hypothalamic neurons that sense glucose suggests a role for neuropeptide Y in glucose sensing. Using in vitro and in vivo techniques to monitor transmitter release, we investigated whether lowering glucose concentration affects the release of neuropeptide Y from the brain, and whether this process is altered in Type I (insulin-dependent) diabetes mellitus. METHODS: Male Sprague-Dawley rats were treated with 48 mg/kg streptozotocin or vehicle intravenously. The effect of reduced glucose on endogenous neuropeptide Y overflow from slices of hypothalamus and medulla incubated in Krebs solution was examined 4 weeks later. The hypothalamus was separated into a dorsal region containing the paraventricular nucleus and a ventral region containing the arcuate nucleus. RESULTS: Streptozotocin-induced diabetes increased basal neuropeptide Y overflow in the dorsal and ventral hypothalamus ( p<0.05) but not the medulla. In vitro neuropeptide Y overflow was reduced by low glucose in the dorsal hypothalamus in diabetic, but not in control rats. No effect of reduced glucose was observed in the ventral hypothalamus or medulla. In vivo push-pull studies in the paraventricular nucleus also showed greater neuropeptide Y overflow in diabetic rats relative to control rats ( p<0.05). Insulin-induced hypoglycaemia induced a decrease in neuropeptide Y overflow in diabetic rats, while an increase was observed in control rats ( p<0.05). CONCLUSION: These region-specific effects of low glucose on neuropeptide Y overflow in diabetic rats support a part for neuropeptide Y in altered glucose sensing in Type I diabetes.

Animals↗
PubMed2001

Alternate cadmium exposure differentially affects the content of gamma-aminobutyric acid (GABA) and taurine within the hypothalamus, median eminence, striatum and prefrontal cortex of male rats.

This work examines changes of gamma aminobutyric acid (GABA) and taurine contents in the hypothalamus, striatum and prefrontal cortex of the rat after an alternate schedule of cadmium administration. Age-associated changes were also evaluated, of those before puberty and after adult age. In control rats GABA content decreased with age in the median eminence and in anterior, mediobasal and posterior hypothalamus, prefrontal cortex and the striatum. Taurine content showed similar results with the exception of mediobasal hypothalamus and striatum, where no changes were detected. In pubertal rats treated with cadmium from 30 to 60 days of life, GABA content significantly decreased in all brain regions except in the striatum. When cadmium was administered from day 60 to 90 of life, GABA content was significantly changed in prefrontal cortex only compared with the age matched controls. Taurine content showed similar results in pubertal rats, with the exception of the median eminence and the mediobasal hypothalamus, neither of which showed a change. However, when cadmium was administered to rats from day 60 to 90 of life, taurine content only changed in prefrontal cortex compared with the age matched controls. These results suggest that cadmium differentially affects GABA and taurine contents within the hypothalamus, median eminence, striatum and prefrontal cortex as a function of age.

Animals↗
PubMed2004

Blood-brain barrier disruption in the hypothalamus of young adult spontaneously hypertensive rats.

Vascular permeability and endothelial glycocalyx were examined in young adult spontaneously hypertensive rats (SHR), stroke-prone SHR (SHRSP), and Wistar Kyoto rats (WKY) as a control, in order to determine earlier changes in the blood-brain barrier (BBB) in the hypothalamus in chronic hypertension. These rats were injected with horseradish peroxidase (HRP) as an indicator of vascular permeability. Brain slices were developed with a chromogen and further examined with cationized ferritin, a marker for evaluating glycocalyx. Staining for HRP was seen around vessels in the hypothalamus of SHR and SHRSP, but was scarce in WKY. The reaction product of HRP appeared in the abluminal pits of endothelial cells and within the basal lamina of arterioles, showing increased vascular permeability in the hypothalamus of SHR and SHRSP, whereas there were no leaky vessels in the frontal cortex of SHR and SHRSP, or in both areas of WKY. The number of cationized ferritin particles binding to the capillary endothelial cells was decreased in the hypothalamus of SHR and SHRSP, while the number decreased in the frontal cortex of SHRSP, compared with those in WKY. Cationized ferritin binding was preserved in some leaky arterioles, while it was scarce or disappeared in other leaky vessels. These findings suggest that BBB disruption occurs in the hypothalamus of 3-month-old SHR and SHRSP, and that endothelial glycocalyx is markedly damaged there without a close relationship to the early changes in the BBB.

Animals↗
PubMed2006

Hypothalamus, sleep and headaches.

The hypothalamus is a key neural region in the regulation of sleep, its anterior part implicated in sleep facilitation, while the posterior hypothalamus acts in a balanced way to maintain wakefulness. The hypothalamus forms part of the so-called central autonomic network, regulating body homeostasis and controlling pain. To this effect, it is strongly wired to more rostral and caudal areas, in particular the brainstem periaqueductal grey, the locus coeruleus and the median raphe nuclei, all involved in sleep mechanisms and also in the descending control of pain perception. The hypothalamus, especially its posterior regions, becomes activated during attacks of the so-called trigeminal autonomic cephalalgias (TACs), while brainstem, especially dorsal pontine, activity shows up during migraine attacks. The hypothalamus and interconnected brainstem areas likely represent the neural sites responsible for the chronobiological features of some headaches, in particular the sleep-related attacks typical of the TACs, migraines and the hypnic headaches.

Headache↗
PubMed2006

Evoked activity in the hypothalamus and amygdala of the cat in conditions of food-related motivation and emotional tension.

The amplitude-time characteristics of potentials evoked by clicks were analyzed in bilateral leads from the lateral hypothalamus and amygdala in cats in conditions of food-related motivation, emotional tension (presentation of dogs), and orientational reactions. In conditions of food-related motivation, as compared with the satiated state, there were decreases in the latent periods and changes in the amplitudes of the P1 and N2 components in the hypothalamus and P1, N2, and N3 in the amygdala. The most marked changes occurred on the left side in both structures. Presentation of dogs induced decreases in the latent periods of all components (including N1) of evoked potentials in the hypothalamus and amygdala, the most marked changes in the hypothalamus occurring on the right side and the most marked changes in the amygdala occurring on the left side. Conversely, orientational reactions to emotionally neutral stimuli induced increases in the latent periods of evoked potentials. It is concluded that there is an increase in sensory reactivity in the hypothalamus and amygdala in motivational-emotional states. It is suggested that the side of dominance in these structures may be associated both with the factor of the activity/passivity of the behavior in conditions of fear and the genesis of the emotion (motivational or informational).

Amygdala↗
PubMed1980

Catecholamine synthesizing enzymes in the hypothalamus during the estrous cycle.

The activities of tyrosine hydroxylase and dopamine-beta-hydroxylase were measured in the medial basal hypothalamus and remaining hyothalamic tissue of female rats at various times during diestrus 2, proestrus and estrus. Tyrosine hydroxylase activity in the medial basal hypothalamus was significantly lower at 12.00 h compared with other times on proestrus. This decrease preceded the elevation of serum prolactin and LH during the afternoon of proestrus. Tyrosine hydroxylase activity did not change significantly during diestrus 2 or estrus nor was it altered at any time in the remainder of the hypothalamus. Dopamine-beta-hydroxylase activity in the basal medial hypothalamus was significantly elevated at 12.00 h on proestrus and at 14.00 h on diestrus. The results provide further evidence for a decrease in dopaminergic neuron activity in the medial basal hypothalamus which may precipitate the series of events leading to the LH surge during proestrus. The increase in dopamine-beta-hydroxylase activity suggests that an increase in noradrenergic neuron activity may also be involved in triggering the release of LH.

Animals↗
PubMed1981

Arterial hypertension elicited either by lesions or by electrical stimulations of the rostral hypothalamus in the rat.

Bilateral anodal lesions performed with stainless steel electrodes placed either in the anterior medial (AMH) or lateral (ALH) hypothalamus, or in the ventromedial nucleus (VMH), induced in unrestrained rats the rapid development of arterial hypertension, tachycardia and death. Similarly placed cathodal lesions performed with platinum electrodes failed to elicit the cardiovascular syndrome. The electrical stimulation of the AMH, ALH or VMH caused an increased in the arterial blood pressure in anesthetized rats. This pressor response was characteristically biphasic and consisted of a sharp increase in arterial pressure at the onset of the stimulation, followed by a second elevation at the end of the stimulation. The hypertension evoked either by lesions or by stimulations of the hypothalamus, appeared to depend largely on a neurally mediated release of adrenal medullary catecholamines, and to some extent on the activation of the sympathetic vasoconstrictor fibers. Bilateral adrenalectomy, or adrenal demedullation, prevented the hypertension evoked by lesions, and selectively blocked the important secondary phase of the pressor response elicited by stimulation, but did not affect the primary phase. The latter was specifically eliminated by the destruction of the sympathetic vasomotor axons with 6-hydroxydopamine (6-OHDA). On the other hand, the tachycardia evoked by lesions or stimulations of the medial hypothalamus, resulted from an increase in sympathetic neural discharges to the heart, and it was abolished either by beta-receptor blockade with sotalol or by chemical sympathectomy with 6-OHDA. In contrast, the tachycardia occurring after lesions of the lateral hypothalamus was entirely due to circulating adrenal medullary catecholamines and it was eliminated by adrenalectomy. It is concluded that acute hypertension and tachycardia produced by anodal lesions performed with stainless steel electrodes results from the excitation of the hypothalamus, possibly due to the irritative action of the metallic ions deposited at the lesion sites. The observations of cardiovascular responses entirely due to adrenomedullary secretions suggests that the control of the adrenal medulla is at least partially distinct from that of the sympathetic vasoconstrictor and cardiac fibers, at the rostral hypothalamic level.

Adrenalectomy↗
PubMed1983

The effect of neonatal testosterone on specific male and female patterns of phosphorylated cytosolic proteins in the rat preoptic-hypothalamus, cortex and amygdala.

This study demonstrates that in the rat there are specific patterns of in vitro phosphorylation of cytosolic proteins for the preoptic-hypothalamus, cortex, and amygdala. Furthermore, there are sex-specific patterns for the male and female preoptic-hypothalamus. These sex-specific patterns are controlled by the sex steroid environment of the neonatal rat. If testosterone was removed by neonatal castration of a male, the female pattern of in vitro phosphorylated proteins was found in the adult preoptic-hypothalamus. Conversely, if a neonatal female was androgenized at 2 days by a single injection of testosterone, a male-like pattern was found in the adult preoptic-hypothalamus. Treatment of neonatal females or males did not alter the adult patterns of in vitro protein phosphorylation in the cortex, but such treatments did give rise to anomalous patterns in the amygdala. Thus, as with behavioral and structural characteristics of the preoptic-hypothalamus, the spectrum of phosphorylated proteins in this region also seems to be organized by neonatal testosterone.

Amygdala↗
PubMed1990

Presence of sex difference of cytochrome P-450 in the rat preoptic area and hypothalamus with reference to coexistence with oxytocin.

Localization of female type cytochrome P-450 (F1) in the preoptic area and hypothalamus of the rat was examined immunocytochemically using antiserum against purified hepatic P-450 (F1). This antiserum recognizes both P-450 (F1) and P-450 (M3). Western immunoblotting using the antiserum demonstrated that female rat brain contains P-450 (F1) but not P-450 (M3), since microsomes from the brain and liver displayed only one immunoreactive band at 50 kD, coinciding with that of P-450 (F1) purified from female rat liver. On the other hand, the male brain has P-450 (M3) but not P-450 (F1), as liver- and brain-derived microsomes produced single band at 49 kD, which represents a mol. wt. identical to that of P-450 (M3) extracted from male rat liver. These results indicate that P-450 (F1)-like immunoreactivity (LI) occurs in the female rat brain, while P-450 (M3)-LI takes place in the male rat brain. Immunocytochemical analysis further demonstrated the detailed cellular localization of these two P-450-LIs in the preoptic area and hypothalamus of female and male rats. Localization of P-450 (F1)-LI in the female rat hypothalamus resembled that of P-450 (M3)-LI in the male rat hypothalamus. Magnocellular neurosecretory neurons in the paraventricular nucleus and supraoptic nucleus were labeled and were found to contain oxytocin but lack vasopressin when serial sections of these areas were analyzed. In addition, groups of immunoreactive cells were seen in the median preoptic nucleus, medial and lateral preoptic area, caudal portion of the bed nucleus of the stria terminalis, lateral hypothalamus at the level of the paraventricular nucleus, periventricular zone from the preoptic area to the paraventricular nucleus, and parvocellular portion of the paraventricular nucleus.

Animals↗