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PubMed1980

Sex steroids and the development of the newborn mouse hypothalamus and preoptic area in vitro. II. Morphological correlates and hormonal specificity.

In studies designed to elucidate morphogenetic mechanisms involved in the neurogenesis of sexual differentiation of the brain, estradiol or testosterone was added to organotypic cultures of the newborn mouse hypothalamus and preoptic area. Both gonadal hormones selectively accelerated and enhanced neuritic proliferation in specific regions of the preoptic area and infundibular/premamillary levels. This regional localization suggests specific induction of neuritic branching perhaps only in those neurons shown by autoradiography to contain the steroid receptor. The significance of estradiol per se is emphasized by the reduction and retardation of neuritic outgrowth in those same regions following exposure to steroid-deficient medium or blockade of the nuclear receptor (CI-628) and by the failure of testosterone alone to induce a significant response. The importance of aromatization of androgen to estradiol is supported by the failure of non-aromatizable 5 alpha-dihydrotestosterone to elicit an effect even in the presence of estradiol. This apparent hormonal specificity suggests that the neuritic response may be a component of sexual differentitation and that the trophic effects of estradiol may influence significantly the ontogeny of target neural circuits in the brain of both genders.

Animals↗
PubMed2005

GABA receptor agonists in the medial preoptic area and maternal behavior in lactating rats.

We studied the effects of injecting agonists of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) muscimol (GABA-A receptor agonist) and baclofen (GABA-B receptor agonist) in the medial preoptic area (MPOA) and neighboring brain regions, the bed nucleus of the stria terminalis (BNST), and lateral preoptic area (LPO) on maternal behavior. Lactating female rats were implanted with bilateral cannulae in the MPOA/BNST on day 1 postpartum. On day 5, a maternal behavior test was conducted in the home cage after females received injections of muscimol or baclofen (0, 12.5, 50 or 200 ng per side). On day 7, after MPOA/BNST injections, a second maternal behavior test was conducted with pups placed at the end of a T-runway projecting from the home cage. Finally, after injections on day 9 maternal aggression, olfaction, and locomotor behavior were tested. The GABA receptor agonists injected in the MPOA/BNST produced dose-dependent deficits in all components of maternal behavior, including maternal aggression, except licking. Muscimol produced deficits in the active component, nest building at lower doses than baclofen, both agonists produced deficits in retrieving, while baclofen produced deficits in passive components (hovering and crouching over pups) at lower doses than muscimol. Both GABA receptor agonists increased locomotor activity and reduced olfactory responsiveness but these were only correlated with deficits in retrieving and crouching in baclofen-treated females.

Analysis of Variance↗
PubMed1995

Differential cellular localization of oestrogen receptor immunoreactivity and oxytocin mRNA and immunoreactivity in the rat preoptic area.

Oestrogen influences both oxytocin mRNA and peptide immunoreactivity in the preoptic area and the rat oxytocin gene contains functional oestrogen response elements. However, using combinations of immunocytochemistry and in situ hybridization for oxytocin and oestrogen receptor, we found that preoptic oxytocin neurons do not possess oestrogen receptors. This finding implies oestrogen actions on oxytocin synthesis in preoptic neurones are unlikely to be mediated directly.

Animals↗
PubMed1995

Gonadal steroid hormone-dependence of beta-endorphin-like immunoreactivity in the medial preoptic area of the rat.

Gonadal steroid hormones are known to alter the expression of proopiomelanocortin (POMC) mRNA in neurons of the arcuate nucleus (ARC). These neurons send projections to the medial preoptic area (MPOA), wherein mu-opiate receptor density is cyclical and gonadal steroid hormone-dependent. Although beta-endorphin-(beta-Endo) content in the MPOA is known to vary across the estrous cycle, the effect of gonadal hormones on the distribution and density of beta-Endo-like immunoreactive (IR) fiber density in the preoptic area is unknown. In the present study, immunohistochemical staining was used to investigate the effects of gonadal steroid hormone treatment on beta-Endo-like IR fibers in the MPOA of ovariectomized (OVX) female rats. The density of beta-Endo-like IR fibers was low in the MPOA of OVX rats, but increased slightly following treatment with 17 beta-estradiol (E2) or 3 h after subsequent progesterone (P) injection. However, beta-Endo-like IR fiber density increased significantly 27 h after E2P treatment, and remained elevated 51 h after E2P treatment in the periventricular zone and in the medial portion of the medial preoptic nucleus, although the general distribution of fibers was unchanged. These results suggest that the density of MPOA beta-Endo innervation is normally gonadal steroid hormone-dependent and that the medial MPOA contains greater opioid tone than the lateral MPOA regardless of the hormonal state. Furthermore, since beta-Endo-like IR fiber density remained elevated even though gonadal hormone levels decreased, additional factors might modulate the release or turnover of beta-Endo in the MPOA during normal estrous cycling.

Animals↗
PubMed1988

Catecholaminergic innervation of luteinizing hormone-releasing hormone and glutamic acid decarboxylase immunopositive neurons in the rat medial preoptic area. An electron-microscopic double immunostaining and degeneration study.

Catecholaminergic innervation of luteinizing hormone-releasing hormone (LHRH) and glutamic acid decarboxylase (GAD) immunoreactive neurons in the rat medial preoptic area (MPO) was studied using electron-microscopic (EM) double-label immunostaining and combinations of single- and double-label immunostaining with acute axonal degeneration. The EM double-immunostaining experiments included double staining for either tyrosine hydroxylase (TH) and LHRH, or TH and GAD. Analysis of TH and LHRH double-immunostained material revealed synaptic connections between TH immunoreactive axons and LHRH immunopositive neurons. The TH and GAD double-staining experiments also demonstrated synaptic connections between axons immunoreactive for TH and GAD immunopositive neurons. Two days following unilateral surgical transection of the ventral and dorsal noradrenergic bundles, synaptic connections were found between degenerated boutons and GAD immunoreactive neurons in the ipsilateral MPO. However, no synapses could be observed in the same area between degenerated axons and the LHRH immunopositive neurons. Following the same operation and immunostaining for TH, a moderate number of degenerating TH axons as well as a large number of nondegenerated TH immunoreactive boutons were observed. Double immunostaining for TH and GAD in MPO sections ipsilateral to the operation revealed synaptic connections between the degenerating TH immunopositive axons and GAD immunoreactive neurons. These results suggest that there are direct synaptic connections between catecholaminergic axons and GAD and LHRH immunoreactive neurons in the medial preoptic area of the rat. Some of the connections between TH immunopositive afferents and GAD immunoreactive neurons may represent connections from noradrenergic neurons in the brain stem, while the majority of TH-GAD and TH-LHRH connections may represent innervation of GABA and LHRH neurons from local dopamine-containing cells.

Adrenergic Fibers↗
PubMed2004

Regulation of galanin receptor GalR1 mRNA expression by ovarian steroids in oestrogen receptor alpha-immunoreactive neurones: identification of distinct populations of neurones in the preoptic area.

This study examined whether gonadal steroids are involved in regulating galanin receptor 1 (GalR1) mRNA expression in neurones that contain oestrogen receptor alpha (ERalpha), in three regions of the preoptic area (POA) known to be involved in the control of gonadotropin secretion. Double-labelling immunohistochemistry using an antibody against the ERalpha and in situ hybridization experiments using a 35S-labelled riboprobe specific for GalR1 mRNAs revealed that ERalpha is expressed in a large proportion of GalR1 mRNA-expressing neurones of the POA in the ovariectomized (OVX) female rat. Oestradiol (E2) and oestradiol plus progesterone (E2 + P) treatments of OVX rats significantly decreased the proportion of GalR1 mRNA/ERalpha immunoreactive (ERalpha-IR) neurones in the anteroventral periventricular nucleus (AVPV), medial preoptic nucleus (MPN) and medial preoptic area (MPO). The expression of GalR1 mRNA in ERalpha-IR neurones varied according the hormonal status of the female animals. In the AVPV, during the oestrous cycle, the hybridization signal significantly increased at oestrus. E2 and E2 + P treatments of OVX rats did not induced significant variation of levels of GalR1 mRNAs in ERalpha-IR neurones. In the MPN, E2 treatment of OVX rats resulted in significant increase in GalR1 mRNA expression in ERalpha-IR neurones. Similarly, levels of the GalR1 hybridization signal increased during afternoon of proestrus and oestrus. In the MPO, treatment of OVX rats with E2 + P significantly decreased GalR1 mRNA expression in ERalpha-IR neurones. The expression of GalR1 mRNA did not change during the oestrous cycle in this area. These findings suggest that the hypothalamic action of galanin on gonadotopin-releasing hormone (GnRH) secretion may pass through the specific population of GalR1/ERalpha-IR neurones of the MPN in mediating the oestrogen action on the GnRH system at the moment of the luteinizing hormone surge.

Animals↗
PubMed2001

Electrophysiological analysis of suprachiasmatic nucleus projections to the ventrolateral preoptic area in the rat.

The circadian pacemaker housed in the suprachiasmatic nucleus (SCN) synchronizes daily sleep-wake cycles, presumably by modulating the sleep-wake regulatory system, including ventrolateral preoptic area (VLPO) neurons. We used whole-cell patch-clamp recording to study the projections from the SCN to the VLPO in horizontal slices of rat hypothalamus. Single-pulse stimulation of the SCN region elicited postsynaptic currents (PSCs) in 20 of 66 neurons (30%) recorded within the VLPO region as verified by intracellular biocytin labelling. At a holding potential of -60 mV, the evoked PSCs had an amplitude of 17.6 +/- 3.2 pA (SEM) and a latency of 6.3 +/- 0.5 ms (n = 10). There was a trend for simple excitatory postsynaptic currents (EPSCs) to be evoked in the VLPO cluster, simple inhibitory postsynaptic currents (IPSCs) in the extended VLPO, and a combination of EPSCs and IPSCs in both regions. IPSCs were blocked reversibly by bicuculline (10 microm, n = 11). In both the presence and absence of bicuculline, EPSCs had fast and slow components that were blocked by 6,7-dinitroquinoxaline-2,3-dione (DNQX; 10 microm; n = 7), and (+/-)3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP; 10 microm, n = 6), respectively. Reversal potentials for the evoked IPSCs and EPSCs were consistent with mediation via GABAA and ionotropic glutamate receptors, respectively. These results suggest that the SCN region provides both inhibitory and excitatory inputs to single VLPO neurons, which are mediated, respectively, by GABAA receptors and by both non-NMDA and NMDA glutamate receptors. These projections may play important roles in conveying circadian input to systems in the preoptic area that regulate sleep and waking.

Animals↗
PubMed1992

Immunocytochemical characterization of afferents to estrogen receptor-containing neurons in the medial preoptic area of the rat.

Double-label immunocytochemistry has been employed to elucidate the chemical nature of the afferent neuronal projections to the estrogen receptor-containing neurons located in the medial preoptic area of the rat brain. To ensure a clear separation of the immunolabelled afferent profiles from the estrogen receptors, the former were visualized first and the diaminobenzidine reaction product was silver-gold intensified. Using a monoclonal antibody raised against purified human estrogen receptors, we observed an intense nuclear immunoreactivity in Vibratome, semithin and ultrathin sections. Neuropeptide-Y, serotonin-, phenylethanolamine N-methyltransferase- and adrenocorticotrophin-immunoreactive axons and varicosities were observed in close apposition to the estrogen receptor-positive cells. At the ultrastructural level, neuropeptide-Y-immunoreactive boutons were seen in synaptic contact with cells showing estrogen receptor immunoreactivity in their nucleus. These results indicate that neurons located in the medial preoptic area, one of the principal sites for the control of female reproductive function, may be influenced by both estrogen and neurotransmitters/neuropeptides via, respectively, nuclear receptors and synaptic contacts.

Adrenocorticotropic Hormone↗
PubMed1994

Estrogen affects calcitonin gene-related peptide- and methionine-enkephalin-immunoreactive neuron in the female rat preoptic area.

The effects of estrogen on the neurons of the medial preoptic area of the ovariectomized rat were immunohistochemically investigated using antisera to calcitonin gene-related peptide (CGRP) and methionine-enkephalin (Met-Enk). To visualize CGRP- and Met-Enk-immunoreactive (IR) cell somata, colchicine was injected into the cerebroventricle. CGRP- and Met-Enk-IR neurons were distributed in the medial preoptic nucleus (MPN) but few in the periventricular preoptic nucleus (PPN) in the ovariectomized rat. After estrogen treatment, CGRP immunoreactivity was markedly increased in the PPN and MPN, whereas Met-Enk immunoreactivity was increased in the MPN. These results, along with our previous data, suggest that estrogen accelerates CGRP- and Met-Enk expression in a different manner in the PPN and MPN neurons.

Animals↗
PubMed1997

Preoptic area infusions of morphine disrupt--and naloxone restores--parental-like behavior in juvenile rats.

As in the adult lactating female, opioids disrupt (and naloxone restores), parental behavior in juvenile rats (approximately 25 days of age). Because the preoptic area regulates the display of parental behavior in lactating females, we examined its parental behavior role in the juvenile rat. At 21 days of age, juvenile rats were implanted with bilateral cannulae aimed at the preoptic area using a modified Kopf stereotaxic and extrapolating from a developing-rat brain atlas [58], and divided into two groups: Initiation and maintenance. On day 25, the initiation group received bilateral infusions of either morphine (0.50 microgram), saline (0.25 microliter), or morphine plus naloxone (0.25 microgram). Thirty minutes later, they were exposed to three 1-6-day-old pups; the maintenance group was exposed to pups until they displayed 2 consecutive days of parental behavior, then infused. Morphine disrupted parental behavior in both the initiation and Maintenance groups, and naloxone restored the behavior to control/ saline levels. Parental behavior in the juvenile animal of both sexes, therefore, is under opioid regulation that parallels the adult female.

Animals↗
PubMed1990

Immunohistochemical localization of cholecystokinin in the medial preoptic area and anterior hypothalamus of the Brazilian gray short-tailed opossum: a sex difference.

We have studied the anatomical localization of cholecystokinin-like immunoreactivity (CCK IR) in somata and fibers in the medial preoptic area (MPA) and anterior hypothalamus (AH) of the Brazilian gray short-tailed opossum, (Monodelphis domestica). With the aid of an avidin-biotin, nickel-enhanced, immunohistochemical technique, CCK IR neuronal elements were found within the MPA and AH. A large number of CCK IR cell bodies were located in the MPA of colchicine-treated opossums. The MPA also contained a CCK IR fiber plexus. Quantitative image analysis revealed that the periventricular preoptic area of noncolchicine-treated male opossums had a significantly higher percent of blocked light measurements than that of the noncolchicine-treated females, indicating a higher density of CCK IR neuronal elements in the males. Neuronal fibers and somata containing CCK IR were also found within the periventricular hypothalamic nucleus (Pe), and the suprachiasmatic nucleus (SCh). These results show that CCK IR neuronal elements are found within the MPA and AH of the Brazilian short-tailed opossum. Furthermore, there is a sexually dimorphic distribution of CCK IR elements within the MPA of this small marsupial.

Animals↗
PubMed1983

Enhanced prolactin release by injection of glycine in the medial preoptic area (mPOA) of the rat.

Injection of glycine into the medial preoptic area (mPOA) in doses of 12.5, 25 and 50 micrograms produced a marked increase in prolactin release in freely-moving male rats. Neither taurine nor beta-alanine had effect on prolactin. These amino acids were unable to modify the resting plasma LH levels. The present studies show that the mPOA is a target site for the prolactin releasing action of glycine. Furthermore, they suggest a participation of this amino acid in the mPOA mechanism for control of prolactin secretion in the rat.

Animals↗
PubMed2001

Sexually dimorphic effects of testosterone on preoptic area calcitonin gene-related peptide mRNA expression depend upon neuron location and differential estrogen and androgen receptor activation.

Experiments examined activational roles of gonadal steroids on the sexually dimorphic, calcitonin gene-related peptide-expressing neurons of the rat preoptic area. Gonadectomy of male rats followed by treatment with testosterone, dihydrotestosterone, or estrogen demonstrated that the tonic suppressive influence of testosterone on cellular levels of calcitonin gene-related peptide mRNA expression in the medial preoptic nucleus and anteroventral periventricular nucleus occurred through either ER- or AR-mediated mechanisms (P < 0.05). The gonadectomy of adult female rats demonstrated little tonic influence of ovarian steroids upon calcitonin gene-related peptide mRNA levels. However, the administration of male levels of testosterone to ovariectomized rats resulted in reduced calcitonin gene-related peptide mRNA expression within the medial preoptic nucleus (P < 0.05) and, strikingly, a 3-fold induction in calcitonin gene-related peptide mRNA expression in the anteroventral periventricular nucleus (P < 0.01). Testosterone's effects in the medial preoptic nucleus and anteroventral periventricular nucleus of the female required both ER and AR activation. Dual labeling immunocytochemical studies revealed that less than 10% of calcitonin gene-related peptide neurons in the male expressed ARs compared with approximately 50% in the female. These investigations reveal that sexually differentiated region- and steroid receptor-specific mechanisms function in association with the sex differences in circulating gonadal steroids to maintain the sexually dimorphic nature of calcitonin gene-related peptide expression in the preoptic area of the adult rat.

Animals↗
PubMed2005

Dopamine d1 and d2 receptor antagonism in the preoptic area produces different effects on maternal behavior in lactating rats.

The preoptic area (POA) is critical for maternal behavior in rats but little is known about what neurotransmitters released here influence maternal responding. POA infusion of 10 microg (but not 2 microg) of the dopamine D1 receptor antagonist SCH-23390 greatly impaired retrieval and licking of pups but not other maternal or nonmaternal behaviors in lactating rats. In contrast, POA infusion of 10 microg (but not 2 microg) of the D2 receptor antagonist raclopride facilitated nursing but did not affect oral maternal behaviors. SCH-23390 in the medial hypothalamus tended to impair licking but not retrieval. Raclopride in the medial hypothalamus had no effects. Therefore, D1 and D2 receptor activity, particularly in the POA, is important for regulating different maternal behaviors.

Analysis of Variance↗
PubMed1982

Acute thermoregulatory effects of unilateral electrolytic lesions of the medial and lateral preoptic area in rats.

Unilateral anodal lesions of the medial or lateral preoptic area (POA) in unanesthetized rats had opposite thermoregulatory effects immediately after the lesion were made. Lesions of the medial POA evoked hyperthermias and accompanying cold defense responses, including vasoconstriction of the tail, increased oxygen consumption, shivering, and heat conservation postures. The hyperthermias had latencies of 0-30 minutes and reached maximum values within 120 minutes postlesion. They were independent of ambient temperature and dissociable from the hyperactivity often seen after such lesions. Damage to the lateroventral POA elicited acute falls in body temperature, as well as vasodilation of the tail, decreased oxygen consumption, inhibition of shivering in cool environments, and prone body extension. Unilateral cathodal lesions throughout the POA yielded only hyperthermia. These results suggest a possible anatomical segregation of heat and cold defense functions within the anterior basal forebrain.

Animals↗
PubMed1998

Castration decreases extracellular, but increases intracellular, dopamine in medial preoptic area of male rats.

Dopamine (DA) is released in the medial preoptic area (MPOA) of male rats in the presence of a female, and it facilities male sexual behavior. Castration blocks the DA response to a female and the male's ability to copulate. The present experiments examined the effects of castration on (1) basal levels of extracellular DA in the MPOA, using the no net flux microdialysis technique, (2) the response of extracellular DA to amphetamine, and (3) tissue levels of DA. Castrated rats had lower basal levels of extracellular DA in the MPOA, compared with gonadally intact rats; in vivo recovery, a measure of uptake, was not different. This suggests that castration decreases DA release in basal conditions, as well as in response to a female. However, systemic amphetamine injections, which induce DA release, resulted in greater DA release in castrates. Finally, tissue levels of DA were higher in the MPOA, the caudate-putamen and the bed nucleus of stria terminalis of castrates. These data suggest that DA synthesis and storage in the MPOA are normal, or even enhanced, in castrates, and uptake is not altered. The deficit in extracellular levels appears to be related to release, perhaps due to decreased nitric oxide.

Amphetamine↗
PubMed1986

Ultrastructure of gonadotropin-releasing hormone neuronal structures derived from normal fetal preoptic area and transplanted into hypogonadal mutant (hpg) mice.

The hpg mutant mouse lacks the neurohormone gonadotropin-releasing hormone (GnRH) and hence has a reproductive deficit. This deficit can be corrected by placement of normal fetal preoptic area into the third ventricle (see Krieger et al., 1985). We have now used ultrastructural immunocytochemistry to investigate the morphology of GnRH neurons in such intraventricular grafts, the routes that their axons take as they exit into the host, and the neurosecretory terminations that they make in the host median eminence. The GnRH cells in the transplant were similar in morphology to that reported for such cells in the preoptic area of other rodents. There was a large central nucleus, frequently indented and containing 1 or 2 nucleoli. The thin rim of cytoplasm was filled with rough endoplasmic reticulum, Golgi stacks, and mitochondria. Both dendritic and axonal profiles were identified, and a modest synaptic input to the former was found. Between the host and the implant a complex multilayered ependymal zone developed, and it was through this region that GnRH axons exited into the host arcuate nucleus and median eminence, usually surrounded by ependymal or glial elements. Within the median eminence, GnRH terminals were in close association with fenestrated blood vessels forming a normal neurosecretory terminus.

Animals↗
PubMed2004

Nicotinic enhancement of the noradrenergic inhibition of sleep-promoting neurons in the ventrolateral preoptic area.

According to multiple lines of evidence, neurons in the ventrolateral preoptic area (VLPO) that contain GABA promote sleep by inhibiting neurons of the arousal systems. Reciprocally, transmitters used by these systems, including acetylcholine (ACh) and noradrenaline (NA), exert an inhibitory action on the VLPO neurons. Because nicotine, an agonist of ACh, acts as a potent stimulant, we queried whether it might participate in the cholinergic inhibition of these sleep-promoting cells. Indeed, we found that ACh inhibits the VLPO neurons through a nicotinic, as well as a muscarinic, action. As evident in the presence of atropine, the non-muscarinic component was mimicked by epibatidine, a nonselective nicotinic ACh receptor (nAChR) agonist and was blocked by dihydro-beta-erythroidine, a nonselective nAChR antagonist. It was not, however, blocked by methyllycaconitine, a selective antagonist of the alpha7 subtype, indicating that the action was mediated by non-alpha7 nAChRs. The nicotinic inhibition was attributed to a presynaptic facilitation of NA release because it persisted in the presence of tetrodotoxin and was blocked by yohimbine and RS 79948, which are both selective antagonists of alpha2 adrenergic receptors. Sleep-promoting VLPO neurons are thus dually inhibited by ACh through a muscarinic postsynaptic action and a nicotinic presynaptic action on noradrenergic terminals. Such dual complementary actions allow ACh and nicotine to enhance wakefulness by inhibiting sleep-promoting systems while facilitating other wake-promoting systems.

Acetylcholine↗