Hypothalamic areas involved in prostaglandin (PG)-induced gonadotropin release. I: effects of PGE2 and PGF2alpha implants on luteinizing hormone release

Ovariectomized rats had a cannula inserted unilaterally within various hypothalamic areas. Several days later they were primed with a sc dose of 10 microng of estradiol benzoate (Eb). Two days after priming they were etherized and an initial blood sample was drawn from the external jugular vein. An inner cannula containing PGE2 or PGF2alpha at its tip was inserted into the previously implanted outer cannula. Blood samples were drawn at 20, 40, 60, and 120 min following the implantation. PGE2 induced a 4-5-fold increase in plasma LH 40 to 60 min following its implantation in the arcuate nucleus-median eminence region (ARH-ME). Levels were already significantly elevated at 20 min. When PGE2 was placed slightly more dorsally, close to the ventromedial nucleus (VMH), LH titers rose to comparable levels but only after a delay of 120 min. PGE2 implanted in the caudal portion of the ARH-ME or dorsally in the VMH-dorsomedial nuclei, barely increased plasma LH, whereas its placement in the anterior portion of the ARH-ME clearly elevated LH titers. PGE2 implants located more than 1 mm lateral from the midline or outside the hypothalamus were ineffective. When PGE2 was placed in the preoptic area (POA) or anterior ventral portion of the anterior hypothalamic area (AHA), plasma LH levels rose strikingly, the first significant increase being observed at 20 min. PGE2 implants located in the vicinity of the paraventricular nucleus-dorsal portion of AHA were much less effective. PGF2alpha implanted in the ARH-ME or POA induced a small increase in plasma LH and the implantation of empty cannulae in the same areas was ineffective. Intrapituitary implants of PGE2 failed to alter plasma LH significantly. The results indicate that PGE2 acts at the ARH-ME region to induce LH release and that an even more effective site of action seems to be located in the POA-AHA. Since these are areas which contain LHRH, the results support the view that PGs can activated LHRH-secreting neurons in these regions.     

Preoptic rather than mediobasal hypothalamic amino acid neurotransmitter release regulates GnRH secretion during the estrogen-induced LH surge in the ovariectomized rat

Inhibitory and excitatory amino acid neurotransmitters have been suggested to participate in the feedback actions of estradiol (E2) on LH secretion. In the rat estrogen-receptive neurons have been demonstrated in the preoptic/anterior hypothalamic area (POA) and mediobasal hypothalamus/median eminence (MBH) and many of these neurons utilize gamma-aminobutyric acid (GABA) as neurotransmitter. The actions of excitatory amino acids (EAA) differ in ovariectomized (ovx) and ovx E2-substituted rats indicating that EAAs also participate in the positive feedback action of E2 on LH release. However, little information is available as to whether in vivo these transmitters exert their effects in the POA, where most of the GnRH perikarya are located, or in the MBH, i.e. at the nerve terminals. Therefore we conducted push pull cannula perfusions to compare the release rates of GABA, aspartate (ASP) and glutamate (GLU) in the MBH and POA. A subcutaneous implant of a silastic tube containing E2 resulted in LH surges in the afternoon of all treated animals. Prior to and during this LH surge the MBH release rates of neither GABA nor ASP nor GLU were significantly altered. In contrast, a conspicuous drop in preoptic GABA release occurred prior to and during the time of estrogen-induced LH surges and this was accompanied by enhanced preoptic secretion of ASP and GLU. In conclusion, we present the first data about amino acid release in the MBH during the E2-induced LH surge. Since only in the POA the LH surge is associated with changes in amino acid release, it appears that both inhibitory and excitatory amino acids act at the level of the GnRH cell bodies and/or dendrites and not on GnRH nerve terminals to mediate the feedback mechanism of E2 on LH release.     

Forebrain lesions differentially affect drinking elicited by dipsogenic challenges and injections of muscimol into the median raphe nucleus.

Injections of muscimol into the median raphe nucleus (MR) elicit intense drinking in normally hydrated rats. To determine whether this response is dependent on forebrain systems mediating other aspects of water intake, the authors examined the effects of lesions of the subfornical organ (SFO), median preoptic nucleus (MnPO), lateral preoptic area (LPO), or lateral hypothalamus (LH) on the drinking. Lesions of the SFO or LH attenuated muscimol-elicited drinking, whereas lesions of the MnPO or LPO increased water intake after the treatment. All of the lesion groups showed a deficit in drinking to injections of polyethylene glycol and at least one of the doses of hypertonic saline. Only the SFO- and LH-lesioned groups showed a suppression of drinking to systemic injections of angiotensin II, suggesting that the drinking elicited by intra-MR injections of muscimol may involve changes in the central circuits mediating angiotensin-induced drinking. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Luteinizing hormone requirements for ovulation in the pentobarbital-treated proestrous rat

The LH requirements for ovulation in the pentobarbital-blocked proestrous CD rat have been studied by increasing serum gonadotropin levels through electrical stimulation of the brain and subsequently comparing the effects of timed hypophysectomy on ovulation and serum LH concentrations. The arcuate nucleus (ARC) or the medial preoptic area (POA) was stimulated unilaterally for 45 min with matched pairs of biphasic rectangular pulses through a coaxial platinum electrode. Serum LH was significantly elevated above basal values at the end of stimulation, but not in sham-stimulated controls. The results of both hormone measurement and hypophysectomy showed that the pituitary continued to release LH after extrinsic stimulation of the hypothalamus had ceased. Animals did not ovulate if they had been hypophysectomized at the end of the 45 min stimulation whereas nearly all ovulated if hypophysectomy was delayed for an additional 20 min. Some evidence suggested that the pituitary could be removed earlier without affecting ovulation if the rate of LH release was increased. The minimum peak LH concentration measured in rats that subsequently ovulated fully was 187 ng/ml, substantially lower than concentrations ordinarily attained in the spontaneous proestrous surge. When serum LH was insufficiently high to cause follicle rupture, there was nevertheless the resumption of meiosis and luteinization of the large ovarian follicles. Attempts were made to restore ovulability in animals presumed to have released a subovulatory quota of gonadotropin. Ovulation was obtained when such animals, prepared by hypophysectomy after the 45 min stimulation, had been bilaterally nephrectomized prior to stimulation. However, multiple injections of progesterone after hypophysectomy were without effect. The results are discussed in relation to variables that affect minimum requirements of LH for ovulation.     

Neuromodulation of transplanted gonadotropin-releasing hormone neurons in male and female hypogonadal mice with preoptic area brain grafts

Implantation of normal preoptic area (POA) tissue into the third ventricle of adult hypogonadal (HPG) mice provides a source of GnRH neurons that innervate the host median eminence and stimulate reproductive development in the sterile mutants. To further evaluate graft-host integration, the effects of N-methyl-D,L-aspartic acid (NMA) and opiate antagonists on LH secretion in HPG mice with POA transplants (HPG/POA) were tested. NMA challenges significantly stimulated LH secretion in 10 of 11 HPG/POA females. Only 5 of 12 HPG/POA males responded to the same treatment. Administration of the opiate antagonists naloxone or naloxone methiodide was ineffective in stimulating LH release in any mice, but opiate antagonist pretreatment significantly potentiated the LH secretory response to NMA in female, but not male, HPG/POA mice. A potential anatomical substrate for this facilitation may be the beta-endorphin-immunoreactive innervation of the POA grafts in all HPG/POA brains examined. beta-Endorphin fibers were also present in the median eminence in the vicinity of GnRH outgrowth from the grafts. However, similar innervation patterns in HPG/POA males that did not respond to opioid antagonism suggests that this is not sufficient. We tested whether the sex difference in HPG/POA responsivity to neuromodulation is related to the steroid milieu in the hosts. 17 beta-Estradiol (E2) treatment facilitated the LH secretory response of male HPG/POA to NMA challenges whether animals were castrated and given an E2 capsule prior to graft implantation or one week before testing two months after graft surgery. Intact or vehicle (sesame oil)-treated, castrated HPG/POA males rarely responded to NMA challenges, yet graft-derived GnRH innervation of the hosts' median eminence was comparable in all treatment groups. GnRH challenge testing indicated that pituitary sensitivity of the HPG/POA males was not significantly altered by E2 treatment, suggesting that estrogen acted centrally. These results indicate that the activity of grafted GnRH neurons may be modulated by endogenous opioids of host origin as well as by the hormonal milieu.     

Effect of fasting and immobilization stress on estrogen receptor immunoreactivity in the brain in ovariectomized female rats

The present study examined the effect of 48-h fasting and 1-h immobilization on estrogen receptor immunoreactivity in selected hypothalamic areas and the nucleus of the solitary tract (NTS) in ovariectomized rats. Fasting induced an increase in ER-immunoreactive cells in the paraventricular nucleus (PVN), periventricular nucleus (PeVN) and NTS compared with the unfasted control group. Similarly, immobilization caused an increase in ER-positive cells in the same areas, PVN, PeVN and NTS, versus the non-immobilized group. There was no significant increase in the number of ER-immunoreactive cells in the preoptic area (POA), arcuate nucleus (ARC) or ventromedial hypothalamic nucleus (VMH) following fasting and immobilization. Our previous work in ovariectomized rats with estrogen microimplants in the brain revealed that the PVN and A2 region of the NTS are the feedback sites of estrogen in activating the neural pathway to suppress pulsatile LH secretion during 48-h fasting. The result in the food-deprived rats suggests that estrogen modulation of the suppression of LH secretion during fasting is partly due to the increase in estrogen receptors in the PVN and A2 region. The physiological significance of the increase in neural ER following immobilization remains to be elucidated.     

A light and electron microscopic study of cytoplasmic phospholipase A2 and cyclooxygenase-2 in the hippocampus after kainate lesions

Tamoxifen, the major adjuvant drug treatment for estrogen-dependent breast cancer, has been shown previously to affect both estrogen-dependent and calcium/calmodulin-dependent pathways. In the current study, we developed an in vitro slice system to study the effects of tamoxifen on ATP levels in hypothalamic (HTH) and preoptic areas (POA) of the rat brain. Baseline data showed that, following a 2-h incubation, HTH and POA slices had comparable ATP levels to hippocampal slices, a system used extensively by researchers examining the metabolic responsiveness of the hippocampal region (HPC) of the brain. HTH-POA slice ATP levels remained steady for 2, 4 and 6 h, but fell to 11% of initial levels by 12 h. Neurons from HTH-POA slices incubated for 4 h appeared healthy and demonstrated robust protein synthesis as measured autoradiographically by incorporation of [3H]leucine. We explored the effects of tamoxifen (TAM), fluphenazine (FLU) and estradiol (E2) on ATP levels in HTH and POA slices. The effects of TAM were complex: a 4-h incubation with 10-6 M TAM led to decreased ATP levels in HTH (but not POA), and a 4-h incubation with 10-8 M led to increased ATP levels in POA (but not HTH); a 15-min exposure to 10-6 M TAM decreased ATP levels in POA (but not HTH) slices, while the exposure of slices to the lower concentration of TAM was without effect in either area. As with higher concentrations of TAM, 4-h incubation with 10-6 M FLU decreased ATP levels in HTH (but not POA), while incubation with E2 did not affect slice ATP levels. These data are consistent with the hypothesis that both TAM and FLU alter ATP levels in HTH slices via calmodulin- or calcium-mediated processes.     

Expression of Fos-like immunoreactivity in the preoptic area of maternally behaving virgin and postpartum rats.

Used Fos immunocytochemistry to show that the medial preoptic area and ventral bed nucleus of the stria terminalis are activated in maternally behaving female rats. In Exp 1, virgin female rats that showed maternal behavior toward pups had more cells in these regions that expressed Fos-like immunoreactivity than did virgin females that were not maternally responsive. In Exp 2, postpartum rats that were exposed to pups and showed maternal behavior had more Fos-labeled cells in these regions than did postpartum rats exposed to candy. Evidence also indicated that functional modifications in the medial amygdala were related to the changes in Fos expression observed in the preoptic area and ventral bed nucleus of the stria terminalis. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Role of the anterior hypothalamus–preoptic area in the regulation of courtship behavior in the male Canadian red-sided garter snake (Thamnophis sirtalis parietalis): Lesion experiments.

Lesions of the medial preoptic area and/or the ventromedial hypothalamus resulted in an abrupt and immediate decline in courtship behavior in 28 male Canadian red-sided garter snakes. Lesions of the more anterior portions of the preoptic area resulted in a more gradual, delayed decline in courtship behavior. Ss sustaining lesions dorsal, ventral, or caudal to the anterior hypothalamus–preoptic area (AH–POA) exhibited no change in courtship behavior relative to controls. Measurements of testis size, spermatogenic stage, and circulation levels of androgens revealed no differences between any of the groups. There were marked differences in the change in hematocrit over time between the groups. Results indicate that the AH–POA is involved in the control of courtship behavior in the adult male red-sided garter snake. Moreover, it is suggested that the stimulus affecting the AH–POA to activate courtship is temperature-related. (32 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The role of neuropeptide Y (NPY) in the control of LH secretion in the ewe with respect to season, NPY receptor subtype and the site of action in the hypothalamus

Neuropeptide Y1-36 (NPY1-36) acts through Y1 and Y2 receptors while the C-terminal NPY fragments NPY18-36 and N-acetyl[Leu28,31]pNPY24-36 act only through the Y2 receptor. We have investigated the effects of intracerebroventricular (i.c.v.) administration of NPY1-36, NPY18-36 and N-acetyl[Leu28,31]pNPY24-36 on LH secretion in the ovariectomised (OVX) ewe. These peptides were administered into a lateral ventricle (LV) or the third ventricle (3V) of OVX ewes during the non-breeding and breeding seasons. Microinjections of NPY were also made into the preoptic area (POA) during both seasons to investigate the effects of NPY at the level of the GnRH cell bodies. Tamed sheep were fitted with 19 gauge guide tubes into the LV, 3V or the septo-preoptic area (POA). Jugular venous blood samples were taken every 10 min for 3 h. Sheep were then given NPY1-36 (10 micrograms), NPY18-36 (100 micrograms) or saline vehicle into the LV; N-acetyl[Leu28,31]pNPY24-36 (100 micrograms), NPY1-36 (10 micrograms or 100 micrograms), NPY18-36 (10 micrograms or 100 micrograms) or saline vehicle into the 3V, or NPY1-36 (1 microgram, 5 micrograms, 10 micrograms) into the POA. Blood sampling continued for a further 3 h. LH was measured in plasma by radioimmunoassay. LV or 3V injection of 10 micrograms NPY1-36 caused a small but significant (P < 0.025) increase in the interval from the last pre-injection pulse of LH to the first post-injection LH pulse during the breeding season. Other LH pulse parameters were not significantly affected. NPY18-36 did not produce any significant change in LH pulsatility when injected into the LV, and neither peptide had any effect on plasma prolactin or GH levels. There was a significant (P < 0.01) reduction in LH pulse frequency after 3V injection of 10 micrograms and 100 micrograms NPY and 100 micrograms NPY18-36. Pulse amplitude was reduced by 3V administration of the Y2 agonist, N-acetyl[Leu28-31]pNPY24-36 and 100 micrograms NPY18-36. When the amplitude of the first post-injection LH pulse was analysed, 10 micrograms NPY also had a significant (P < 0.05) suppressive effect. During the non-breeding season, 100 micrograms NPY1-36 (but not 10 micrograms) decreased (P < 0.01) LH pulse frequency. LH pulse amplitude was significantly (P < 0.01) decreased by 100 micrograms NPY18-36. Doses of 10 micrograms NPY1-36 and 100 micrograms NPY18-36 had greater inhibitory effects on pulse frequency during the breeding season but the suppressive effect of 100 micrograms NPY was similar between seasons. Microinjections of NPY into the POA decreased (P < 0.01) average plasma LH levels during the non-breeding season at a dose of 10 micrograms but did not significantly affect pulse frequency or amplitude. We conclude that a substantial component of the inhibitory action of NPY on LH secretion in the absence of steroids is mediated by the Y2 receptor. This inhibition is probably exerted by way of a presynaptic action on GnRH terminals in the median eminence as NPY does not modulate the frequency or amplitude of LH pulses at the level of the GnRH cell bodies in the POA.     

Increased ipsilateral expression of Fos following lateral hypothalamic self-stimulation

Immunohistochemical labeling of Fos protein was used to visualize neurons activated by rewarding stimulation of the lateral hypothalamic level of the medial forebrain bundle (MFB). Following training and stabilization of performance, seven rats were allowed to self-stimulate for 1 h prior to anesthesia and perfusion. Brains were then processed for immunohistochemistry. Two control subjects were trained and tested in an identical manner except that the stimulator was disconnected during the final 1 h test. Among the structures showing a greater density of labeled neurons on the stimulated side of the brains of the experimental subjects were the septum, lateral preoptic area (LPO), medial preoptic area, bed nucleus of the stria terminalis, substantia innominata (SI), and the lateral hypothalamus (LH). Several of these structures, the LPO, SI, and LH, have been implicated in MFB self-stimulation by the results of psychophysical, electrophysiological, and lesion studies.     

Motherhood and nursing stimulate c-FOS expression in the rabbit forebrain.

Mother rabbits nurse once daily with circadian periodicity. The authors investigated brain structures involved in regulating this activity by quantifying c-FOS-immunoreactive (IR) cells in the forebrain of: (1) mothers killed on postpartum Day 1 (PPD 1) after nursing (Group 1) or not given pups (Group 2); (2) mothers killed on PPD 7 after nursing (Group 3) or not given pups on such day (Group 4); (3) unmated virgins (Group 5). Groups 1 through 4 showed similar numbers of c-FOS-IR cells in the preoptic area, an amount around three to fourfold larger than that found in virgins. Nursing increased, on PPD 1 and 7, c-FOS-IR cell number in the lateral septum and paraventricular and supraoptic nuclei. No differences were seen among Groups 1 through 5 in the suprachiasmatic nucleus. In the ventromedial hypothalamus virgins had more c-FOS-IR cells compared with Groups 1 and 2. Results suggest that specific forebrain structures participate in regulating particular aspects of rabbit maternal behavior: the POA and LS seem associated with the establishment of motherhood and the magnocellular nuclei with the occurrence of milk letdown. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Hypothalamic sites of action for testosterone, dihydrotestosterone, and estrogen in the regulation of luteinizing hormone secretion in male sheep

Testosterone (T) inhibits LH secretion partly by acting at unknown sites within the brain to inhibit GnRH secretion. We tested the hypothesis that the preoptic area (POA) and arcuate-ventromedial region (ARC/VMR), areas rich in androgen and estrogen (E) receptors, are neural sites at which T and the T metabolites, dihydrotestosterone (DHT) and estrogen (E), act to suppress LH secretion. Bilateral guide cannulae were surgically implanted into either the POA or ARC/VMR of castrated male sheep. Experiments were conducted under a long day photoperiod to maximize the inhibitory effect of the steroids. In Exp 1, all sheep (n = 6/site) sequentially received bilateral implants of cholesterol (CHOL), T, or E at each site. Jugular blood samples were taken at 10-min intervals for 4 h both immediately before implant insertion and 5 days later. In Exp 2, all sheep (n = 6/site) sequentially received bilateral implants of CHOL, DHT, or E at each site according to a latin square design. Blood samples were taken before and 7 days after implant insertion. In Exp 3, which followed the same design as Exp 2, implants of E, T, or DHT were placed only in the ARC/VMR. In the final experiment, the effects of T and CHOL implants in the ARC/VMR were compared. Neither T, DHT, nor CHOL implants at either site affected LH secretion. In contrast, E treatment in the ARC/VMR suppressed mean plasma LH levels (P < 0.01), primarily due to an increase in interpulse interval (P < 0.01). Estrogen implants in the POA caused a small, but nonsignificant (P > 0.05), decrease in mean LH levels in the first experiment and an increase in LH interpulse interval (P < 0.05) in the second experiment. These results suggest that the ARC/VMR and possibly the POA are sites at which E acts to reduce GnRH secretion in male sheep.     

Morphine amplifies norepinephrine (NE)-induced LH release but blocks NE-stimulated increases in LHRH mRNA levels: comparison of responses obtained in ovariectomized, estrogen-treated normal and androgen-sterilized rats

In these studies we examined the temporal effects of intracerebroventricular (i.c.v.) infusions of norepinephrine (NE) on plasma LH and on LHRH mRNA levels in the organum vasculosum of the lamina terminalis (OVLT) and in neurons located in the rostral (r), middle (m) and caudal (c) preoptic areas (POA) of ovariectomized, estrogen-treated rats. Thereafter, we compared these responses to those which occur in androgen-sterilized rats (ASR). NE infusions not only increased plasma LH concentrations but within 1 h after NE, LHRH mRNA levels also were increased significantly in the OVLT and rPOA but not in the mPOA or cPOA. By 4 h, these message levels still were elevated in the OVLT and rPOA and they now also were significantly higher than control values in the mPOA and cPOA. While NE also increased LH secretion in ASR, the plasma LH concentrations obtained were markedly blunted compared to control values. Moreover, NE infusions did not alter single cell levels of LHRH mRNA in any region of the rostral hypothalamus. Previously, we have reported that morphine (s.c.) markedly amplifies NE-induced LH release and questioned whether these responses are accompanied by concomitant augmented increases in LHRH mRNA levels. Morphine alone did not affect basal LHRH mRNA or plasma LH levels. However, when rats were pretreated with morphine (-15 min) and NE was infused i.c.v. at 0 time, significant amplification of LH release occurred but, unexpectedly, morphine completely blocked NE-induced increases in LHRH mRNA levels in all of the neurons we examined. Morphine also amplified LH release in ASR but these responses were significantly less than those obtained in control rats.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cytochrome Oxidase Activity in the Preoptic Area Correlates With Differences in Sexual Behavior of Intact and Castrated Male Leopard Geckos (Eublepharis macularius).

Although the utility of analyzing behavioral experience effects on neural cytochrome oxidase (CO) activity is well recognized, the behavioral correlates of endogenous differences in CO activity have rarely been explored. In male leopard geckos (Eublepharis macularius), the incubation temperature experienced during embryogenesis (IncT) and age affect CO activity in the preoptic area (POA), an area that modulates copulatory behavior. In this study, the authors assessed whether differences in POA CO activity correlate with differences in sexual behavior in intact and castrated geckos. Males with IncT- and age-dependent increases in POA CO activity mounted females with shorter latencies while intact and after castration and ejaculated more frequently after castration. The authors discuss the predictive value of CO activity and propose similar parallels in other species. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Dorsolateral connections of the medial preoptic area and maternal behavior in rats.

The lateral connections of the medial preoptic area (MPOA) are essential for maternal behavior in rats. The purpose of this study was to more exactly specify the nature of this pathway. Exp 1 found that knife cuts that severed the dorsolateral connections of the MPOA were as effective as complete cuts in disrupting maternal behavior, whereas knife cuts that severed the ventrolateral MPOA connections were ineffective. These results suggest that MPOA efferents and afferents critical for maternal behavior leave or enter the MPOA dorsolaterally. Exp 2 located possible sources of critical afferent input. Lactating rats received MPOA lateral cuts with a horseradish peroxidase (HRP)-coated wire knife. Full lateral cuts and dorsolateral cuts disrupted maternal behavior and labeled more cells with HRP in the nucleus of the solitary tract and the locus coeruleus than did ventrolateral cuts, which did not disrupt maternal behavior. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Co-infusion with a TrkB-Fc receptor body carrier enhances BDNF distribution in the adult rat brain

Intraspecific confrontation between male rats represents a biologically relevant form of social stress. C-fos expression has been used to map the pattern of neural activation following either a single (acute) or repeated (10 times) exposure of an intruder male to a larger male in the latter's home cage. These conditions induce high levels of aggressive interaction. Sixty minutes after a single defeat, there was intense c-fos expression (quantified using image analysis) in restricted areas of the basal forebrain (including lateral septum, bed nucleus of stria terminalis, lateral preoptic area, lateral hypothalamic area, paraventricular nucleus, and medial and central amygdala) as well as in the autonomic and monoaminergic nuclei of the brainstem (central grey, dorsal and median raphe, locus coeruleus and nucleus of the solitary tract). After the tenth defeat, this pattern was modified despite persistently high levels of aggression. Some areas in the forebrain (bed nucleus of stria terminalis, paraventricular nucleus and medial amygdala) continued to express increased c-fos; others (the septum, lateral hypothalamic area, lateral preoptic area and central amygdala) no longer expressed c-fos. The brainstem response was equally varied: the central grey and the raphe nuclei continued to respond after repeated defeat, whereas the solitary nucleus and locus coeruleus did not. On the other hand, there was no change in the behaviour of intruder rats after repeated defeat. This study shows the pattern of adaptation at a cellular level in the basal forebrain and brainstem to repeated defeat. As in our previous studies of repeated restraint, modulation in the expression of c-fos following repeated stress is highly regionally specific, suggesting that differential neural processing is involved in adaptation to social stress.     

Progesterone and 3α-androstanediol conjugated to bovine serum albumin affects estrous behavior when applied to the MBH and POA.

Ovariectomized rats with cannula over the medial basal hypothalamus (MBH) received implants of 3α-diol conjugated to bovine serum albumin (BSA; 3α-diol:BSA), free 3α-diol diluted with BSA (3α-diol&BSA), progesterone (PRE) conjugated to BSA (PRE:BSA), free PRE diluted with BSA (PRE&BSA), or BSA alone. 3α-diol:BSA or 3α-diol&BSA facilitated receptivity within 90 min. Other estradiol-treated rats received steroid implants in the preoptic area (POA); those receiving PRE:BSA or PRE&BSA showed significant elevations in lordosis in 5 min. When systemic PRE was given, 3α-diol:BSA and 3α-diol&BSA applied to the MBH or POA inhibited receptivity. When 3α-diol was given systemically, 3α-diol:BSA implants to the MBH and POA produced facilitatory effects. These data suggest 3α-diol can act at the membrane and that these effects are influenced by circulating steroids; yet membrane-mediated actions do not account for all of PRE-facilitated sexual behavior in the MBH and POA. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Functional mapping of neural sites mediating prolactin-induced hyperphagia in doves

Microinjections of prolactin (PRL) into the ventromedial nucleus of the hypothalamus (VMN) or the preoptic area (POA) have been previously shown to increase food intake and body weight in ring doves. In an attempt to corroborate these results and to provide a more complete map of PRL-sensitive brain sites mediating the orexigenic action of PRL, a microinjection procedure was employed in the present study that delivered PRL or saline vehicle in extremely small volumes (10 nl/injection) to a variety of diencephalic sites in dove brain that had been previously demonstrated to contain high concentrations of PRL receptors. Estimates obtained from one female subject given a single 10 nl injection of [125I]ovine PRL into the VMN supported the claim that such injection volumes resulted in limited diffusion, as 80% of the tissue radioactivity was found within a 280 mm area surrounding the injection site at 30 min after injection. Food intake of cannulated male doves in the mapping study was monitored daily during a 6 day baseline period, an initial 4 day treatment period, a 6-12 day post-treatment recovery period, and a second 4 day treatment period. Approximately half of the birds received PRL injections (50 ng/10 nl twice daily) and saine vehicle injections (10 nl twice daily) during the first and second treatment periods, respectively, while remaining birds received these treatments in the reverse order. No significant changes in food intake across baseline, vehicle, post-treatment, or PRL treatment periods were observed in birds with injection sites in the lateral POA, paraventricular nucleus of the hypothalamus (PVN), or the medial-basal hypothalamic region between the tuberal hypothalamus (TU) and VMN. In contrast, injections of PRL into the VMN area, medial POA, or TU resulted in average daily food intake values that significantly exceeded those recorded during other periods. The most robust feeding response was seen in the VMN group, where PRL injections resulted in a 58% increase in food intake over that recorded during injection of vehicle. This increase was significantly greater than that observed following PRL injections into the mPOA (26%) or the TU (32%). These findings suggest that the VMN may be a primary site of PRL action in promoting hyperphagia in this species, although PRL effects at other diencephalic loci, such as the mPOA and TU, may also contribute to the orexigenic action of this hormone.