Comparison of the effects of ether and restraint stress on the activity of tuberoinfundibular dopaminergic neurons in female and male rats

The purpose of the present study was to characterize the acute inhibitory effects of restraint stress on the activity of tuberoinfundibular dopamine (DA) neurons as estimated by measuring concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence. The time course of the effects of two types of physical restraint (immobilization in the supine position or confinement in an acrylic cylindrical tube) was determined in unanesthetized and diethylether (ether)-exposed female and male rats. The combination of brief (2 min) exposure to ether followed by 10 and 20 min of supine restraint increased concentrations of prolactin in plasma and decreased DOPAC concentrations in median eminence of both female and male rats. Thirty minutes of supine restraint decreased DOPAC concentrations in the median eminence of female rats that were not exposed to ether, and brief exposure to ether enhanced this effect. By contrast, 30 min of supine restraint failed to alter DOPAC concentrations in the median eminence in either unanesthetized or ether-exposed male rats. Tube restraint in the absence of ether failed to alter DOPAC concentrations in the median eminence of either female or male rats; but in female rats preexposed to ether, 30 min of tube restraint decreased DOPAC concentrations in the median eminence. On the other hand, in the absence of physical restraint, 2 min ether exposure caused a transient increase in prolactin secretion and a concurrent decrease of DOPAC concentrations in median eminence of both female and male rats.(ABSTRACT TRUNCATED AT 250 WORDS)     

Restraint stress decreases the neurosecretory activity of tuberoinfundibular dopaminergic neurons in young but not in aged female rats

The regulation of prolactin secretion by tuberoinfundibular dopamine (DA) neurons appears to be altered in the aged rat: the concentration of prolactin in the serum increases and the activity of the tuberoinfundibular DA neurons decreases. In the young female rat a brief period of stress reduces the tuberoinfundibular DA neurosecretory activity and increases the secretion of prolactin. The purpose of the present study was to determine if the responsiveness of tuberoinfundibular DA neurons to restraint stress is altered in the aged female rat. The activity of these neurons was estimated from the rate of DA synthesis in their terminals in the median eminence, as measured by the rate of accumulation of dihydroxyphenylalanine (DOPA) after the administration of a decarboxylase inhibitor. Thirty minutes of restraint stress increased serum prolactin concentrations in both young (3 months) and aged (26 months) constant estrous rats, but reduced the rate of DOPA accumulation in the median eminence of only the young rats. Restraint also decreased the rate of DOPA accumulation in the median eminence of intermediate-aged rats (14 months) independently of whether the rats were exhibiting normal ovarian cycles (measured on the day of estrus) or were in a constant estrus. This suggests that the loss of ovarian cyclicity per se is not associated with the age-related change in the response of tuberoinfundibular DA neurons to restraint stress.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute restraint stress decreases dopamine synthesis and turnover in the median eminence: a model for the study of the inhibitory neuronal influences on tuberoinfundibular dopaminergic neurons

The effects of acute stress on serum prolactin concentrations and tuberoinfundibular dopaminergic (TIDA) neuronal activity were studied in female rats. TIDA neuronal activity was estimated by measuring the rate of dihydroxyphenylalanine (DOPA) accumulation after the administration of a decarboxylase inhibitor (NSD 1015) and the rate of decline of dopamine (DA) after the administration of a tyrosine hydroxylase inhibitor (alpha-methyltyrosine) in the median eminence. Serum prolactin concentrations were increased following 30 min of supine immobilization (restraint stress), but returned to control levels by 2, 8, and 16 h after the onset of this stress. The rate of DOPA accumulation was decreased during the 30 min of restraint; it was still further reduced 2 h later but had returned to control levels 8 and 16 h later. No change in the rate of DOPA accumulation was observed in the striatum or neurointermediate lobe of the pituitary at any time after the start of restraint. Restraint stress also decreased the rate of DA turnover in the median eminence, but was without effect on the rates of DA turnover in the striatum or neurointermediate lobe. These results suggest that restraint stress activates an inhibitory neuronal pathway which decreases the activity of TIDA neurons and may be responsible, at least in part, for the increase in serum prolactin concentrations. The responsiveness of TIDA neurons to the stress-induced decrease in activity was not influenced by the time of day or the stage of the estrous cycle. Not all stressful manipulations decreased TIDA neuronal activity.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute and chronic galanin administration decreases hypothalamic galanin synthesis in both male and female adult rats: evidence for a long-loop galanin autofeedback

The secretion of growth hormone (GH) in both male and female rats is controlled by two main neuropeptides, GH-releasing hormone (GHRH), which is stimulatory, and somatostatin, which is inhibitory. Recently, it has been shown that galanin (GAL) also stimulates GH secretion, although the underlying mechanism is still unknown. It was the aim of this study to begin to elucidate if and how GAL regulates its own production at the hypothalamic and pituitary level. Rats underwent the following experimental trials. In experiment 1, adult male and female rats had blood samples collected at -15 minutes, -7.5 minutes, and immediately preceding a subcutaneous (s.c.) injection of GAL at a dose of either 50 or 200 microg/kg. Blood samples were collected at 5, 10, 15, 30, and 60 minutes, and the GH concentration was measured using a radioimmunoassay. The tissues were collected and analyzed for mRNA levels of hypothalamic and pituitary GAL. In experiment 2, adult male and female rats were treated long-term with 200 microg/kg GAL for 7 days s.c., and the pituitary and hypothalamus were analyzed for GAL mRNA. Serum GH concentrations were significantly increased in acutely dosed male and female rats regardless of the dosage level. For the male and female animals acutely dosed with both 50 and 200 microg/kg GAL, hypothalamic GAL mRNA was decreased, whereas pituitary GAL mRNA was affected by 200 microg/kg GAL only in females (increased). For the animals treated long-term with GAL, hypothalamic GAL mRNA was decreased while mRNA for pituitary GAL was increased. We conclude that regardless of the dosage and duration of treatment, administration of GAL negatively regulates hypothalamic GAL mRNA in a non-gender-specific way. Pituitary GAL synthesis appears to be stimulated particularly during chronic SCGAL administration.     

Time course of induction of prolactin-secreting pituitary tumors with diethylstilbestrol in male rats: response of tuberoinfundibular dopaminergic neurons

3,4-Dihydroxyphenylalanine (Dopa) accumulation and dopamine (DA) and noradrenaline levels were measured in the median eminence (ME) of Fisher 344-derived inbred male rats. These animals had been treated with Silastic capsules containing 8-9 mg diethylstilbestrol (DES) or with empty capsules for 3, 7, 14, or 30 days and had the pellets removed 22 days before killing. In an additional group of rats, the DES pellets were continuously present until killing. Blood was collected before treatment was started, at pellet removal, 2 days before killing, and at killing. All rats received 50 mg/kg hydroxybenzylhydrazine (NSD-1015), an L-aromatic amino acid decarboxylase inhibitor, iv 30 min before killing, and the subsequent accumulation of Dopa provided an indirect measure of DA synthesis. Treatment with DES for 7, 14, or 30 days produced an elevation of circulating PRL. Although this elevation of PRL levels was substantially reduced after pellet removal, this parameter was still elevated in the 30-day DES-treated rats at the time of killing. Pituitary levels of PRL and PRL secretion in vitro were elevated in both the 14- and the 30-day DES-treated rats. Rats treated continuously with DES had markedly elevated circulating PRL levels, and the pituitary content and in vitro release of this hormone were also enhanced. DA synthesis, as evidenced by the accumulation of Dopa after NSD-1015 treatment, was significantly elevated in the ME of rats treated with DES for 14 or 30 days while the concentration of DA was reduced in the 30-day treated rats. DA synthesis in the ME was not different from controls in rats treated continuously with DES, although DA levels were markedly suppressed. Pituitary weights were elevated, and BWs were reduced in rats continuously treated with DES. Pituitary weights were also elevated in rats treated with DES for 30 days although not as much as in rats treated continuously with DES. A progressive reduction in seminal vesicles and testes weights was observed with longer periods of DES treatment. Testosterone levels were suppressed in rats treated continuously with DES. In a second study in which rats received DES pellets for 2 months and then the pellets were removed for 4 months, 1 mg bromocriptine sc markedly suppressed the elevated levels of circulating PRL. Collectively, these results show that 14 to 30 days of DES treatment are sufficient to induce PRL-secreting adenohypophysial tumors in adult male rats, although considerable involution of the tumor appears to occur after pellet removal.(ABSTRACT TRUNCATED AT 400 WORDS)     

A sex difference in the stimulatory afferent regulation of tuberoinfundibular dopaminergic neuronal activity

The involvement of afferent neuronal systems in the maintenance of basal and prolactin-stimulated tuberoinfundibular dopaminergic (TIDA) neuronal activity was examined in female and male rats. The synthesis and turnover of dopamine (DA) was measured in the median eminence, the terminal region of the TIDA neurons, to estimate the activity of these neurons. Complete and retrochiasmatic deafferentations of the mediobasal hypothalamus were made 7 days prior to experimentation to either completely isolate the TIDA neurons from the rest of the brain or to interrupt neuronal connections from rostral brain regions to the TIDA neurons, respectively. Both complete and retrochiasmatic deafferentations decreased the basal rate of DA synthesis and turnover in the median eminence of female, but not of male rats. These results suggest that neuronal afferents originating rostral to the mediobasal hypothalamus stimulate TIDA neurons in the female but not in the male rat. Intracerebroventricular administration of rat prolactin increased DA synthesis in the median eminence of both sham and retrochiasmatic deafferentiated female and male rats showing that the stimulatory action of prolactin is not blocked by retrochiasmatic deafferentation. Ovariectomy reduced the rate of DA synthesis in the median eminence but retrochiasmatic deafferentation did not cause a further decrease in ovariectomized rats. These results suggest that retrochiasmatic deafferentation and ovariectomy may remove a stimulatory input to the TIDA neurons which is mediated through a common afferent neuronal pathway. These afferent influences do not appear to be operational in the adult male rat since retrochiasmatic deafferentation did not reverse the castration-induced increase in the rate of DA synthesis in the median eminence of male rats.     

Hypoprolactinemia induced by hypophysectomy and long-term bromocriptine treatment decreases tuberoinfundibular dopaminergic neuronal activity and the responsiveness of these neurons to prolactin

The effect of long-term decreases in circulating concentrations of prolactin was determined on the responsiveness of tuberoinfundibular dopamine (DA) neurons to this hormone. The activity of these neurons in ovariectomized rats was estimated by measuring the rate of DA synthesis (DOPA accumulation after the administration of a decarboxylase inhibitor) in the median eminence at various times after serum concentrations of prolactin had been reduced by hypophysectomy or the chronic administration of a DA agonist (bromocriptine, 3 mg/kg/day). The concentration of DA in the median eminence, but not in striatum, declined progressively up to 12 days after hypophysectomy, but did not change at any time during bromocriptine treatment. On the other hand, norepinephrine concentrations in the median eminence were increased 12 days after both treatments. Within 24 h after hypophysectomy or the first injection of bromocriptine the rate of DA synthesis in the median eminence was decreased; this decrease was maintained for at least 12 days suggesting that tuberoinfundibular DA neuronal activity is normally maintained by endogenous prolactin. Intracerebroventricular (ICV) injections of prolactin (10 micrograms, 12 h prior to sacrifice) increased the rate of DA synthesis in the median eminence of control, 24-hour hypophysectomized and 24-hour bromocriptine-treated rats. After longer periods (6-12 days) of bromocriptine treatment or after hypophysectomy the responsiveness of tuberoinfundibular DA neurons to prolactin was reduced. Dose-response studies revealed that the sensitivity and magnitude of response to ICV prolactin was markedly reduced in 12-day hypophysectomized rats.(ABSTRACT TRUNCATED AT 250 WORDS)     

Role of LHRH in the gonadotrophin response to restraint stress in intact male rats

A hypothalamic site of action has been hypothesized for the inhibitory effect of chronic stress on gonadotrophin secretion. The aim of the present study was to examine the temporal changes in hypothalamic LHRH content and gonadotrophin secretion during restraint stress, and the pituitary responsiveness to LHRH stimulation in chronically stressed rats. Adult male rats were killed after being restrained for 0, 20, 45, 90, 180 and 360 min or for 6 h daily over 2, 3 and 4 days. After 20-45 min of stress there was an increase in plasma concentrations of LH (P less than 0.01) and a decrease in hypothalamic LHRH content (P less than 0.01), suggesting a negative correlation between plasma LH and hypothalamic LHRH concentrations. Plasma concentrations of FSH were also increased by restraint, but the FSH response was slower and less than the plasma LH response, being significant after 90 min of restraint. Plasma LH and FSH and hypothalamic LHRH concentrations were decreased in chronically stressed rats. In rats restrained for 6 h daily over 4 days, the response of plasma gonadotrophins to administration of 500 ng LHRH was enhanced 45 min after the injection. On the basis of these observations we concluded that in the intact rat, stress may acutely stimulate LHRH and gonadotrophin secretion, and the inhibitory effect of chronic stress on plasma LH and FSH seems not to be due to a reduction in pituitary responsiveness to LHRH, but rather to a decrease in LHRH secretion.     

Evidence for a permanent decline in tuberoinfundibular dopaminergic neuronal function after chronic estrogen treatment is terminated in Fischer 344 rats

Long-term 17 beta-estradiol (E2) treatment in rats decreases tuberoinfundibular dopaminergic (TIDA) neuronal function. The objective of this study was to determine if the decline in TIDA function after E2 treatment in Fischer 344 (F344) rats is sustained long after removal of E2. Ovariectomized (OVX) F344 rats were each implanted with an E2-containing or empty Silastic capsule for 4 weeks; the capsule was then removed, and 26 weeks later acute experiments were performed. Release of 3H from median eminence tissue in vitro in response to electrical stimulation after 3H-DA accumulation was not different between E2-treated rats and OVX controls, even though serum prolactin (PRL) was 4-fold greater in E2-treated animals. Acute administration of apomorphine hydrochloride, a DA receptor agonist, at 2 doses, reduced serum PRL values as much in E2-treated animals as in OVX control rats. Injection of morphine sulfate or nomifensine maleate, which directly influence TIDA neurons, resulted in nonsignificant serum PRL responses in animals long after E2 withdrawal as compared to the greater response in OVX control rats. To further evaluate TIDA neuronal function, OVX non-E2-treated rats and animals 26 weeks after E2 withdrawal received a 3-day E2 challenge which increased the stimulation-evoked release of 3H from the median eminence tissue in vitro 2-fold in OVX control rats but had no effect in rats given E2 26 weeks previously. The difference in the stimulation-evoked release occurred in the presence of similar circulating serum PRL levels in the two groups as a result of the 3-day E2 treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute restraint stress activates functional NK1 receptor in the colon of female rats: involvement of steroids

BACKGROUND AND AIMS: Psychological factors have been implicated in the aetiology of irritable bowel syndrome characterised by intestinal altered motility and visceral hypersensitivity. Similar disorders have been found in rats under stressful conditions. The role of tachykinins in bowel dysfunctions caused by stress is not fully documented. Therefore, we investigated the influence of stress on NK1 receptor activation at the colonic level in female rats. METHODS: The stress procedure used consisted of two hours of partial restraint. Histamine release was measured from colonic samples of control and stressed animals and the effect of SR140333, a NK1 receptor antagonist, on substance P induced histamine release was determined. Involvement of steroids has been evaluated in this response. RESULTS: NK1 receptor antagonist was found to inhibit substance P induced histamine release in samples from stressed female rats but not in samples from control animals. Previous treatment of female rats with RU 486 abolished this effect observed in stressed animals. Similarly, in samples from stressed female rats previously ovariectomised, SR140333 failed to inhibit substance P induced histamine release but previous treatment with both progesterone and oestrogen restored its effect. CONCLUSIONS: Stress induces NK1 receptor activation in the colon, and ovarian steroids are involved in this response.     

Circadian rhythms of neuroendocrine dopaminergic neuronal activity in ovariectomized rats

Prolactin (PRL) secretion is inhibited by dopamine (DA) released from hypothalamic neuroendocrine neurons designated tuberoinfundibular (TIDA), tuberohypophyseal (THDA) and periventricular hypophyseal (PHDA) dopaminergic (DAergic) neurons. Since PRL is secreted in many physiological states with a circadian rhythm, the purpose of these experiments was to determine if patterns of neuroendocrine DAergic neuronal activity in rats are also circadian. The activity of neuroendocrine DAergic neurons, defined as DA turnover rate in nerve terminals and quantitated as the ratio of DOPAC (a primary DA metabolite) to DA content, was measured by high-performance liquid chromatography with electrochemical detection (HPLC-EC) in these populations of DA neurons of OVX rats. TIDA neurons exhibit a rhythm of activity in a light:dark cycle which free-runs in constant dark (DD) and is entrained by light, indicating that TIDA neuronal activity is circadian. THDA and PHDA neurons also display daily rhythms entrained to a photoperiod and PHDA neuronal activity free-runs in DD with a period of approximately 24 h. However, a significant rhythm of THDA neuronal activity was not detected under DD. In the OVX rat, the activities of TIDA and PHDA neurons, but not THDA neurons, describe all the characteristics of a circadian rhythm as they are both entrained by light, but only TIDA and PHDA neurons maintain a significant rhythm of activity under DD.     

An endogenous serotonergic rhythm acting on 5-HT(2A) receptors may be involved in the diurnal changes in tuberoinfundibular dopaminergic neuronal activity and prolactin secretion in female rats

The central serotonergic system has long been known to have a stimulatory role on the secretion of prolactin (PRL). The integrity of serotonergic neurotransmission is essential for the expression of the estrogen-induced afternoon PRL surge. Whether its effect on PRL involves change in the activity of tuberoinfundibular dopaminergic (TIDA) neurons has not been ascertained. In adult ovariectomized rats treated with estrogen, depletion of central serotonin (5-HT) by 5,7-dihydroxytryptamine (5,7-DHT, 200 microg/rat, i.c.v.) effectively prevented the afternoon fall in TIDA neuronal activity (using the levels of 3,4-dihydroxyphenylalanine and 3, 4-dihydroxyphenylacetic acid (DOPAC), and the ratio of DOPAC/dopamine in the median eminence as indices), and blunted the afternoon PRL surge. A single injection of a 5-HT(2A) receptor antagonist, ketanserin (5 mg/kg, i.p. at 12.00 h), also had the same effects on the diurnal changes in TIDA neuronal activity and PRL secretion as the treatment with 5,7-DHT did. Intracerebroventricular injection of a 5-HT(2) receptor agonist 2, 5-dimethoxy-4-iodoamphetamine (DOI) in the morning inhibited the TIDA neuronal activity and stimulated PRL secretion in a dose-dependent manner; while injection of a 5-HT(1) agonist, 8-hydroxy-dipropylaminotetralin, was without effect. Injection of DOI in 5,7-DHT-pretreated rats at 14.30 h also lowered the TIDA neuronal activity and reinstated the PRL surge. In all, endogenous 5-HT, acting through the 5-HT(2A) receptor, appears to exhibit an inhibitory effect on TIDA neuronal activity during the afternoon, which is essential for the PRL surge.     

Profound decrement of mesolimbic dopaminergic neuronal activity during ethanol withdrawal syndrome in rats: electrophysiological and biochemical evidence.

Activity of the mesolimbic dopaminergic system was investigated in rats withdrawn from chronic ethanol administration by single-cell extracellular recordings from dopaminergic neurons of the ventrotegmental area, coupled with antidromic identification from the nucleus accumbens, and by microdialysis-technique experiments in the nucleus accumbens. Spontaneous firing rates, spikes per burst, and absolute burst firing but not the number of spontaneously active neurons were found drastically reduced; whereas absolute and relative refractory periods increased in rats withdrawn from chronic ethanol treatment as compared with chronic saline-treated controls. Consistently, dopamine outflow in the nucleus accumbens and its acid metabolites were reduced after abruptly stopping chronic ethanol administration. All these changes, as well as ethanol-withdrawal behavioral signs, were reversed by ethanol administration. This reversal suggests that the abrupt cessation of chronic ethanol administration plays a causal role in the reduction of mesolimbic dopaminergic activity seen in the ethanol-withdrawal syndrome. Results indicate that during the ethanol-withdrawal syndrome the mesolimbic dopaminergic system is tonically reduced in activity, as indexed by electrophysiological and biochemical criteria. Considering the role of the mesolimbic dopaminergic system in the reinforcing properties of ethanol, the depressed activity of this system during the ethanol-withdrawal syndrome may be relevant to the dysphoric state associated with ethanol withdrawal in humans.     

Relation of gonadal hormones to differential LH response to naloxone in prepubertal male and female rats

Naloxone (NAL) has been shown to induce LH release in female but not in male rats 10-25 days of age. The purpose of this study was to examine the role of neonatal gonadal hormones on NAL-induced LH release in male and female rats 15, 25, and 35 days of age. On each of these days rats received a s.c. injection of either NAL (5 mg/kg) or physiological saline, and blood was collected 30 min later by decapitation. At 15 days of age, NAL induced LH release in intact and ovariectomized (OVX) female rats, and in male rats castrated (CAST) on the 1st day of life (neonate CAST males). Injection of 10 micrograms estradiol benzoate (EB) 24 h prior to NAL administration blocked NAL-induced LH release in these rats. NAL had no effect on LH release in 15- or 25-day-old intact and CAST male rats or in female rats given 2 mg testosterone propionate at 3 days of age (androgenized female rats). At 35 days of age, NAL induced LH release in intact, OVX, and OVX-EB treated female rats, and in neonate CAST and neonate CAST-EB treated male rats. NAL had no effect on serum LH levels in androgenized female rats. NAL induced LH release in intact and CAST 35-day-old male rats, but pretreatment with estrogen prevented NAL from eliciting LH release. These results indicate that neonatal exposure to androgen is responsible for the sex difference in the LH response to NAL observed in prepubertal male and female rats before 30 days of age.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hypoprolactinemia decreases tyrosine hydroxylase activity in the tuberoinfundibular dopaminergic neurons acutely by protein dephosphorylation and chronically by changes in gene expression

This study evaluated the roles of protein dephosphorylation or suppressed gene expression in reducing tyrosine hydroxylase activity in tuberoinfundibular dopaminergic neurons after acute or chronic bromocriptine (BROMO) administration. Diestrous or ovariectomized rats were injected with BROMO (3 mg/kg, s.c.) at 1000 h and were sacrificed 4 h later or were injected with BROMO at 12 h intervals for 3 days.In vitro tyrosine hydroxylase activity was assessed by incubating hypothalamic explants with brocresine, an L-aromatic amino acid decarboxylase inhibitor, and measuring 3,4-dihydroxyphenylalanine (DOPA) accumulation in the stalk-median eminence (SME). The incubation medium also contained either 2 μM okadaic acid, a protein phosphatase 1 and 2A inhibitor, or its vehicle (0.25% dimethylsulfoxide). Acute (4 h) and chronic (3 days) BROMO treatment suppressed circulating PRL levels from 10–12 ng/ml to<1 ng/ml and reduced tyrosine hydroxylase activity in the SME by 60% or 40% in diestrous or ovariectomized rats, respectively. Okadaic acid increased tyrosine hydroxylase activity in the SME 2-fold in control diestrous or ovariectomized rats. The reduced tyrosine hydroxylase activity in the SME after acute BROMO treatment was increased by okadaic acid 5-or 3-fold in diestrous or ovariectomized rats respectively, to a value similar to the controls. In sharp contrast, after chronic BROMO treatment, the response to okadaic acid was blunted. As assessed byin situ hybridization, tyrosine hydroxylase mRNA signal levels in the arcuate nucleus of diestrous rats were not altered after acute BROMO treatment, but were reduced by 70% after chronic BROMO treatment. The acute BROMO-induced decrease in tyrosine hydroxylase activity was reversed by co-administration of oPRL or rPRL, indicating that the action of BROMO is via a reduction in PRL. The data suggest that protein dephosphorylation may be a primary mechanism for the rapid BROMO-dependent suppression of tyrosine hydroxylase activity, whereas suppression of tyrosine hydroxylase gene expression may contribute to the lower tyrosine hydroxylase activity after chronic BROMO treatment.     

Acute stress differentially affects aromatase activity in specific brain nuclei of adult male and female quail

The rapid and temporary suppression of reproductive behavior is often assumed to be an important feature of the adaptive acute stress response. However, how this suppression operates at the mechanistic level is poorly understood. The enzyme aromatase converts testosterone to estradiol in the brain to activate reproductive behavior in male Japanese quail (Coturnix japonica). The discovery of rapid and reversible modification of aromatase activity (AA) provides a potential mechanism for fast, stress-induced changes in behavior. We investigated the effects of acute stress on AA in both sexes by measuring enzyme activity in all aromatase-expressing brain nuclei before, during, and after 30 min of acute restraint stress. We show here that acute stress rapidly alters AA in the male and female brain and that these changes are specific to the brain nuclei and sex of the individual. Specifically, acute stress rapidly (5 min) increased AA in the male medial preoptic nucleus, a region controlling male reproductive behavior; in females, a similar increase was also observed, but it appeared delayed (15 min) and had smaller amplitude. In the ventromedial and tuberal hypothalamus, regions associated with female reproductive behavior, stress induced a quick and sustained decrease in AA in females, but in males, only a slight increase (ventromedial) or no change (tuberal) in AA was observed. Effects of acute stress on brain estrogen production, therefore, represent one potential way through which stress affects reproduction.     

Acute stress rapidly decreases plasma testosterone in a free-ranging male songbird: Potential site of action and mechanism

We used a free-ranging, seasonally breeding adult male songbird, the rufous-winged sparrow, Aimophila carpalis, to investigate the effects of acute stress-induced by capture followed by restraint, on the hypothalamo-pituitary-testicular axis. Intra- and interindividual comparisons revealed that males decreased their plasma testosterone (T) by 37-52% in response to acute stress. The decrease occurred within 15 min of capture and persisted for at least another 15 min. Within 15 min, the decrease in plasma T was not associated with a reduction in plasma luteinizing hormone (LH). Thirty minutes after capture and restraint, the decrease in plasma T either was likewise not associated with decreased plasma LH (intraindividual comparison) or concurred with a reduction in plasma LH (interindividual comparison). These observations indicate that effects of stress may have been mediated at the pituitary gland and also directly at the testicular levels. To address this question, we measured the hormonal response to an injection of the glutamate receptor agonist N-methyl-d,l-aspartate (NMA) to stimulate to stimulate the release of gonadotropin-releasing hormone (GnRH) or of GnRH to stimulate the release of LH. Treatment with NMA did not change plasma LH, presumably because the birds were in breeding condition and already secreting GnRH at a maximum rate. Administration of GnRH increased plasma LH equally in birds that were or were not stressed before the treatment. An injection of purified ovine LH (oLH) increased plasma T equally in birds that were or were not acutely stressed before the hormone injection. Thus, the observed acute stress-induced decrease in plasma T was apparently not mediated by decreased responsiveness of the pituitary gland to GnRH or of the testes to LH. Decreased plasma T following stress may involve a direct impairment of the testicular endocrine function.