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A Sahu

Publications and source records attributed to A Sahu.

At least 19 recordsLinked to original sources
PubMed1992

Evidence that long-term estrogen treatment disrupts opioid involvement in the induction of pituitary LH surge.

Recent evidence suggests that a decrease in the inhibitory opioid influence is a necessary hypothalamic neural event in the preovulatory and ovarian steroid-induced luteinizing hormone (LH) surge. Whether shifts in ovarian steroidal milieu disrupts this neural event is not known. Therefore, the effects of short-term (3 days) and long-term (13 or 17 days) estradiol 17 beta (E2) exposure on spontaneous, naloxone (NAL) and progesterone (P)-induced LH surges were assessed in ovariectomized (ovx) rats. Two weeks after ovariectomy, rats received subcutaneous Silastic capsules filled with crystalline E2. In rats exposed to E2 for 3 days and infused with saline intravenously between 11.00-14.00 h, plasma LH rose significantly at 17.00 h. NAL infusion between 11.00-14.00 h in these rats to decrease the inhibitory opioid influence, advanced both the onset of LH rise and amplified the secretion of LH in the afternoon. Continuation of E2 exposure for 13 days produced no deleterious effects on either the spontaneous or NAL-induced augmentation in LH responses. However, uninterrupted E2 exposure for 17 days abolished the spontaneous afternoon LH rise and drastically diminished the ability of NAL to advance and amplify the LH response. In the next experiment, we evaluated the effect of P injection (2 mg/rat) at 11.00 h on the afternoon LH release in rats similarly exposed to E2 for either 3 or 17 days. In rats exposed to E2 for 3 days, the P-induced LH release was significantly greater than that observed after saline or NAL infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

A selective sexually dimorphic response in the median eminence neuropeptide Y.

Recent studies show that neuropeptide Y (NPY) is widely distributed in the hypothalamus and that it stimulates luteinizing hormone-releasing hormone (LHRH) release from the medial basal hypothalamus (MBH) of male and female rats. The neuroendocrine factors that regulate NPY neurosecretion in two sexes are not well understood. We have previously observed that orchidectomy (orch) in male rats decreased and testosterone (T) replacement increased NPY levels selectively in the median eminence (ME), arcuate nucleus (ARC) and ventromedial nucleus (VMN) and the KCl-evoked in vitro release of NPY from the MBH was likewise decreased after orch and restored by testosterone replacement. Now we report that these NPY responses are different in female rats following removal of the ovaries. Ovariectomy (ovx) decreased NPY concentrations in the ARC and VMN and not in the ME. Estrogen replacement restored NPY concentrations in the ARC and VMN, however, in the ME NPY concentration decreased significantly. Further, the KCl-evoked NPY release in vitro from either the MBH or ME of intact and ovx rats was similar. In an additional concurrent comparative study in male and female rats, we observed that of the 6 microdissected hypothalamic sites, NPY levels were approximately 50% less in the ME of intact females than in those of intact male rats. Again, in male rats there was a significant decrease in NPY levels in the ME, ARC and VMN after orch, whereas in female rats, NPY levels in the ARC and VMN, but not in the ME decreased after ovx.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Hypothalamic neuropeptide Y gene expression in rats on scheduled feeding regimen.

Recent evidence suggests that neuropeptide Y (NPY) is an important signal in the neural circuitry that controls feeding behavior. Previously we observed that in rats entrained to 4 h daily scheduled feeding regimen (SFR), NPY content and release in the paraventricular nucleus (PVN) was elevated but decreased rapidly in association with food consumption. In the present study, we investigated the pattern of hypothalamic NPY gene expression in SFR rats before and after food consumption by measuring the content of preproNPY mRNA in the medial basal hypothalamus (MBH). Adult male rats were maintained on either ad libitum diet (control) or on SFR. Rats were killed before food presentation at 11.00 h and at the end of 4 h food consumption at 15.00 h. The levels of preproNPY mRNA in the MBH were determined by solution hybridization/RNase protection assay using a cRNA probe complementary to rat NPY precursor mRNA. We observed that, as compared to that in control rats on ad libitum diet, preproNPY mRNA levels in the MBH were increased two-fold in the SFR rat at 11.00 h and remained elevated even after 4 h of food consumption. These results show a simultaneous enhancement in PVN NPY release and hypothalamic gene expression in advance of scheduled feeding time, but food intake rapidly decreases PVN NPY release and content, with little impact on hypothalamic gene expression.

Animals↗
PubMed1992

Anti-leprosy drugs inhibit the complement-mediated solubilization of pre-formed immune complexes in vitro.

Incubation of pre-formed immune complexes (IC) (125I-HSA--anti-HSA) with normal human serum resulted in solubilization of IC. When various anti-leprosy drugs were added to human sera, solubilization of IC was fairly explicit with clofazimine, whereas this effect was marginal with dapsone. Rifampicin hardly displayed this effect. Aspirin, chloroquine, and prednisolone, the drugs used in addition to multi-drug therapy to control reactions in leprosy, were in a position to inhibit the solubilization of 125I HSA--anti-HSA by normal serum only at a very high dose. From the current data of the inhibition of solubilization of pre-formed IC along with our earlier observations on the modulation of complement-mediated haemolysis by these drugs, it may be possible to postulate that clofazimine as well as chloroquine affect early complement components. This may in turn be responsible for preventing the deposition of C3 complement onto IC.

Antigen-Antibody Complex↗
PubMed1992

In vivo effects of anti-leprosy drugs on the rat peritoneal macrophages and lymphocyte subpopulations.

The present study describes the in vivo effects of anti-leprosy drugs on rat peritoneal macrophages and T-cell homeostasis. It was observed that BCG-elicited rat peritoneal macrophages produced more H2O2 and expressed more Ia antigen on their cell surfaces compared with resident peritoneal macrophages. Furthermore, elicited macrophages isolated from rats administered multidrug therapy (MDT), consisting of dapsone, clofazimine and rifampicin in high dose (10 x MDT) released more O2-. On the contrary, there was a significant decrease in the Ia antigen expression on these macrophages. Anti-leprosy drug treatment in high dose (10 x MDT) decreased the total number of blood T-helper (W3/25+) cells and increased the total number of blood T-suppressor (OX-8+) cells which resulted in a significant decrease in a W3/25: OX-8 ratio. Electron microscopy of elicited macrophages isolated from 10 x MDT treated rats showed development of many filipodia compared with control macrophages. These data show that 10 x MDT treatment in rats for 1 month alters the homeostasis of blood T-cell subpopulations which perhaps decreases the Ia expression on macrophages. However, the increase in O2- production and the appearance of filipodia on the macrophages is due to a direct effect of drugs on the macrophages. MDT treatment for 1 month in a therapeutic dose has no effect on the above-mentioned parameters.

Animals↗
PubMed1992

Effect of d-fenfluramine on neuropeptide Y concentration and release in the paraventricular nucleus of food-deprived rats.

Recent evidence indicates that Neuropeptide Y (NPY) is an important signal in the hypothalamic neural circuitry that stimulates feeding in the rat. Administration of d-fenfluramine (FEN) has been shown to rapidly inhibit feeding in the rat. Because food deprivation increases the levels and release of NPY in the paraventricular nucleus (PVN) of the hypothalamus, the aim of this study was to investigate whether the rapid anorectic effects of FEN in food-deprived (FD) rats are associated with alterations in the hypothalamic NPYergic system. In the first experiment, the effect of FEN (10 mg/kg) on NPY concentrations in nine microdissected hypothalamic sites was assessed by radioimmunoassay (RIA) in rats either food deprived for 3 days or fed ad lib during the experimental period. In response to food deprivation, NPY concentrations increased significantly in the PVN and arcuate nucleus, but NPY levels remained unchanged in the remaining seven hypothalamic sites. In control rats maintained on ad lib food supply, FEN injection produced little effect on NPY concentration in hypothalamic sites. However, FEN suppressed NPY levels selectively in the PVN of FD rats, so that NPY concentrations measured in the nucleus were within the range found in satiated control rats. In the second experiment, the effect of FEN on NPY release in the PVN was examined in FD rats by the push-pull cannula (PPC) technique. NPY levels in the PPC perfusate were unchanged in FD rats during the period 30-120 min after saline or FEN injection. Also, the mean rate of NPY release was similar in vehicle- and FEN-treated FD rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1992

Effects of tachykinins on luteinizing hormone release in female rats: potent inhibitory action of neuropeptide K.

Tachykinins, a family of biologically active related peptides, are found in variable amounts in the rat hypothalamus. We assessed the effects of five tachykinins, substance P (SP), neurokinin A (NKA), neuropeptide K (NPK), neuropeptide gamma (NP gamma), and neurokinin B (NKB), on LH release in different experimental model systems in ovariectomized rats. In the first series of experiments rats were ovariectomized and implanted with permanent cannulae in the third cerebroventricle of the rat brain. Two weeks later, the effects of intracerebroventricular injection of 0.5 or 1.25 nm various tachykinins on LH release were studied. The results showed that whereas SP, NKA, and NKB were ineffective, and NP gamma was marginally effective, NPK produced a long-lasting suppression of LH release. NPK decreased LH release in a dose- and time-related fashion. Similarly, in the second series of experiments, whereas SP and NKA were inactive, NPK completely suppressed the LH surge induced by progesterone in estrogen-primed ovariectomized rats. In the third series of experiments we observed that NK-2 receptor agonist [Nle10]NKA4-10, and not NK-1 receptor agonist [Sar9,Met(O2)11]SP, suppressed both the release of LH in vivo and basal and KCl-induced hypothalamic LHRH release in vitro. These results show that NPK is the most effective tachykinin in suppressing LH release, and the inhibitory response is mediated by hypothalamic NK-2 receptors. These findings are in accord with the hypothesis that NPK may serve as a hypothalamic inhibitory neurotransmitter/neuromodulator of LHRH secretion.

Animals↗
PubMed1992

Steroidal regulation of hypothalamic neuropeptide Y release and gene expression.

Neuropeptide Y (NPY) readily stimulates the release of hypothalamic LHRH and pituitary LH release in intact and gonadal steroid-primed gonadectomized rats. We have now tested the hypothesis that the release and synthesis of hypothalamic NPY may be regulated by gonadal steroids. To measure the effects of gonadal hormones on NPY release, a permanent push-pull cannula was implanted in the anterior pituitary (AP) of sham castrated (controls) or castrated (CAST) male rats, and 1 week later, the AP was perfused with artificial cerebrospinal fluid over a 3-4 h period. NPY concentrations in the perfusates collected at 10-min intervals were measured by RIAs. The NPY release pattern in the AP was episodic in both intact and CAST rats, and the frequency of NPY episodes was similar in two groups. However, the amount of NPY detected in the AP of CAST rats was significantly less than that of intact rats because the mean rate of release and the amplitude of NPY episodes in the perfusates of CAST rats were significantly reduced. This observation of attenuated hypothalamic NPY output in vivo and previous evidence of decreased hypothalamic NPY contents after CAST implied that the synthesis of hypothalamic NPY may be regulated by testicular secretions. Therefore, the effects of testosterone (T)-replacement on preproNPY messenger RNA (mRNA) in the medial basal hypothalamus (MBH) was evaluated. Rats were CAST and received either empty or T-filled Silastic capsules sc. Two weeks later, the level of perproNPY mRNA in the MBH was determined by solution hybridization/ribonuclease protection assay using a complementary RNA probe complementary to the rat NPY precursor mRNA. We observed that the levels of preproNPY mRNA were 2-fold higher in the MBH of T-replaced CAST as compared to control CAST rats. These findings are consistent with the hypothesis that gonadal steroids enhance the neurosecretory activity of hypothalamic NPYergic neurons, and for the first time reveal a coupling between the level of gene expression and the secretion of a neuropeptide involved in the regulation of hypothalamic LHRH and pituitary LH release.

Animals↗
PubMed1992

Neuropeptide Y release is elevated from the microdissected paraventricular nucleus of food-deprived rats: an in vitro study.

Intracerebroventricular injection of neuropeptide Y (NPY) stimulates a robust dose-related feeding response in the rat. Experimental evidence attests to the view that the release of NPY in the paraventricular nucleus (PVN), a site richly innervated by NPY immunopositive fibers, is responsible for stimulation of feeding behavior. However, there is little information on the neuroendocrine factors involved in regulation of NPY release, in part due to the unavailability of reliable techniques to monitor PVN NPY release. In this study, we have validated an in vitro technique to assess NPY release from the PVN and other neighboring hypothalamic sites of the rat brain. In the first experiment, freshly dissected brains from male rats were processed for 300-microns thick sections with a vibratome. The PVNs were microdissected from the brain sections under a stereomicroscope and incubated in 250 microliters Krebs Ringer bicarbonate buffer at 37 C for basal and KCl-induced NPY release. The results showed that basal NPY efflux from the excised PVN was detectable and increased in relation to the number of PVNs in the incubation chambers. Addition of KCl at the end of the 60-min basal incubation period increased NPY release further, the increments were again closely related to the number of PVN punches in the incubation chambers. In the second experiment, the assumption that in vitro basal and KCl-evoked NPY release from the PVN reflected the in vivo pattern of PVN NPY secretion was validated. The effects of 4-day food deprivation (FD), an experimental paradigm known to augment in vivo PVN NPY secretion, on the in vitro NPY release from PVN and ventromedial nucleus were evaluated. The results showed that both basal and KCl-evoked NPY release was significantly higher from the PVN of food-deprived than control rats on ad libitum rat chow. This FD-induced incremental NPY response was site-specific because the basal and KCl-evoked NPY effluxes from the ventromedial nucleus of FD and control rats were similar. Thus, in agreement with previous in vivo findings, NPY release in vitro is also augmented selectively from the PVN in response to fasting. Cumulatively, these results demonstrate that NPY release in vitro from hypothalamic sites microdissected from fresh brains can be assessed in a reliable fashion and are in accord with the proposal that enhanced NPY action within the PVN is responsible for increased drive for food.

Animals↗
PubMed1992

Diverse effects of tachykinins on luteinizing hormone release in male rats: mechanism of action.

The tachykinins are a group of structurally related peptides found in the rat hypothalamus and anterior pituitary. We have evaluated the effects of four tachykinins on LH release in male rats. In intact male rats, intracerebroventricular (icv) injection of neurokinin A (NKA), neuropeptide K (NPK), and neuropeptide-gamma (NP gamma) elicited dose-related, transient increases in plasma LH. Substance P (SP) was ineffective under these conditions. A further examination showed that in vitro incubation with either NPK or NP gamma of hemipituitaries from intact but not castrated male rats promoted release of LH into the medium, thereby revealing that the excitatory effects of tachykinins in intact male rats may, in part, be a result of stimulation of LH release directly from the anterior pituitary. On the other hand, the effects of these four tachykinins on LH release were different in castrated rats. Intracerebroventricular injection of NPK, NKA, and NP gamma as well as SP, which was ineffective in intact male rats, evoked a long-lasting suppression of LH release. Comparatively, NPK was the most effective tachykinin in eliciting LH responses in both of these tests involving different endocrine environments. We next evaluated the possibility that the inhibitory effects of tachykinins (NPK) may be mediated by activation of inhibitory endogenous opioid peptides. The results showed that iv infusion of the opiate receptor antagonist naloxone, to block the possible inhibitory effects of endogenous opioid peptides, only partially counteracted the suppressive effects of icv NPK on plasma LH levels. Thus, in addition to revealing the diverse effects of structurally related tachykinins on LH release, the results of these investigations showed specifically that the NK-2 receptor agonists NPK, NP gamma, and NKA stimulated LH release in intact rats, in part, by a direct action at the level of the pituitary, whereas the NK-1 receptor agonist SP was inactive under these conditions. These findings imply a paracrine/autocrine mode of excitatory action on LH release involving pituitary NK-2 receptor subtypes. On the other hand, in castrated rats, all four tachykinins readily suppressed LH release by a central action involving, in part, an activation of hypothalamic opioid systems.

Animals↗
PubMed1992

Neuropeptide Y release from the paraventricular nucleus increases in association with hyperphagia in streptozotocin-induced diabetic rats.

We tested the hypothesis that the hyperphagia observed in streptozotocin (STZ)-induced diabetic rats is due to increased release of neuropeptide Y (NPY) in the paraventricular nucleus (PVN) of the hypothalamus. In the first experiment, male rats were injected with STZ or vehicle (control) via the tail vein and 18-20 days later, NPY levels in seven hypothalamic sites and release in vitro from selected hypothalamic sites were evaluated. The results showed that in association with STZ-produced marked hyperglycemia and hyperphagia, NPY concentrations were increased in four hypothalamic sites, including the PVN. Evaluation of NPY release in vitro showed that both basal and KCl-induced release was significantly higher from the micro-dissected PVN of STZ-treated than control rats. A similar augmentation in the NPY efflux in vitro was detected from the median eminence arcuate nucleus, but not from the neighboring ventromedial nucleus of STZ-treated rats. In the second experiment, rats were treated with STZ or vehicle and received permanent push-pull cannula (PPC) in the PVN for evaluation of NPY release in vivo 18-21 days after STZ treatment. The results showed that mean NPY levels in the perfusates collected from the PVN of diabetic rats were significantly higher as compared to control rats. Since NPY is the most potent naturally occurring orexigenic signal and the PVN is an important initial site of NPY action in the stimulatory pathway regulating feeding, our findings of augmented PVN NPY release in vivo and in vitro are in accord with the hypothesis that increased NPY secretion in the PVN may be responsible for hyperphagia in diabetic rats.

Animals↗
PubMed1992

Delayed clearance of circulating immune complexes in mice following administration of antileprosy drugs.

In this report we describe an animal experiment which showed delayed clearance of preformed 125I-HSA-anti-HSA immune complexes (with five times excess HSA) from the circulation of mice treated with antileprosy drugs (dapsone, clofazimine, and rifampin--multidrug therapy for 7 days) in comparison with normal (untreated) mice. The results also showed delayed retention of the preformed immune complexes in the spleen and kidneys of the antileprosy-drug-treated animals. The exact mechanism of the delayed handling of preformed immune complexes in mice fed antileprosy drugs could not be ascertained. However, in light of the anticomplementary effects of clofazimine and dapsone, as reported earlier, and in light of the large accumulation of clofazimine and rifampin in macrophages, it has been postulated that in the drug-fed animals either the immune complexes could not be phagocytosed by macrophages, through the avenue of their C3b receptors, or the immune complexes could not be downgraded easily within the macrophages overloaded with clofazimine and rifampin. These results might have clinical significance and might throw some light on the prolonged persistence of circulating immune complexes in the vascular bed of lepromatous patients even after clinical remission of erythema nodosum leprosum.

Animals↗
PubMed1991

Neuropeptide Y secretion increases in the paraventricular nucleus in association with increased appetite for food.

Feeding in mammals is a periodic behavior; however, knowledge of how the brain signals an intermittent eating pattern is scanty. Recent indirect evidence indicates that one of the signals encoded in the structure of neuropeptide Y (NPY) is to stimulate robust feeding. Therefore, two series of experiments were undertaken to characterize NPY secretion within the paraventricular nucleus (PVN) in association with eating behavior in the rat. Dynamic changes in NPY concentration in several hypothalamic sites and release in the PVN were assessed before and during the course of food consumption in rats trained to eat daily only for 4 h. Only in the PVN were NPY concentrations elevated before the introduction of food and, thereafter, levels decreased significantly during the course of eating. A similar temporal pattern in NPY release into the PVN interstitium was evident in samples collected by push-pull cannula perfusion in unrestrained rats. In addition, in food-deprived rats displaying a robust drive for feeding, NPY release in the PVN was also markedly enhanced in the shape of high-amplitude secretory episodes as compared to a lower release rate in rats receiving food ad libitum. The higher rate of NPY release in fasted rats returned to the control range after 24 h of ad libitum food supply. These findings of intense and dynamic NPY neurosecretory activity within a discrete hypothalamic site in association with an increased drive for food consumption demonstrate that NPY release in the PVN is an important orexigenic signal for periodic eating behavior. These results have important global implications for elucidating the underlying causes of the pathophysiology of eating disorders--anorexia nervosa, bulimia, and obesity--as well as constituting a specific contextual model for the formulation and testing of suitable NPY receptor agonists and antagonists for therapeutic intervention.

Animals↗
PubMed1991

Effect of anti-leprosy drugs on superoxide anion production by rat peritoneal macrophage with special reference to light exposed clofazimine.

The present study describes the in vitro effect of anti-leprosy drugs on superoxide anion (O2-) production by rat resident peritoneal macrophages. Of the three drugs tested i.e. clofazimine, rifampicin and dapsone, the first was most effective in increasing O2- production in a dose dependent manner, while rifampicin had some stimulatory effect and dapsone exhibited minimal action. Furthermore, when clofazimine and dapsone were added together it was observed that the increase of O2- production by macrophages due to clofazimine was not significantly altered by the addition of dapsone. Moreover, it was found that killed Mycobacterium leprae could induce a lesser amount of O2- production in comparison to that of Staphylococcus aureus and the enhancement of O2- release due to clofazimine was stimulus dependent. This increase of O2- release after addition of clofazimine was inhibited by the addition of p-bromophenacyl bromide. Another interesting finding was that the enhancement of O2- production by clofazimine gradually decreased as clofazimine was exposed to light for days. On further investigation it was found that ultraviolet, NMR, infrared and mass spectra of the light unexposed and exposed drug were similar, but the diffusion current of the polarogram of light exposed drug was remarkably more than that observed in light unexposed drug, indicating, thereby, a possible increase in the electron accepting capacity of the light reacted molecule. As far as we know this is the first report describing the effect of light exposed clofazimine on the respiratory burst activity of macrophages.

Animals↗
PubMed1991

Effects of various tachykinins on pituitary LH secretion, feeding, and sexual behavior in the rat.

Our investigations of the four tachykinines tested have shown that NPK characteristically evoked a spectrum of biological effects in male and female rats. NPK suppressed pituitary LH release by inhibiting the release of hypothalamic LHRH, presumably by activation of NK-2 tachykinin receptor subtypes. However, NPK may also act at the level of gonadotrophs to stimulate LH release in male rats. Central injection of NPK rapidly disrupted copulatory behavior in sexually active male rats. NPK also suppressed feeding, but, in this case, peripheral injections were more effective than central injections. Taken together, these observations strongly imply that NPK may be an inhibitory messenger molecule in the hypothalamic control of reproduction, sexual, and feeding behaviors.

Animals↗
PubMed1991

Sexual function and neuropeptide Y levels in selected brain regions in male spontaneously hypertensive rats.

Sexual function was examined in spontaneously hypertensive rats (SHR) from 8 to 20 wk of age and compared with normotensive Wistar-Kyoto (WKY) and Long-Evans rats (LE). Blood pressures (evaluated indirectly) were elevated in SHR (185 +/- 2 and 195 +/- 3 mmHg at 16 and 19 wk of age, respectively) relative to WKY and LE (135-144 mmHg). SHR exhibited good copulatory behavior but displayed fewer erections (less than 20% of the number displayed by WKY or LE) in ex copula tests. At the conclusion of the study (20 wk of age), body weights were lowest in SHR, intermediate in WKY, and greatest in LE. Relative weights of testes were greater in SHR, whereas relative weights of accessory organs, pituitary and adrenal glands, and kidneys were equivalent across strains, as were circulating levels of aldosterone. Circulating levels of testosterone were higher in SHR and WKY than in LE. Neuropeptide Y (NPY) levels in the median preoptic and arcuate nuclei were significantly greater in SHR than in WKY or LE, whereas NPY levels in the medial preoptic area and the suprachiasmatic, hypothalamic dorsomedial, and hypothalamic paraventricular nuclei were equivalent in SHR and WKY, with both greater than LE. No strain differences were evident in the medial nucleus of the amygdala, the bed nucleus of the stria terminalis, the median eminence, the anterior hypothalamic nucleus, or the hypothalamic dorsomedial nucleus.

Aldosterone↗
PubMed1990

Aging in male rats modifies castration and testosterone-induced neuropeptide Y response in various microdissected brain nuclei.

Neuropeptide Y (NPY) is localized in several hypothalamic sites which are implicated in the control of hypothalamic luteinizing hormone-releasing hormone (LHRH) and pituitary luteinizing hormone (LH) release. We have observed previously that in young rats castration decreases and testosterone (T) replacement restores NPY levels in selected hypothalamic sites. However, in aged male rats, NPY levels were decreased in all hypothalamic sites studied. Since testicular function is diminished in aged rats, we reasoned that decreased T feedback may be responsible for the reduction of NPY in the hypothalamus. Therefore, we compared the effects of castration and T-replacement on NPY levels in microdissected hypothalamic sites of 2.5-month- (young) and 15-month-old (aged) male rats. Serum LH and T levels were markedly reduced in aged as compared to those observed in young rats. In association with the decreased hormone levels, NPY levels were significantly reduced in each of the 7 hypothalamic sites of aged as compared to young rats. Further, in young rats, castration reduced and T-replacement prevented the castration-induced depletion in only 3 sites, viz. the ventromedial hypothalamic nucleus (VMN), arcuate nucleus (ARC) and median eminence (ME). In contrast, castration in aged rats reduced NPY levels not only in the VMN as in young rats, but also in the medial preoptic area (MPOA) and dorsomedial nucleus (DMN). However, the marked reduction in the ME and ARC NPY levels of young rats following castration was not observed in the ME and ARC of aged rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗