Biomedical subjects

Horacio E Romeo

Publications and source records attributed to Horacio E Romeo.

7 recordsLinked to original sources

PubMed2006

Site-specific estrogen and progestin regulation of orphanin FQ/nociceptin and nociceptin opioid receptor mRNA expression in the female rat limbic hypothalamic system.

The distributions of orphanin FQ (OFQ/N; also known as nociceptin) and its cognate receptor, opioid receptor-like receptor-1 (NOP), overlap steroid-responsive regions throughout reproductive circuits of the limbic system and hypothalamus. For example, in the ventromedial nucleus of the hypothalamus (VMH), OFQ/N facilitates lordosis in female rats through estrogen and progesterone regulation of nociceptin activity. We studied estrogen and progesterone regulation of OFQ/N and NOP mRNA expression in limbic-hypothalamic reproductive circuits. Ovariectomized rats were treated with 17beta-estradiol-benzoate (2 microg) and 26 hours later with oil or progesterone (500 microg) and were killed 30 hours after initial treatment. Alternate brain sections were processed for OFQ/N or NOP mRNA in situ hybridization. High levels of hybridization for NOP and OFQ/N and overlapping distributions were observed throughout the limbic hypothalamic reproductive circuits; however, in VMH, only NOP expression was observed. Estrogen treatment increased NOP mRNA expression in anteroventral periventricular nucleus (AVPV), median preoptic nucleus, and VMH. Subsequent progesterone treatment did not alter estrogen-induced expression of NOP mRNA in VMH or median preoptic nucleus but reduced expression in the AVPV. OFQ/N mRNA levels were also regulated by steroids. In the caudal part of the posterodorsal medial amygdala, estrogen increased OFQ/N mRNA levels, and progesterone did not alter this increase, whereas, in the medial part of the medial preoptic nucleus, estrogen and progesterone were needed to increase OFQ/N mRNA levels. Steroid regulation of OFQ/N and NOP in the medial preoptic nucleus and VMH is consistent with emerging data indicating that this opioid system regulates female reproduction.

Animals↗

PubMed2006

Differential effects of alcohol consumption and withdrawal on circadian temperature and activity rhythms in Sprague-Dawley, Lewis, and Fischer male and female rats.

BACKGROUND: Hypothalamic synthesis and secretion of corticotropin-releasing hormone (CRH), a putative mediator of various behavioral and physiological responses to ethanol (EtOH), is defective in inbred Lewis (LEW) rats in comparison with their genetically related inbred Fischer 344 (F344) and outbred Sprague-Dawley (S-D) strains. We aimed to characterize the effects of continuous EtOH consumption and withdrawal on circadian patterns of body temperature and spontaneous locomotor activity in males and females of these 3 strains. METHODS: Adult LEW, F344, and S-D males and randomly cycling females were fed an EtOH-containing liquid diet or the control (pair-fed or lab chow and water) diet for 14 days. Biotelemetric body temperature data for the last 3 days of EtOH diet feeding and the first 3 days of withdrawal were subjected to cosinor analysis of the circadian rhythm parameters of midline-estimating statistic of rhythm (MESOR), amplitude, and acrophase. Mean dark-phase activity during these periods was also computed. RESULTS: In the control diet condition, the MESORs and amplitudes of LEW males were lower than those of F344 males. MESORs of rhythms of LEW females were lower than those of both F344 and S-D females. Ethanol consumption caused hypothermia with reduced MESORs and amplitudes of LEW and F344 males and amplitudes of F344 and S-D females. Upon withdrawal, MESORs of the males increased during each day as the amplitudes decreased, reflective of their initial withdrawal-induced dark-phase hypothermia, which was most pronounced in the LEW males, followed by light-phase hyperthermia. MESORs of females were not affected by withdrawal; their amplitudes were differentially affected. Acrophase of LEW males shifted from dark to light on the first day of withdrawal. All rats responded to EtOH exposure with a reduction of dark-phase spontaneous locomotor activity and an immediate increase upon withdrawal. CONCLUSIONS: Body temperature rhythms of the males were generally more affected by EtOH consumption and withdrawal than the females; within each sex, LEW and F344 rats differed significantly. The specific hormonal factors that mediate the differential temperature responses remain to be defined.

Animals↗

PubMed2005

The febrile response to intraperitoneal lipopolysaccharide: strain and gender differences in rats.

The acute-phase febrile responses of the inbred Lewis (LEW) and Fischer 344 (F344) rat strains and their parent Sprague-Dawley (S-D) strain to immune challenge with lipopolysaccharide (LPS) were compared. LEW and S-D males and females displayed a biphasic febrile response with a markedly attenuated second phase in F344 rats. At 2 h after LPS (50 microg/kg), corticosterone was significantly higher in F344 than in LEW rats, but serum interleukin-1beta was higher only in F344 than LEW males. These data suggest that the greater LPS-induced corticosterone response of F344 rats mediates differences between febrile responses of F344 and LEW males and females.

Analysis of Variance↗

PubMed2003

Effects of glossopharyngeal nerve transection on central and peripheral cytokines and serum corticosterone induced by localized inflammation.

Bilateral transection of the glossopharyngeal nerves (GLOx) disrupts the immune-to-brain communication from the posterior oral cavity. The current report tested whether this effect is due to the afferent (sensory) or efferent (parasympathetic motor) components of the nerve. Injection of lipopolysaccharide (LPS) into the soft palate (ISP) of GLOx or sham-operated (SHAM) rats increased the circulating levels of interleukin-1beta (IL-1beta), interleukin-1 receptor antagonist (IL-1ra) and corticosterone (CORT), as well the hypothalamic content of IL-1beta; no difference in circulating levels and hypothalamic content was found between GLOx and SHAM at 2 and 4.5 h after LPS injection. These results indicate that glossopharyngeal neural efferents do not mediate the effects of GLOx on the immune-to-brain communication.

Afferent Pathways↗

PubMed2002

Site-specific decrease of progesterone receptor mRNA expression in the hypothalamus of middle-aged persistently estrus rats.

Middle-aged females gradually become acyclic and spontaneously develop a persistently estrus (PE) state. PE rats, acyclic for 30 days (early PE), are unresponsive to the positive feedback action of estrogen, but respond to a progesterone challenge with a luteinizing hormone (LH) surge and ovulation; unlike long-term PE rats, acyclic for 90 days, neither estrogen nor estrogen plus progesterone will elicit an LH surge [10th International Congress of Endocrinology, San Francisco, P3 (1996) 1061]. We hypothesize that the PE state may develop due to a diminished level of estrogen-induced progesterone receptor (PR) expression in the hypothalamus that prevents progesterone from stimulating LH regulating circuits. To test this hypothesis, PR mRNA levels were measured in hypothalamic regions of young, proestrus (2-3 months of age), early PE (10-12 months) and long-term PE (13-15 months) rats. The anteroventral periventricular nucleus (AVPV), an important regulatory site of the LH surge, had decreased PR mRNA levels in early and long-term PE rats compared with proestrus rats. However, PR mRNA levels were reduced only in long-term PE rats in the ventromedial nucleus (VMH) and arcuate nucleus (ARH). In the medial preoptic nucleus (MPN), levels of PR mRNA did not change. A previous report showed that exogenous progesterone stimulates an LH surge in young and early PE animals, indicating that the expression of PR mRNA demonstrated in this study is sufficient to mediate progesterone facilitation of the LH surge in early PE rats. In acyclic, long-term PE rats, diminished estrogen-induced expression of progesterone receptors is correlated with a previously shown inability to respond to exogenous progesterone.

Aging↗

PubMed2002

Alcohol consumption in traumatic brain injury: attenuation of TBI-induced hyperthermia and neurocognitive deficits.

Clinical and animal studies indicate that hyperthermia during or after traumatic brain injury (TBI) is associated with poor outcome. Alcohol intoxication, a complicating risk factor in many cases of head injury, has been found to both worsen or attenuate posttraumatic neural damage and outcome. The purpose of the present study was to determine whether chronic ethanol consumption would affect TBI-induced hyperthermia and deficits in spatial learning. TBI was produced by cortical contusion injury in adult male rats. We first characterized the TBI-induced febrile response using probes implanted intraperitoneally (ip) or intracerebroventricularly for continuous biotelemetric recording of core body and brain temperatures and locomotor activity. In another experiment, rats, implanted with ip probes, were fed a liquid diet containing ethanol (5% w/v, 35% ethanol-derived calories); control rats were pair-fed the isocaloric liquid diet (P-P). At 14 days after commencement of diet feeding, TBI or sham surgery was performed, and the ethanol-fed rats were divided into two groups: half were transferred to the isocaloric diet (E-P) and the other half remained on the ethanol-containing diet (E-E). TBI produced a significant febrile response in all rats, that persisted for at least 6 days in the E-P and P-P groups but lasted for only 2 days in the E-E group. When tested at 3-4 weeks after TBI, E-E rats required significantly fewer trials than E-P rats to reach criterion in the Morris water maze. In sum, continuous consumption of ethanol before and after TBI attenuated TBI-induced hyperthermia and deficits in spatial learning. Whereas the results suggest that this ethanol regimen may be neuroprotective, a causal relationship between the two outcomes remains to be determined.

Alcohol Drinking↗

PubMed2002

Maternal adrenalectomy abrogates the effect of fetal alcohol exposure on the interleukin-1beta-induced febrile response: gender differences.

Fetal alcohol exposure (FAE) has been shown to blunt the febrile component of the primary host-defense response to infection induced experimentally by systemic administration of interleukin (IL)-1beta. Given that maternal adrenalectomy (ADX) can prevent various postnatal effects of FAE, the present experiments were designed to determine whether maternal ADX would prevent the blunted IL-1beta-induced febrile response of fetal alcohol-exposed offspring and whether the effects of maternal ADX would be gender related. Timed-pregnant rats underwent ADX or were sham-operated on gestation day (GD) 7, or remained intact (without any surgery), and were fed ethanol-containing (E) or pair-fed (PF) liquid diets or normal (N) rat chow and water from GD 8 to GD 21. As adults, male and female E, PF and N offspring were injected with saline on day 1 and with IL-1beta (2 microg/kg, i.p.) on day 2 at 09.00 h and the body temperature was recorded biotelemetrically for 8.5 h. IL-1beta produced significantly lower febrile responses in female than in male offspring of intact dams, irrespective of prenatal diet. Furthermore, prenatal surgical stress differentially affected the IL-1beta-induced febrile response of male and female normally fed offspring. Additionally, in both male and female offspring of intact dams, FAE significantly attenuated the IL-1beta-induced febrile response. In males, FAE also attenuated the febrile response in the offspring of maternal sham-operated dams, and this effect was completely reversed by maternal ADX. In females, both maternal sham surgery and ADX reversed the effect of FAE on the febrile response. These findings suggest that maternal adrenal mediators are essential for the long-term effect of FAE on the febrile response in male offspring. In females, early prenatal surgical stress is sufficient to reverse the effects of FAE, possibly via adrenal-independent mechanisms that affect the thermoregulatory system.

Adrenalectomy↗