The present experiments sought to identify the physiological signals that inhibit thirst when dehydrated rats drink water or NaCl solution. Rats were deprived of drinking fluid but not food overnight. When allowed to drink again, the dehydrated animals consumed water or saline (0.05 M, 0.10 M, 0.15 M, or 0.20 M NaCl solution) almost continuously for 5-8 min before stopping. The volumes consumed were similar regardless of which fluid they ingested, but blood analyses indicated that increased plasma osmolality and decreased plasma volume, or both, still remained when drinking terminated. These results suggest that the composition of the ingested fluid is less significant than its volume in providing an early signal that inhibits thirst and fluid consumption by dehydrated rats. Analyses of the gastrointestinal tracts revealed that the cumulative volume in the stomach and small intestine correlated highly with the amount consumed regardless of which fluid was ingested. These and other results suggest that the volume of fluid ingested by dehydrated rats is sensed by stretch receptors detecting distension of the stomach and small intestine, which provide an early inhibitory stimulus of thirst. dehydration; gastrointestinal distension; visceral osmoreceptors; water deprivation WATER DEPRIVATION ELICITS thirst and secretion of neurohypophyseal vasopressin (VP), the antidiuretic hormone, in rats and other animals (31). When dehydrated animals drink water, both responses are inhibited before systemic rehydration is evident. In dogs and human subjects, the early signal that inhibits thirst and VP secretion has been related to the volume of fluid consumed, apparently detected by oropharyngeal receptors that monitor the swallowing of liquids regardless of whether water, isotonic saline, or hypertonic saline solution is consumed (2,13,24,32). However, recent experiments indicate that early inhibition of VP secretion in rats is not mediated by oropharyngeal receptors (17, 29) because plasma VP levels (pVP) were not affected either when dehydrated rats ingested isotonic saline or when water was consumed but drained from the stomach through an open gastric fistula (29). In contrast, water ingested normally by thirsty rats initiated a rapid decline in pVP that began while systemic plasma Na ϩ concentrations (pNa) still were elevated (17, 29), suggesting that the inhibitory effect was not mediated by cerebral osmoreceptors but by a potent presystemic stimulus, related to the composition of ingested fluid, which might arise from osmoreceptors or Na ϩ receptors in the viscera (4, 19). Furthermore, the signal that terminated an initial bout of water consumption occurred a few minutes later, in association with a reduction of systemic pNa but continued plasma volume deficits (29). Because the intake of isotonic saline also ceased after similar volumes were consumed, without any associated change in pNa (29), these observations allow the hypothesis that thirst in rats is inhibited by signals related to the volume of ingested fluid rath...

High strength static magnetic fields are thought to be benign and largely undetectable by mammals. As magnetic resonance imaging (MRI) machines increase in strength, however, potential aversive effects may become clinically relevant. Here we report that rats find entry into a 14.1 T magnet aversive, and that they can detect and avoid entry into the magnet at a point where the magnetic field is 2 T or lower. Rats were trained to climb a ladder through the bore of a 14.1 T superconducting magnet. After their first climb into 14.1 T, most rats refused to re-enter the magnet or climb past the 2 T field line. This result was confirmed in a resistive magnet in which the magnetic field was varied from 1 to 14 T. Detection and avoidance required the vestibular apparatus of the inner ear, because labyrinthectomized rats readily traversed the magnet. The inner ear is a novel site for magnetic field transduction in mammals, but perturbation of the vestibular apparatus would be consistent with human reports of vertigo and nausea around high strength MRI machines.

Advances in magnetic resonance imaging are driving the development of higher-resolution machines equipped with high-strength static magnetic fields (MFs). The behavioral effects of high-strength MFs are largely uncharacterized, although in male rats, exposure to 7 T or above induces locomotor circling and leads to a conditioned taste avoidance (CTA) if paired with a novel taste. Here, the effects of MFs on male and female rats were compared to determine whether there are sex differences in behavioral responses and whether these can be explained by ovarian steroid status. Rats were given 10-min access to a novel saccharin solution and then restrained within a 14-T magnet for 30 min. Locomotor activity after exposure was scored for circling and rearing. CTA extinction was measured with two-bottle preference tests. In experiment 1, males were compared with females across the estrous cycle after a single MF exposure. Females circled more and acquired a more persistent CTA than males; circling was highest on the day of estrus. In experiment 2, the effects of three MF exposures were compared among intact rats, ovariectomized females, and ovariectomized females with steroid replacement. Compared with intact rats, ovariectomy increased circling; estrogen replacement blocked the increase. Males acquired a stronger initial CTA but extinguished faster than intact or ovariectomized females. Thus the locomotor circling induced by MF exposure was increased in females and modulated by ovarian steroids across the estrous cycle and by hormone replacement. Furthermore, female rats acquired a more persistent CTA than male rats, which was not dependent on estrous phase or endogenous ovarian steroids.

Exposure of rats to high strength static magnetic fields of 7 T or above has behavioral effects such as the induction of locomotor circling, the suppression of rearing, and the acquisition of conditioned taste aversion (CTA). To determine if habituation occurs across magnetic field exposures, rats were pre-exposed two times to a 14 T static magnetic field for 30 min on two consecutive days; on the third day, rats were given access to a novel 0.125% saccharin prior to a third 30-min exposure to the 14 T magnetic field. Compared to sham-exposed rats, pre-exposed rats showed less locomotor circling and an attenuated CTA. Rearing was suppressed in all magnet-exposed groups regardless of pre-exposure, suggesting that the suppression of rearing is more sensitive than other behavioral responses to magnet exposure. Habituation was also observed when rats under went pre-exposures at 2-3 hour intervals on a single day. Components of the habituation were also long lasting; a diminished circling response was observed when rats were exposed to magnetic field 36 days after 2 pre-exposures. To control for possible effects of unconditioned stimulus pre-exposure, rats were also tested in a similar experimental design with two injections of LiCl prior to the pairing of saccharin with a third injection of LiCl. Pre-exposure to LiCl did not attenuate the LiCl-induced CTA, suggesting that 2 pre-exposures to an unconditioned stimulus are not sufficient to explain the habituation to magnet exposure. Because the effects of magnetic field exposure are dependent on an intact vestibular apparatus, and because the vestibular system can habituate to many forms of perturbation, habituation to magnetic field exposure is consistent with mediation of magnetic field effects by the vestibular system.

The pontine parabrachial nucleus (PBN) has been implicated in the modulation of ingestion and contains high levels of μ-opioid receptors (MOPRs). In previous work, stimulating MOPRs by infusing the highly selective MOPR agonist enkephalin (DAMGO) into the lateral parabrachial region (LPBN) increased food intake. The highly selective MOPR antagonist d-Phe-Cys-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) prevented the hyperphagic action of DAMGO.The present experiments aimed to analyze both the pattern of neural activation and the underlying cellular processes associated with MOPR activation in the LPBN. Male SpragueDawley rats received a unilateral microinfusion of a nearly maximal hyperphagic dose of DAMGO into the LPBN. We then determined the level of c-Fos immunoreactivity in regions throughout the brain. MOPR activation in the LPBN increased c-Fos in the LPBN and in the nucleus accumbens, hypothalamic arcuate nucleus, paraventricular nucleus of the thalamus and hippocampus. Pretreatment with CTAP prevented the increase in c-Fos translation in each of these areas. CTAP also prevented the coupling of MOPRs to their G-proteins which was measured by [ 35 S]GTPγS autoradiography. Together, these data strongly suggest that increasing the coupling of MOPRs to their G-proteins in the LPBN disinhibits parabrachial neurons which subsequently leads to excitation of neurons in regions associated with caloric regulation, ingestive reward and cognitive processes in feeding. Keywordsobesity; brainstem; nucleus accumbens; arcuate nucleus; hippocampus; paraventricular nucleus of the thalamus Numerous studies have examined the role of μ-opioid receptors (MOPRs) in the neural control of feeding behavior. Opioid receptor ligands have been administered centrally into multiple brain regions such as the nucleus tractus solitarius (NTS), parabrachial nucleus (PBN), hypothalamus, amygdala, ventral tegmental area (VTA) and nucleus accumbens (NAcc), in rats (Carr et al., 1991, Kotz et al., 1997, Giraudo et al., 1998b, Lamonte et al., © 2009 IBRO. Published by Elsevier Ltd. All rights reserved.Corresponding Author: Kenny J. Simansky PhD, 245 N 15 th St, 19 th floor MS 400, Philadelphia, PA 19102, Phone: (215) Fax: (215)762-2299, kenny.simansky@drexelmed.edu. Section Editor: Dr. Geoffrey Schoenbaum, University of Maryland School of Medicine, Department of Anatomy and Neurobiology, 655 W. Baltimore Street, Baltimore, MD 21201, USA Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2012 July 8. 2002, MacDonald et al., 2...