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      Involvement of Mesolimbic Structures in Short-Term Sodium Depletion: In situ Hybridization and Ligand-Binding Analyses

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          Acute treatment with the diuretic furosemide (Lasix) produces a reduction in plasma Na<sup>+</sup> and volume as well as increased thirst and salt appetite. The resulting hypovolemia stimulates the well-known counter-regulatory physiological response from the renin-angiotensin-aldosterone system. However, the neurochemical players underpinning the behavioral responses of thirst and salt appetite are less clear. Previously, we have reported that salt-replete deoxycorticosterone (DOCA) treatment activates mesolimbic structures associated with reward and goal-seeking behavior. The present study was designed to test whether the same brain regions are affected in a salt-depleted state. In experiment 1, two groups of adult male Sprague-Dawley (SD) rats were injected with Lasix (10 mg/rat, s.c.) and 18 h later were allowed access either to 2% NaCl solution (‘Lasix+salt’) or only to tap water (‘Lasixnosalt’) for 2 h. For comparison purposes, a third group received an isotonic saline injection instead of Lasix and was allowed access to the 2% salt solution (Vehicle). All groups were permitted 24 h access to tap water. We found no differences in dynorphin-mRNA levels in any striatal and accumbal regions among any of the treatment groups. However, as found previously in DOCA-treated rats, there were increased enkephalin (ENK)-mRNA and decreased dopamine transporter (DAT) binding levels throughout the striatum in Lasix+salt and decreased ENK-mRNA in Lasixnosalt rats versus Vehicle. In experiment 2, the involvement of the ENKergic and/or dopaminergic system was tested in rats divided into the same three groups described in experiment 1. However, before access to salt or water, the Lasix+salt and the vehicle groups were administered either a δ-opioid, naltrindole or a dopamine D<sub>2</sub> antagonist, raclopride. Only the naltrindole-treated rats showed a blunted intake of salt solution. Thus, these findings along with our neurochemical results suggest that mesolimbic enkephalin might impact salt intake through dopaminergic systems.

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          Most cited references 16

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          Neurotransmitter regulation of dopamine neurons in the ventral tegmental area

           Peter Kalivas (1993)
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            Role of the central nucleus of the amygdala and bed nucleus of the stria terminalis in experimentally-induced salt appetite.

            The contributions of the central nucleus of the amygdala (CeA) and the bed nucleus of the stria terminalis (BST) to salt appetite were evaluated with two treatments which induce sodium chloride (NaCl) ingestion. Cumulative 3 h intakes of 2% NaCl after sodium depletion using furosemide, or subcutaneous (s.c.) injections of yohimbine (YOH), were measured in male, Sprague-Dawley rats both before and after electrolytic lesions of the CeA or the BST. Before surgery, sham-lesion and lesion groups drank equivalent amounts of 2% NaCl in response to furosemide depletion and YOH treatment. After surgery, rats with sham lesions increased their intakes of 2% NaCl following YOH while rats with CeA or BST lesions showed significant decreases. Rats with CeA or BST lesions also showed significant decreases in their intake of 2% NaCl after furosemide depletion, while intakes of the sham lesion groups remained unchanged. Lesions of either nucleus virtually eliminated 24 h need-free salt intake. Before and after surgery, all groups drank equivalent amounts of water in response to s.c. angiotensin II and to s.c. hypertonic saline, indicating the lesions specifically affected salt appetite. The results indicate that the CeA and the BST may be important sites for processing inputs mediating salt appetite.
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              Plasmalemmal mu-opioid receptor distribution mainly in nondopaminergic neurons in the rat ventral tegmental area.

               V Pickel,  M Garzón (2001)
              Opiate-evoked reward and motivated behaviors reflect, in part, the enhanced release of dopamine produced by activation of the mu-opioid receptor (muOR) in the ventral tegmental area (VTA). We examined the functional sites for muOR activation and potential interactions with dopaminergic neurons within the rat VTA by using electron microscopy for the immunocytochemical localization of antipeptide antisera raised against muOR and tyrosine hydroxylase (TH), the synthesizing enzyme for catecholamines. The cellular and subcellular distribution of muOR was remarkably similar in the two major VTA subdivisions, the paranigral (VTApn) and parabrachial (VTApb) nuclei. In each region, somatodendritic profiles comprised over 50% of the labeled structures. MuOR immunolabeling was often seen at extrasynaptic/perisynaptic sites on dendritic plasma membranes, and 10% of these dendrites contained TH. MuOR-immunoreactivity was also localized to plasma membranes of axon terminals and small unmyelinated axons, none of which contained TH. The muOR-immunoreactive axon terminals formed either symmetric or asymmetric synapses that are typically associated with inhibitory and excitatory amino acid transmitters. Their targets included unlabeled (30%), muOR-labeled (25%), and TH-labeled (45%) dendrites. Our results suggest that muOR agonists in the VTA affect dopaminergic transmission mainly indirectly through changes in the postsynaptic responsivity and/or presynaptic release from neurons containing other neurotransmitters. They also indicate, however, that muOR agonists directly affect a small population of dopaminergic neurons expressing muOR on their dendrites in VTA and/or terminals in target regions. Copyright 2001 Wiley-Liss, Inc.

                Author and article information

                S. Karger AG
                June 2003
                08 July 2003
                : 77
                : 6
                : 406-415
                Laboratory of Neuroendocrinology, The Rockefeller University, New York, N.Y., USA
                71312 Neuroendocrinology 2003;77:406–415
                © 2003 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 2, References: 57, Pages: 10
                Stress and Central Neurotransmitters


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