Cellular localization of vasopressin V1a receptor messenger ribonucleic acid in adult male rat brain, pineal, and brain vasculature

Abstract

Vasopressin V1a receptor (V1aR) transcripts were localized in brain, pineal, and superficial brain vascular tissues of adult male rats using hybridization histochemistry and an [35S]riboprobe complementary to the messenger ribonucleic acid (mRNA) encoding the fifth to the midseventh transmembrane regions of the receptor. V1aR mRNA was extensively distributed throughout brain and was expressed in 1) superficial cells of the granule cell layers of the main olfactory bulb, hippocampal dentate gyrus, and cerebellum; 2) numerous anatomically distinct brain nuclei; 3) isolated cells dispersed throughout the central nervous system; 4) cells of the choroid plexus, occasional blood vessels in the olfactory bulb and interpeduncular nucleus, and extraparenchymal intracranial vasculature; and 5) some white matter structures. Numerous cells expressing V1aR transcripts were found in forebrain structures, including primary olfactory (piriform) cortex, the anterior and posterior olfactory nuclei; dorsal, intermediate, and ventral lateral septal nuclei; the septo-fimbrial nucleus and accumbens nucleus; and numerous hypothalamic regions with the most intense hypothalamic labeling in the arcuate, stigmoid, suprachiasmatic, and periventricular nuclei and the lateral hypothalamic area. Cells expressing V1aR transcripts were ubiquitous throughout the midbrain, pontine, and medullary regions. A lower intensity signal was found in cells of the parvocellular paraventricular and anteroventral nucleus of the thalamus, circumventricular organs including the pineal, and the subfornical organ. V1aR transcripts were not generally detected in parenchymal vasculature, but could be found over large blood vessels in the interpeduncular nucleus and medial olfactory bulb; transcripts were commonly detected in perivascular brain cells. V1aR mRNA was abundantly expressed by choroid plexus, endothelial cells of midline blood vessels between the main olfactory bulbs, and superficial vascular tissue on all brain surfaces. These data confirm the presence of the vascular/hepatic-type V1aR gene in brain tissue and document an extensive expression. The distribution of V1aR mRNA suggests that there are at least two types of vasopressin-responsive cells in brain: one type exemplified by lateral septal ara neurons innervated by classical axodendritic/somatic synaptic vasopressinergic terminals and a second, perivascular/vascular type that would facilitate humoral vasopressinergic signaling in the brain.

Vasopressin indirectly excites dorsal raphe serotonin neurons through activation of the vasopressin1A receptor

“…Although V 1A R activation is the predominant receptor (Ostrowski et al, 1992, Ostrowski et al, 1994), the source of AVP innervation differs greatly across brain regions (De Vries and Buijs, 1983, Rood et al, 2012). Innervation of the brainstem and spinal cord as well as the central amygdala comes primarily from the paraventricular nucleus (Sawchenko and Swanson, 1982, Rood et al, 2012), whereas innervation to the lateral septum and DR comes primarily from the extended amygdala (De Vries and Buijs, 1983, Rood et al, 2012).…”

Selective vasopressin-1a receptor antagonist prevents brain edema, reduces astrocytic cell swelling and GFAP, V1aR and AQP4 expression after focal traumatic brain injury

“…Subsequent evidence highlighted the link between increased GFAP and concomitant elevation of AQP4 and V1a receptors (V1aR) (Verkman, 2009) that may respond to injury-induced discharge of the hormone arginine vasopressin (AVP). V1aR are the predominant AVP receptor subtype in the CNS and are widely distributed in neurons, cortical astrocytes, and endothelial cells (Hernando et al, 2001, Landgraf, 1992, Ostrowski et al, 1994, Szmydynger-Chodobska et al, 2011, Szot et al, 1994). AVP is elevated in serum and cerebrospinal fluid (CSF) in humans following TBI (Huang et al, 2008, Kleindienst et al, 2010, Sorensen et al, 1985), and centrally released AVP may be instrumental in the development of brain edema (Cserr and Latzkovits, 1992, Landgraf, 1992).…”

Plasma Vasopressin, an Etiologic Factor of Motion Sickness in Rat and Human?

“…Further studies are obviously needed to clarify the underlying mechanisms, although the medulla oblongata, hypothalamus and thalamus are believed to play critical roles in MS, and are potential targets of AVP antagonists. AVP receptors have been detected in these areas [55,56,57]. …”