Developmental and Diurnal Expression of the Synaptosomal-Associated Protein 25 (Snap25) in the Rat Pineal Gland

Abstract

Snap25 (synaptosomal-associated protein) is a 25 kDa protein, belonging to the SNARE-family (soluble N-ethylmaleimide-sensitive factor attachment protein receptors) of proteins, essential for synaptic and secretory vesicle exocytosis. Snap25 has by immunohistochemistry been demonstrated in the rat pineal gland but the biological importance of this is unknown. In this study, we demonstrate a high expression of mRNA encoding Snap25 in all parts of the rat pineal complex, the superficial-, and deep-pineal gland, as well as in the pineal stalk. Snap25 showed a low pineal expression during embryonic stages with a strong increase in expression levels just after birth. The expression showed no day/night variations. Neither removal of the sympathetic input to the pineal gland by superior cervical ganglionectomy nor bilateral decentralization of the superior cervical ganglia significantly affected the expression of Snap25 in the gland. The pineal expression levels of Snap25 were not changed following intraperitoneal injection of isoproterenol. The strong expression of Snap25 in the pineal gland suggests the presence of secretory granules and microvesicles in the rat pinealocyte supporting the concept of a vesicular release. At the transcriptional level, this Snap25-based release mechanism does not exhibit any diurnal rhythmicity and is regulated independently of the sympathetic nervous input to the gland.

Loss of Cervical Sympathetic Chain Input to the Superior Cervical Ganglia Affects the Ventilatory Responses to Hypoxic Challenge in Freely-Moving C57BL6 Mice

“…The morphology, neurophysiology and neuropharmacology of the mouse CSC-SCG has received considerable investigation over the years (Black et al, 1972;Yokota and Yamauchi, 1974;Banks and Walter, 1975;Inoue, 1975;Lewis and Burton, 1977;Forehand, 1985;Kidd and Heath, 1988;Gibbins, 1991;Kasa et al, 1991;Little and Heath, 1994;Jobling and Gibbins, 1999;El-Fadaly and Kummer, 2003;David et al, 2010;Cadaveira-Mosquera et al, 2012;Pashai et al, 2012;Alberola-Die et al, 2013;Liu and Bean, 2014;Martinez-Pinna et al, 2018;Mitsuoka et al, 2018;Feldman-Goriachnik and Hanani, 2019;Simeone et al, 2019;Rivas-Ramírez et al, 2020). Mouse tissues that receive post-ganglionic projections from the SCG have also been heavily investigated (Krieger et al, 1976;García et al, 1988;Kawaja and Crutcher, 1997;Maklad et al, 2001;Pankevich et al, 2003a,b;Ivanusic et al, 2013;Karlsen et al, 2013;Lindborg et al, 2018;Ziegler et al, 2018;Teshima et al, 2019). Nonetheless, there is no direct evidence that the CSC-SCG complex innervates the carotid bodies of mice, and this is likely on the basis of the presence of sympathetic (i.e., tyrosine-hydroxylase-positive) nerve terminals and adrenergic receptors in these structures (Prieto-Lloret et al, 2007;Roux et al, 2008;Kåhlin et al, 2010;…”

“…The effects of bilateral transection of the CSC (CSCX) or bilateral removal of the SCG (SCGX) have been investigated on a variety of physiological functions/variables in the mouse (Krieger et al, 1976;García et al, 1988;Kawaja and Crutcher, 1997;Pankevich et al, 2003a,b;Karlsen et al, 2013;Lindborg et al, 2018;Ziegler et al, 2018). However, to our knowledge, no studies, in any species, have determined the roles of the CSC-SCG complex on ventilatory functions and responses to hypoxic challenges in vivo.…”

GABAergic signaling in the rat pineal gland

“…Perhaps, the focus on melatonin release obscures other interesting actions. Rather than simple prevention of secretion, GABA may mediate more subtle fine tuning of NE release, adjusting timing and responsiveness of pinealocytes, or rather it may modulate the circadian activity of thyroid hormones by affecting the rhythmic expression of type II iodothyronine deiodinase , or it might modulate the secretion of peptides within the gland , or it might underlie even longer term remodeling of the gland with time of day and season.…”

SNAREs and developmental disorders

“…Null mutants of Drosophila SNAP25 die at the pharate adult stage and exhibit varying defects in synaptic transmission (Vilinsky et al, 2002). There are two SNAP25 splice isoforms in mammals, SNAP25A and SNAP25B, which differs in levels of expression during development and their localizations (Karlsen et al, 2013; Prescott & Chamberlain, 2011). SNAP25B's stronger postnatal expression (Bark et al, 1995) and its localization at the synaptic termini of central synapses and motor endplates (Yamamori et al, 2011) suggest that it is the major splice isoform mediating regulated SV exocytosis.…”