1.Galanin microinjection into the dorsal periaqueductal gray matter produces paradigm-dependent anxiolytic effects.
Soares FR1, Silote GP1, Almeida-Santos AF2, Aguiar DC2, Schenberg LC1, Beijamini V3. Brain Res Bull. 2016 Mar;121:42-7. doi: 10.1016/j.brainresbull.2015.12.006. Epub 2016 Jan 2.
Galanin is a peptide that is present in the central nervous system in mammals, including rodents and humans. The actions of galanin are mediated by three types of metabotropic receptors: GAL1, GAL2, and GAL3. GAL1 and GAL3 increase K(+) efflux, and GAL2 increases intracellular Ca(2+) levels. The distribution of galanin and its receptors suggests its involvement in fear and/or anxiety. The periaqueductal gray matter (PAG) is a key mediator of defensive behaviors that is both targeted by galaninergic projections and supplied with GAL1 receptors and, less markedly, GAL2 receptors. We examined the effects of galanin microinjections in the dorsal PAG (dPAG) on the performance of rats in different models of anxiety. Male Wistar rats (n=7-12) were implanted with guide cannulae in the dPAG. They received microinjections of either galanin (0.3, 1.0, and 3.0nmol) or vehicle and were tested in the Vogel conflict test (VCT), elevated plus maze (EPM), and elevated T-maze (ETM).
2.Galanin and galanin-like peptide modulate vasopressin and oxytocin release in vitro: the role of galanin receptors.
Wodowska J1, Ciosek J2. Neuropeptides. 2014 Dec;48(6):387-97. doi: 10.1016/j.npep.2014.10.005. Epub 2014 Nov 10.
Galanin (Gal) and galanin-like peptide (GALP) may be involved in the mechanisms of the hypothalamo-neurohypophysial system. The aim of the present in vitro study was to compare the influence of Gal and GALP on vasopressin (AVP) and oxytocin (OT) release from isolated rat neurohypophysis (NH) or hypothalamo-neurohypophysial explants (Hth-NH). The effect of Gal/GALP on AVP/OT secretion was also studied in the presence of galantide, the non-selective galanin receptors antagonist. Gal at concentrations of 10(-10 )M and 10(-8 )M distinctly inhibited basal and K(+)-stimulated AVP release from the NH and Hth-NH explants, whereas Gal exerted a similar action on OT release only during basal incubation. Gal added to the incubation medium in the presence of galantide did not exert any action on the secretion of either neurohormone from NH and Hth-NH explants. GALP (10(-10 )M and 10(-9 )M) induced intensified basal AVP release from the NH and Hth-NH complex as well as the release of potassium-evoked AVP from the Hth-NH.
3.G protein-gated inwardly rectifying potassium channel subunits 1 and 2 are down-regulated in rat dorsal root ganglion neurons and spinal cord after peripheral axotomy.
Lyu C1,2, Mulder J3, Barde S4, Sahlholm K5, Zeberg H6, Nilsson J7, Århem P8, Hökfelt T9, Fried K10, Shi TJ11,12. Mol Pain. 2015 Jul 22;11:44. doi: 10.1186/s12990-015-0044-z.
BACKGROUND: Increased nociceptive neuronal excitability underlies chronic pain conditions. Various ion channels, including sodium, calcium and potassium channels have pivotal roles in the control of neuronal excitability. The members of the family of G protein-gated inwardly rectifying potassium (GIRK) channels, GIRK1-4, have been implicated in modulating excitability. Here, we investigated the expression and distribution of GIRK1 and GIRK2 in normal and injured dorsal root ganglia (DRGs) and spinal cord of rats.
4.Identifying neuropeptide Y (NPY) as the main stress-related substrate of dipeptidyl peptidase 4 (DPP4) in blood circulation.
Wagner L1, Kaestner F2, Wolf R3, Stiller H4, Heiser U5, Manhart S5, Hoffmann T6, Rahfeld JU7, Demuth HU7, Rothermundt M8, von Hörsten S9. Neuropeptides. 2016 Feb 27. pii: S0143-4179(16)30010-5. doi: 10.1016/j.npep.2016.02.007. [Epub ahead of print]
BACKGROUND: Dipeptidyl peptidase 4 (DPP4; EC 188.8.131.52; CD26) is a membrane-bound or shedded serine protease that hydrolyzes dipeptides from the N-terminus of peptides with either proline or alanine at the penultimate position. Substrates of DPP4 include several stress-related neuropeptides implicated in anxiety, depression and schizophrenia. A decline of DPP4-like activity has been reported in sera from depressed patient, but not fully characterized regarding DPP4-like enzymes, therapeutic interventions and protein.