The galanin peptide family: Receptor pharmacology, pleiotropic biological actions, and implications in health and disease

Central nervous system regulation of food intake and energy expenditure: role of galanin-mediated feeding behavior

“…In mammals, acute injection of galanin or active fragments such as galanin (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16), into the PVN, lateral and ventromedial hypothalamic nuclei, and the central nucleus of the amygdala, significantly increases food intake and produces rapid increases in the feeding response and total caloric intake [4,5,11,12] . The effects of galanin on feeding be-…”

“…Galanin, a 29-amino-acid neuropeptide, is mainly distributed in central and peripheral nervous systems [6] . Currently, it is known that the galanin receptor subtypes include GalR1, GalR2 and GalR3, all of which are G protein-coupled receptors [7] and are distributed in the hypothalamus, amygdala, hippocampus, thalamus, brainstem, spinal cord and dorsal root ganglia [7][8][9] . Both GalR1 and GalR3 act through the Gi/o receptor, inhibiting adenyl cyclase and causing a decrease of cAMP [7,9] .…”

“…Currently, it is known that the galanin receptor subtypes include GalR1, GalR2 and GalR3, all of which are G protein-coupled receptors [7] and are distributed in the hypothalamus, amygdala, hippocampus, thalamus, brainstem, spinal cord and dorsal root ganglia [7][8][9] . Both GalR1 and GalR3 act through the Gi/o receptor, inhibiting adenyl cyclase and causing a decrease of cAMP [7,9] . Distinct from GalR1 and GalR3, the GalR2 subtype activates the stimulatory pathway of Gq/ 11 , resulting in the hydrolysis of inositol phosphate, activation of atypical protein kinase C, and an increase of intracellular Ca 2+ [7,10] .…”

“…Both GalR1 and GalR3 act through the Gi/o receptor, inhibiting adenyl cyclase and causing a decrease of cAMP [7,9] . Distinct from GalR1 and GalR3, the GalR2 subtype activates the stimulatory pathway of Gq/ 11 , resulting in the hydrolysis of inositol phosphate, activation of atypical protein kinase C, and an increase of intracellular Ca 2+ [7,10] .…”

Unraveling the biological mechanisms in Alzheimer's disease — Lessons from genomics

“…Subsequent replication studies have shown mixed results regarding confirmation of the identified loci, with GWA_14q32.13, TNK1 and GALP showing the strongest association. Galanine and galanine-like peptides (GALP) have been implicated in inhibition of long term potentiation in the hippocampus, as well in suppression of cholinergic neurotransmission (Lang et al, 2007), and have been shown to be overexpressed in 9 the AD brains. On the other hand, tyrosine kinase, non receptor 1 (TNK1) has been shown to enable tumor necrosis factor α induced necrosis, providing a possible mechanisms for increased neuronal death in AD patients.…”