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In the present study, the functional coupling of Gi/o protein-coupled receptors to GalR1, and the CB1 receptor subtype for endocannabinoids were analyzed in the 3xTg-AD mice model of Alzheimer's disease in the prodromal and advanced stages. In addition, the activity mediated by Gi/o protein-coupled M2/4 muscarinic receptor subtypes was also analyzed in brain areas involved in anxiety and cognition.
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Galanin, acting via the GAL1 receptor and Gi -coupled signalling in L and K cells, is a potent inhibitor of GLP-1 and GIP secretion
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endogenous Gal-1 may influence T. cruzi infection by fueling tolerogenic circuits that hinder anti-parasite immunity.
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Experiments with a GalR1-preffering galanin analog, NAX-5055, show that GalR1 is involved in regulating glucose and insulin homeostasis
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two different models of chronic pain requires a galanin receptor 1-triggered depression of excitatory synaptic transmission in indirect pathway nucleus accumbens medium spiny neurons.
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GalR1 expression is increased in the nucleus accumbens after chronic restraint stress.
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Galanin opposes the actions of morphine which leads to opiate dependence and withdrawal, an effect that is mediated via GalR1
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Galanin receptor 1 deletion exacerbates hippocampal neuronal loss after systemic kainate administration in mice
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Rotavirus infection of murine small intestine causes colonic secretion via age restricted galanin-1 receptor expression.
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Homozygous Galr1-/- mice are viable, capable of breeding, and exhibit no significant difference in growth rate. They have reduced circulating levels of insulin-like growth factor-I (IGF-I) and exhibit spontaneous tonic-clonic seizures.
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The distribution of galanin receptor 1 messenger RNA in the mouse brain is abundantly expressed in many brain regions, including numerous hypothalamic and other forebrain regions associated with neuroendocrine function.
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The duration of pain-like behaviours is significantly increased in mice lacking the galanin receptor 1 gene (Galr1-/-) after photochemically induced partial sciatic nerve ischemic injury.
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Galanin receptor 1 knockout mice show increased anxiety-like behavior on the elevated plus-maze test, a finding that is consistent with the hypothesis that galanin exerts anxiolytic actions via the GAL-R1 receptor.
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GAL-R1 knockout mice are unimpaired on a number of tests of learning and memory with the exception of the trace version of cued fear conditioning.
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GalR1 mediate galanin protection from seizures and seizure-induced hippocampal injury in Li-pilocarpine and perforant-path- stimulation models of limbic status epilepticus, but not under conditions of kainic acid-induced seizures.
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Increased levels of GalR1 mRNA and galanin binding (attributed to GalR1) in the external granule cell layer at P10-12/(14) coincide with granule cell migration from the external to the inner granule cell layer.
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Changes in levels of GalR1 may play an important role in modulating signaling events and neuroplasticity underlying physiological functions of the locus coeruleus.
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mice lacking the GALR1 receptor (Galr1-/-) exhibited only slight increase in heat nociception in the hot plate, but not tail flick, test and showed no increase in spinal sensitization
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GalR1 knockout mice showed no difference with respect to acute nociception, but showed a modest tendency towards increased hyperalgesia after tissue injury and inflammation
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Knockout mice deficient in the GAL-R1 receptor subtype were normal on most memory tasks, while showing a small deficit in trace cued fear conditioning
