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Galanin (GAL) is a neuropeptide composed of 29 to 30 amino acids, and its N-terminus and C-terminus are glycine and alanine residues, respectively. GAL is widely distributed in the central and peripheral nervous systems and participates in various biological functions such as feeding, pain, endocrine, neuroprotection, learning and memory, and sexual and reproductive. In particular, it is closely related to the pathogenesis of Alzheimer’s disease (AD), neuronal development and regeneration, and pain sensitivity caused by nerve damage. GAL also protects nerve cells. The galanin receptor (GalR), which is GalR1, GalR2, and GalR3, respectively, belongs to the G protein-coupled receptor. The galanin-message-associated peptide (GMAP) is a peptide consisting of 59 or 60 amino acid residues immediately following galanin in pre pro-galanin. It has only been found to have a role in spinal cord injury repair and has been less studied.
As an inhibitory tempering, galanin regulates neurotransmitter release through hyperpolarization. In depression, anxiety and stress response, galanin has important regulatory effects on NE and 5-HT neurons. Studies have shown that galanin inhibits the release of NE and 5-HT from neurons in the blue spot and dorsal raphe nucleus. In hippocampus and hypothalamic slices, galanin inhibits depolarization-induced glutamate release, hyperpolarizing post-synaptic neurons, and producing endogenous anticonvulsant effects. GalR1 activation of Gi/o protein also opens G protein-coupled inward-rectifying K+ channels and promotes mitogen-activated protein kinase (MAPK) activation. GalR2 promotes a variety of intracellular pathways by transmitting signals coupled to multiple types of G proteins. The GalR3 signal coupling mechanism is similar to GalR1.
The numerous physiological functions of galanin and GalR suggest that they play important roles in a variety of related diseases such as Alzheimer' disease, epilepsy, alcoholism, diabetes, neuropathic pain, depression, and cancer. GalR can be used as a new potential drug target, bringing new solutions to the treatment of these diseases. In patients with AD, a large number of cholinergic neurons were lost and galanin expression was up-regulated. Galanin stimulates cholinergic neurons and promotes the release of acetylcholine (ACTH) from all remaining cells in the brain of patients with AD.
References
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