Galanin Human


  • Description

  • Application Data


Galanin is a neuropeptide released by the locus coeruleus with neuroprotective properties and a major role in appetite regulation.

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Application Data

Catalogue number crb1000200
Molecular Weight 3157.41
Sequence (one letter code)


Sequence (three letter code)


Purity >95%
cas 119418-04-1

Weinshenker and Holmes (2016) Regulation of neurological and neuropsychiatric phenotypes by locus coeruleus-derived galanin. Brain Res. 1641 320.

Laque et al (2013) Leptin receptor neurons in the mouse hypothalamus are colocalized with the neuropeptide galanin and mediate anorexigenic leptin action. Am. J. Physiol-Endocrinol. Metab. 304(9) E999-E1011

Manufactured in: United Kingdom
Data Sheet Material Safety Data Sheet (MSDS)

Galanin is a neuropeptide synthesised and released by the brainstem locus coeruleus (LC). Galanin is expressed in most LC neurons in rodents and humans. Galanin has been shown to inhibit LC activity by hyperpolarising LC neurons, suppressing their spontaneous firing rate, and enhancing α2-adrenergic receptor-mediated negative feedback. Galanin is also a potent trophic and neuroprotective factor throughout the nervous system.

Galanin is widely distributed from the central nervous system, peripheral regions and endocrine system. Galanin’s overarching function is as an inhibitory, hyper-polarizing neuromodulator for classical neurotransmitters like acetylcholine and serotonin. Galanin interacts with 3 receptor subtypes GalR1-3 which are G protein-coupled receptors and are inserted into the plasma membrane. GalR1 is believed to activate a Gβγ pathway to regulate MAPK activation. GalR2 can also activate the MAPK pathway but unlike GalR1 there is detectable inositol phosphate production. GalR3 is associated with the Gαi/o pathway, activation of the receptor leads to cellular influx of K+. Each receptor has been associated with neurological diseases such as GalR3 and epilepsy.

Galanin protects against a variety of physiological insults in vitro, including excitotoxicity and β-amyloid toxicity. Changes in galanin have been widely studied in relation to Alzheimer’s disease and galaninergic neurons have been shown to be spared in late-stage Alzheimer’s relative to non-galaninergic neurones.

Galanin Human

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