Introduction of ADRA2B

The alpha-2B adrenergic receptor (ADRA2B), is a G-protein coupled receptor that in humans is encoded by the ADRA2B gene. ADRA2B is a subtype of the adrenergic receptor family and has been identified in several mammals. ADRA2B orthologs have been identified in several mammals. α2-adrenergic receptors have 3 highly homologous subtypes: α2A, α2B, and α2C, all of which is essential in regulating neurotransmitter release from sympathetic nerves and from adrenergic neurons in the central nervous system. The ADRA2B gene encodes the α2B subtype, which was observed to associate with eIF-2B, a guanine nucleotide exchange protein that functions in regulation of translation.

Function of ADRA2B Membrane Protein

Several diseases are associated with ADRA2B including Epilepsy, Familial Adult Myoclonic, and Benign Adult Familial Myoclonic Epilepsy. Among its related pathways are response to elevated platelet cytosolic Ca²⁺ and Monoamine GPCRs. A deletion variant of the α_2B adrenergic receptor has been shown to be associated with emotional memory. This variant also predisposed people who had it to focus more on negative aspects of a situation. The deletion variant of the ADRA2B gene is related to enhanced emotional memory and amygdala responses to emotional stimuli. It may increase susceptibility to post-traumatic stress disorder (PTSD) or related phenotypes by increasing the likelihood of traumatic memory formation. This tendency is still present in people who carry the variant gene and take a single dose of the noradrenergic antidepressant reboxetine but is attenuated in people without the variant.

Fig.1 Clinical uses of α₂-Adrenergic Agonists. (Beak, 2017)

Application of ADRA2B Membrane Protein in Literature

1. Zoladz PR., et al. ADRA2B deletion variant influences time-dependent effects of pre-learning stress on long-term memory. Neurobiol Learn Mem. 2017, 140: 71-81. PubMed ID: 28254464

Authors in this group investigated whether ADRA2B deletion variant influences time-dependent effects of pre-learning stress on long-term memory. The accumulating evidence regarding this ADRA2B genetic variant implicates it as a susceptibility factor for traumatic memory formation and PTSD-related phenotypes.

2. Wirz L., et al. A Deletion Variant of the α2b-Adrenoceptor Modulates the Stress-Induced Shift from "Cognitive" to "Habit" Memory. J Neurosci. 2017, 37(8): 2149-2160. PubMed ID: 28115477

The article reports that carriers exhibited a significantly reduced bias toward habit memory after stress compared with noncarriers of the ADRA2B deletion variant. The variant modulates the stress-induced shift from cognitive to habit memory.

3. Luhrs L., et al. Function of brain α_2B-adrenergic receptor characterized with subtype-selective α_2B antagonist and KO mice. Neuroscience. 2016, 339: 608-621. PubMed ID: 27751959

The results show that α_2B receptor is involved in CNS behaviors associated with sensorimotor gating and compulsivity. It may be therapeutically relevant for disorders such as schizophrenia, ADHD, post-traumatic stress disorder, addiction, and obsessive-compulsive disorder.

4. Mammarella N., et al. The modulating role of ADRA2B in emotional working memory: Attending the negative but remembering the positive. Neurobiol Learn Mem. 2016, 130: 129-34. PubMed ID: 26899992

Authors in this group investigated the role of ADRA2B in emotional working memory. The results show that deletion variants of ADRA2B may show greater levels of cognitive-affective flexibility compared to non-carriers.

5. Che P., et al. Spinophilin Is Indispensable for the α2B Adrenergic Receptor-Elicited Hypertensive Response. PLoS One. 2015, 10(8): e0135030. PubMed ID: 26244553

This article reveals that interaction with spinophilin is indispensable for the α2BAR to elicit the hypertensive response and spinophilin may represent a useful therapeutic target for treatment of hypertension.

ADRA2B Preparation Options

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Reference

1. Beak J, et al. (2017). An Oral Selective Alpha-1A Adrenergic Receptor Agonist Prevents Doxorubicin Cardiotoxicity. JACC Basic Transl Sci. 2(1), 39-53.

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