个人简介

B.S. – Biology, University of Montevallo; Ph.D., University of Alabama at Birmingham

研究领域

Adrenergic receptor biology & molecular pharmacology

Research in Cottingham's lab is aimed broadly at understanding the biological functions of adrenergic receptors (ARs), which belong to the G protein-coupled receptor (GPCR) superfamily of cell surface receptors. In mammalian organisms, including humans, the ARs mediate cellular responses to epinephrine and norepinephrine, important neurotransmitters and endocrine factors. We are also interested in the molecular pharmacology associated with the ARs. Put another way, Cottingham and his team are interested in understanding how drugs interact with and modify receptor function. Presently, the team's major effort is focused specifically on investigating a potential role for the alpha2A AR subtype in the biological mechanisms underlying antipsychotic-induced weight gain. Antipsychotic drugs are used in the clinical management of the debilitating psychiatric disorder known as schizophrenia, and are close molecular relatives of antidepressants, the team's previous drugs of interest. Many currently available antipsychotics cause dramatic metabolic side effects, including weight gain, in a significant subset of patients. Given the complex molecular interactions of these drugs with numerous receptors and other targets, it has been difficult to understand how antipsychotics drive these effects. Our goal, then, is to provide new biological and pharmacological insights into this unresolved problem. The goal of Cottingham's research is to contribute to the development of improved treatment strategies.

近期论文

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C. Cottingham, C. Ferryman, and Q. Wang. 2015. Alpha2 adrenergic receptor trafficking as a therapeutic target in antidepressant drug action. In Progress in Molecular Biology and Translational Science: Trafficking of GPCRs. G. Wu, Ed. Academic Press. [http://www.ncbi.nlm.nih.gov/pubmed/26055060] C. Cottingham, S. Percival, T. Birky, and Q. Wang. 2014. Tricyclic antidepressants exhibit variable pharmacological profiles at the alpha2A adrenergic receptor. Biochem Biophys Res Commun 451: 461-466. [http://www.ncbi.nlm.nih.gov/pubmed/25128275] C. Cottingham, R. Lu, K. Jiao, and Q. Wang. 2013. Cross-talk from beta adrenergic receptors modulates alpha2A adrenergic receptor endocytosis in sympathetic neurons via protein kinase A and spinophilin. J Biol Chem 288: 29193-29205. [http://www.ncbi.nlm.nih.gov/pubmed/23965992] C. Cottingham and Q. Wang. 2012. Alpha2 adrenergic receptor dysregulation in depressive disorders: implications for the neurobiology of depression and antidepressant therapy. Neurosci Biobehav Rev 36: 2214-2225. [http://www.ncbi.nlm.nih.gov/pubmed/22910678] C. Cottingham, A. Jones, and Q. Wang. 2012. Desipramine selectively potentiates norepinephrine-elicited ERK1/2 activation through the alpha2A adrenergic receptor. Biochem Biophys Res Commun 420: 161-165. [http://www.ncbi.nlm.nih.gov/pubmed/22405824] C. Cottingham, Y. Chen, K. Jiao, and Q. Wang. 2011. The antidepressant desipramine is an arrestin-biased ligand at the alpha2A adrenergic receptor driving receptor downregulation in vitro and in vivo. J Biol Chem 286: 36063-36075. [http://www.ncbi.nlm.nih.gov/pubmed/21859713]