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Shane T. Hentges, PhD

Associate Professor
Department of Biomedical Sciences
Colorado State University
Fort Collins, CO 80523

Phone: 970-491-5086
Fax: 970-491-7907
Email: Shane.Hentges@colostate.edu

Member
Program in Molecular, Cellular and Integrative Neurosciences

Education
PhD, Washington State University

ST Hentges PubMed

Picture of Dr. Hentges

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Research Interests

The regulation of energy balance is a complex physiologic process. At the level of the central nervous system, food intake and energy metabolism are regulated by extensive neural networks using a variety of transmitters. To understand how energy balance is coordinated in this complex neuronal circuitry, a detailed understanding of the cellular physiology of each type of neuron involved is necessary. My lab studies how neurons in the hypothalamus are regulated and how these neurons communicate synaptically with each other as well as other neurons in the larger neural networks that affect energy balance.

Current studies in this lab are primarily focused on the proopiomelanocortin neurons in the arcuate nucleus of the hypothalamus. These neurons play a critical role in maintaining energy balance through the release of the peptide alpha-MSH and affect aspects of food reward through the release of the endogenous opioid beta-endorphin. These neurons also release classical neurotransmitters and endogenous cannabinoids (cell-derived lipids that act at the same receptors as the active compound in marijuana). We are currently working to determine what the release of these transmitters means in terms of food intake and the regulation of downstream neurons.

Proopiomelanocortin neurons express opioid and cannabinoid receptors and receive synaptic input from other neurons that also express these receptors. This provides a great system for us to study the release of endocannabinoids, retrograde inhibition, and both presynaptic and postsynaptic actions at the mu opioid receptor. Thus, we can learn about synaptic regulation, G-protein coupled receptor signaling and cellular physiology while working towards a better understanding of the circuits that regulate food intake and reward. The primary methods used in the lab are patch clamp electrophysiology in brain slices and primary neuronal cell cultures, retrograde labeling by sterotaxic microinjection, immunofluorescence and confocal imaging. Transgenic and knock-out mice are used routinely for our studies.


Teaching Interests

I coordinate and teach a significant portion of BMS325 - Cellular Neurobiology. I have previously taught in a graduate level systems neuroscience course and give occasional lectures in other graduate and undergraduate courses. My teaching activities outside of formal lectures are primarily in training undergraduate and graduate students in the laboratory.


Representative Publications

Pennock RL, Dicken MS, Hentges ST. 2012. Multiple inhibitory G-protein-coupled receptors resist acute desensitization in the presynaptic but not postsynaptic compartments of neurons. J Neurosci 32:10192-10200 http://www.ncbi.nlm.nih.gov/pubmed/22836254.

Jarvie BC, Hentges ST. 2012. Expression of GABAergic and glutamatergic phenotypic markers in hypothalamic proopiomelanocortin neurons. J Comp Neurol 527:3863-3872 http://www.ncbi.nlm.nih.gov/pubmed/22522889.

Dicken MS, Tooker RE, Hentges ST. 2012. Regulation of GABA and glutamate release from proopiomelanocortin neuron terminals in intact hypothalamic networks. J Neurosci 32:4042-4048 http://www.ncbi.nlm.nih.gov/pubmed/22442070.

King CM, Hentges ST. 2011. Relative number and distribution of murine hypothalamic proopiomelanocortin neurons innervating distinct target sites. PLoS ONE 6:e25864 http://www.ncbi.nlm.nih.gov/pubmed/21991375.

Pennock RL, Hentges ST. 2011. Differential expression and sensitivity of pre- and postsynaptic opioid receptors regulating hypothalamic proopiomelanocortin neurons. J Neurosci 31:281-288 http://www.ncbi.nlm.nih.gov/pubmed/21209213.

Hentges ST, Otero-Corchon V, Pennock RL, King CM, Low MJ. 2009. Proopiomelanocortin expression in both GABA and glutamate neurons. J Neurosci 29:13684-13690 http://www.ncbi.nlm.nih.gov/pubmed/19864580.