Matthew Kirchner, PhD

Education and Training

• College of Wooster, Neuroscience and Philosophy, BA, 2013
• University of Tennessee Health Science Center, Neuroscience, PhD, 2018
• Georgia State University, Neurophysiology, Postdoctoral Fellow, 2018-2025

Research Interests

• My primary research interest is the neurophysiology of oxytocin (OT) and vasopressin (VP) magnocellular neurons in the supraoptic nucleus. These neurons are the final link in a chain of central neuroendocrine information processing, projecting their axons to the posterior pituitary where they release OT/VP into the bloodstream for action at peripheral targets. These neuropeptides maintain hydromineral balance critical for survival. My focus is on the mechanisms underlying these neurons’ intrinsic excitability, specifically the calcium-dependent potassium channels that generate afterhyperpolarization (AHP) currents, which hyperpolarize the neuron during spiking. The slow component (sAHP) is of particular interest as its explicit channel identity remains elusive. My lab studies these mechanisms using simultaneous whole cell patch clamp and live calcium imaging in an acute rat brain slice preparation.
• A unique feature of the OT/VP magnocellular neurons is that they have the ability release their respective peptides at soma and dendrites in addition to classic axonal release. This somatodendritic release (SDR) coordinates population activity within the supraoptic and paraventricular nuclei of hypothalamus, acting independently of axonal release. Much is unknown about the underlying mechanisms. My lab studies SDR and its potential involvement in AHP modulation.
• The lab also has a high interest in heart failure (HF), a progressive disease marked by increased circulating VP and hyperexcitable VP neurons. Interestingly, VP neurons in HF rats exhibit abolished AHPs, indicating that this hyperexcitability is underlain in part by a lack of inhibitory intrinsic excitability mechanisms. Though this is initially a compensatory mechanism to maintain blood volume, chronic VP activation causes excessive water retention in the kidneys, leading to hyponatremia and contributing to progression of the disease. Our lab studies how VP neurons change during HF, focusing on intrinsic excitability and SDR. Understanding the mechanisms that underly the disease may help improve therapeutics for these patients.

Teaching Interests

• Cellular Neuroscience
• Endocrinology