Graduate Program in Neuroscience

Dianne Lattemann

lattemann-diannePhone: 206-768-5240
Dept.: VA Senior Research Career Scientist; Research Professor, Department of Psychiatry & Behavioral Sciences(VA); Adjunct, Department of Psychology; Adjunct, Medicine Concurrent
Neuroscience Focus Groups:
Lab Link:


My lab studies the modulation and regulation of CNS function by metabolic hormones (insulin, leptin) and metabolic status. One ongoing project involves the study (in rats) of midbrain dopamine neurons, which are implicated in drug addiction/abuse and in the ‘translation’ of information provided by normal stimuli into appropriate motor program responses. One such normal stimulus is food. Food restriction enhances the reinforcing property of several addictive drugs; and food as a rewarding stimulus normally activates midbrain dopamine neurons. We are investigating the reinforcing properties of food in models of diet-induced obesity and food restriction to determine how this attribute of food modifies the function of brain circuitry involved in the physiological regulation of food intake and body weight (see project description of Dr. Denis Baskin). Our experimental approaches range from the molecular to the behavioral as needed.

A second project of the lab is the investigation of altered CNS activity in a clinically important syndrome, hypoglycemia-associated autonomic failure (HAAF). This syndrome has been identified in diabetic patients who self-administer insulin frequently in order to maintain their blood sugar levels within the normal range. Because this is, at best, an imperfect approach to the regulation of blood sugar, patients experience numerous episodes of low blood sugar, or ‘hypoglycemia’. These frequent bouts lead to the loss of activation of the normal protective neuroendocrine response. We are investigating the hypothesis that CNS centers which regulate the activation of several arms of the neuroendocrine response (e.g., the adrenal medulla and the adrenal cortex) are vulnerable to the repeated bouts of low blood sugar and ultimately do not become appropriately activated. We have mapped forebrain activation in response to experimentally induced hypoglycemia (c-fos measurement) and identified areas which do not activate in response to multiple bouts of hypoglycemia. Current studies are now focusing on afferent inputs to these vulnerable CNS areas in order to elucidate specific mechanisms by which their activation is impaired.