Ph.D., University of California, Irvine, 1993 Associate Professor Director of Graduate Studies mbparent@gsu.edu 204F Kell Hall 404-413-6286

Current Research Interests

My research program is aimed at understanding how chemical reactions in the brain contribute to memory and memory dysfunction. My main experimental subject is the laboratory rat, and for comparative purposes I also examine memory in monkeys and humans. My lab members and I combine a variety of techniques (biochemistry and molecular biology, systemic and intracranial drug infusions, in vivo microdialysis, high performance liquid chromatography, permanent and reversible lesions, and behavioral measures of learning and memory) to ask the following questions regarding the neurobiology of memory:

How does diet influence brain and behavior?

We are very excited about a new line of research in my laboratory examining the effects of a high fructose diet on brain and behavior.  Over the past 30 years, there has been an alarming increase in the consumption of fructose from sweeteners in the North American diet.  In humans and rodents, extensive intake of fructose is associated with a variety of pathological changes, including insulin insensitivity, obesity, cardiovascular disease, and type II diabetes. In rodents, some of the pathological changes are observed as soon as two weeks after consumption of a high fructose diet.  The findings of a study conducted by our collaborator demonstrated for the first time that the damaging effects of a high fructose diet extend to the brain.  Specifically, fructose feeding produces hippocampal insulin resistance and impairs hippocampal synaptic plasticity in hamsters. We recently determined that a high fructose diet impairs spatial water maze memory and will present those data at the 2007 Society for Neuroscience meeting. We are currently investigating whether these deficits may result from impaired insulin signaling in the hippocampus.

How do the medial septum and hippocampus interact in memory?

In another line of research, my lab members and I are investigating how chemical communication between two neural regions, the medial septum and the hippocampus, influences memory. Our findings show that neurochemical interactions between the septum and hippocampus during memory can be directly and effectively investigated by combining behavioral tests of learning and memory with simultaneous drug injections into both regions. We have shown, for example, that the effects of drugs injected into the medial septum on memory are often prevented by simultaneous infusions of other drugs into the hippocampus (Parent et al., 1997; Degroot& Parent, 2000, 2001, Krebs & Parent, 2005ab). These findings support the possibility that neurotransmitters in the septum influence memory, in part, by influencing the hippocampus. We have also combined in vivo microdialysis with site-specific drug injections and found that infusions of drugs into the medial septum influence a variety of neurotransmitters in the hippocampus (Degroot et al., 2003, Parent et al, in preparation). Recently, we initiated projects aimed at characterizing the specific projections between the two regions that contribute to these interactions.

What are the neurochemical and behavioral effects of hyperglycemia?

We are also investigating the neurochemical mechanisms that underlie the memory-enhancing and –impairing effects of glucose. Our research indicates that glucose does not affect memory through a non-specific mechanism, such as hyperosmolarity (Shah & Parent, 2003, 2004). Rather, glucose appears to enhance or impair memory through interactions with specific neurotransmitters in different brain regions. For example, we have shown that elevating glucose in the septum creates memory deficits when septal GABA receptors are activated (Parent et al. 1997; Parent & Gold, 1997; Shah & Parent, 2003; Erickson, Watts, & Parent, 2006). In contrast, elevating glucose in the hippocampus prevents memory deficits (Parent et al., 1997; Krebs & Parent, 2005a, 2007), and this enhancing effect of glucose appears to be mediated, at least in part through an interaction with the neurotransmitter acetylcholine (Degroot et al., 2003; Parent & Baxter, 2004).

Comparative Research

We are currently examining the effects of glucose administration on cognitive performance in monkeys (rhesus macaque).  We have conducted studies to determine whether findings observed in rodents can be extended to humans.  For instance, Evidence from studies of rodent memory suggests that glucose may be part of the biochemical mechanism that allows emotion to enhance memory. This led us to  examine the contributions of glucose to emotional memory in humans. If glucose contributes to the memory-enhancing effects of emotion, then stimuli that are considered emotional and that enhance memory should increase blood glucose levels. Indeed, we have shown that blood glucose levels increase after subjects hear an emotional story, but do not change in subjects who hear a neutral story (Parent, Varnhagen, & Gold, 1999). As in rodents, this increase in blood glucose is correlated with enhanced memory of the emotional information. We later replicated these findings using pictures, rather than narratives (Blake, Varnhagen, & Parent, 2001). We recently completed a project using fMRI to identify the neural correlates of the effects of glucose administration on memory encoding. We also just finished a project looking at the relationship between glycemic regulation and inflammation and cognitive performance in elderly African American patients with Type 2 diabetes.

Currently Funded Grants

Principal Investigator, “The effects of a high fructose diet on brain and behavior.  CDC/GSU Seed Grant Award for Social and Behavioral Science Research, 2007-2008, $59,964 (direct costs).

Principal Investigator, “The effects of a high fructose diet on hippocampal-dependent memory”.  Georgia State University Brains and Behavior Program, 2007, $30,365 (direct costs).

Co-investigator, “A multidisciplinary approach to Learning,” Georgia State University Research Program Enhancement, $50,000 (direct costs).

Representative Publications

Parent, M.B., Tomaz, C. & McGaugh, J.L. (1992). Increased training in an aversively-motivated task attenuates the memory-impairing effects of N-methyl-D-aspartate-induced lesions of the amygdala. Behavioral Neuroscience, 106(5), 789-797.

McGaugh, J.L., Introini-Collison, I. Cahill, L.F., Castellano, C., Dalmaz, C., Parent, M.B., & Williams, C.L. (1993). Neuromodulatory systems and memory storage: Role of the amygdala. Behavioral Brain Research, 58, 81-90.

Parent, M.B., West, M., & McGaugh, J.L. (1994). Memory of rats with amygdala lesions induced 30 days after footshock-motivated escape training reflects degree of original training. Behavioral Neuroscience, 108(6), 1080-1087.

Parent, M.B., & McGaugh, J.L. (1994). Posttraining infusion of lidocaine into the amygdala basolateral>complex impairs retention of inhibitory avoidance training. Brain Research, 661, 97-103.

Parent, M.B., Quirarte, G.L., Cahill, L., & McGaugh, J.L. (1995). Spared retention of inhibitory avoidance following posttraining amygdala lesions. Behavioral Neuroscience, 109, 803-807.

Parent, M.B., Avila, E., & McGaugh, J.L. (1995). Footshock facilitates the expression of aversively-motivated memory in rats with posttraining amygdala basolateral complex lesions. Brain Research, 676, 235-244.

Parent, M.B. & Gold, P.E. (1997). Intra-septal infusions of glucose potentiate inhibitory avoidance deficits when co-infused with the GABA agonist muscimol. Brain Research, 745, 317-320.

Parent, M.B., Laurey, P.T., Wilkniss, S., & Gold, P.E. (1997). Intra-septal infusions of muscimol impair spontaneous alternation performance: Infusions of glucose into the hippocampus, but not the medial septum, reverse the deficit. Neurobiology of Learning and Memory, 68, 75-85.

Parent, M.B., Varnhagen, C. & Gold, P.E. (1999). A memory-enhancing emotional narrative elevates blood glucose levels in human subjects. Psychobiology, 27, 386-396.

Lehmann, H., Treit, D., & Parent, M.B. (2000). Amygdala lesions do not impair shock-probe avoidance retention performance. Behavioral Neuroscience, 114, 107-116.

DeGroot, A & Parent, M.B. (2000). Increasing acetylcholine levels in the hippocampus or entorhinal cortex reverses the impairing effects of septal GABA receptor activation on spontaneous alternation. Learning and Memory, 7, 293-302.

Blake, T., Varnhagen, C. & Parent, M.B. (2001). Emotionally-arousing pictures increase blood glucose levels and enhance recall. Neurobiology of Learning and Memory, 75, 262-273.

DeGroot, A & Parent, M.B. (2001). Infusions of physostigmine into the hippocampus or the entorhinal cortex attenuate avoidance retention deficits produced by intra-septal infusions of the GABA agonist muscimol. Brain Research, 920, 10-18.

Parent, M., Bush, D., Rauw, G., Master, S., Vaccarino, F., & Baker, G. (2001). Analysis of amino acids and catecholamines, 5-hydroxytryptamine, and their metabolites in brain areas in the rat using in vivo microdialysis. Methods, 23, 11-20.

Shah, A.A., & Parent, M.B. (2003). Septal infusions of glucose or pyruvate, but not fructose, produce avoidance deficits when coinfused with the GABA agonist muscimol. Neurobiology of Learning and Memory, 79, 243-251.

Degroot, A. Kornecook, T. Quirion, R., De Bow, S., & Parent, M.B. (2003). Glucose increases hippocampal acetylcholine upon activation of septal GABA receptors. Brain Research, 979, 71-77.

Lehman, H., Treit, D., & Parent, M.B. (2003). Spared anterograde memory for shock-probe fear conditioning after inactivation of the amygdala. Learning and Memory, 10, 261-269.

Shah, A.A., & Parent, M.B. (2003). Septal infusions of glucose or pyruvate, but not fructose, produce avoidance deficits when coinfused with the GABA agonist muscimol. Neurobiology of Learning and Memory, 79, 243-251.

Shah, A.A., & Parent, M.B. (2004). Septal infusions of glucose or pyruvate with muscimol impair spontaneous alternation. Brain Research, 996, 246-250.

Parent, M.B. & Baxter, M.G. (2004). Septo-hippocampal acetylcholine: Involved in but not necessary for learning and memory? Learning and Memory, 11: 9-20.

Krebs, D.L. & Parent, M.B. (2005a). The enhancing effects of hippocampal infusions of glucose are not restricted to spatial working memory. Neurobiology of Learning and Memory, 83,168-172

Krebs, D.L. & Parent, M.B. (2005b). Hippocampal infusions of the glycolytic metabolite pyruvate reverse the memory-impairing effects of septal GABA receptor activation. European Journal of Pharmacology, 520, 91-99.

Erickson, E.J, Watts, K. & Parent, M. B.  (2006).  Septal infusions of glucose with a GABA-B agonist impair memory. Neurobiology of Learning and Memory, 85, 66-70.

Gore, J.B., Krebs, D.L., & Parent, M. B.  (2006).  Changes in blood glucose and salivary cortisol are not necessary for arousal to enhance memory in young or older adults.  Psychoneuroendocrinology, 31, 589-600.

Spetch, M.L. & Parent, M.B. (2006). >Age and sex differences in children’s spatial search strategies. Psychonomic Bulletin and Review, 13(5), 807-812.

Krebs-Kraft, D.L & Parent M.B. (2007). Hippocampal infusions of glucose reverse memory deficits produced by co-infusions of a GABA receptor agonist. Neurobiology of Learning and Memory.