The Lab

Learning-related changes in the strength of neuronal connections in the brain not only underlie memory formation and storage but are also effected by neurological and mental disorders such as Alzheimer's disease and addiction. The goal of our research is to use genetic, pharmacological, behavioral, and electrophysiological techniques to study the neurobiology of learning and memory.

Specific Interests :

· Molecular & cellular substrates of classical conditioning of the eye blink reflex

· Nicotine & alcohol neurobiological effects on acquisition and consolidation of learning

· Nicotinic & b-amyloid interactions on cellular and learning-related processes during aging and Alzheimer's disease



The Molecular Substrates of Classical Conditioning

The ability of the nervous system to modify the strength of synaptic connections between neurons underlie development and storage of long-term memories. It is a goal of our research, in collaboration with Dr. Ted Abel (Department of Biology University of Pennsylvania), to identify the pre and postsynaptic molecular substrates of long-lasting memories formed during classical conditioning of an eye blink reflex in transgenic mice. Eye blink conditioning is a form of motor learning mediated by a well-defined circuit within the cerebellum and deficits in eye blink conditioning have been reported for both developmental and age-related disorders. Because of the known neural circuitry of eye blink conditioning, potential neural areas and synapses involved in learning-related changes have been identified. Inducible transgenic techniques can be applied to increased or decrease molecular substrates of cellular signal transduction through specific expression of gene products in neurons. Applying inducible transgenic techniques to control cell-specific expression of molecular substrates potentially involved in eye blink conditioning will further understanding of the molecular substrates of associative processes.

Nicotinic Modulation of Learning and Memory

In 1988, the US Surgeon General concluded that tobacco products are addictive and nicotine is the main pharmacological agent in tobacco responsible for tobacco's addictive nature. Many questions remain, however, about nicotine. It is not completely understood what nicotine's effects on neurological/behavioral function are nor is it understood why nicotine is addictive. One reason for the incomplete understanding of nicotine addiction may be that addiction is a complex disorder with many factors contributing to the disease. Three of many possible factors that may contribute to nicotine addiction are use of “gateway” substances that sensitize an individual to addictive properties of nicotine, genetics, and learning-related processes. The limbic/striatal system is involved in both learning and addiction and thus may interact to facilitate cognitive influences on addiction. The goals of our research are to identify the neurobiological effects of nicotine on learning and the effects of learning on nicotine use, to identify how alcohol may serve as a gateway substance to nicotine use and abuse, and to identify genetic factors that may contribute to nicotine-associated neurobehavioral effects.

The Neurobiology of Aging and Alzheimer's Disease

Both aging and Alzheimer's disease are associated with changes in nicotinic acetylcholinergic function. These changes may not only contribute to cognitive impairment but may underlie deficits in learning and memory. In collaboration with Dr. Diana Woodruff-Pak (Department of Psychology, Temple University), we are using transgenic, electrophysiological, behavioral, and neurochemical techniques to investigate the age and Alzheimer's disease-related changes in nicotinic receptor function and associated learning processes. Emphasis of our research also focuses on ameliorative agents for age and Alzheimer's disease related changes in learning and memory.