My research explores the neurobiology of learning and memory, focusing on particular brain substrates activated in response to the acquisition and expression of Pavlovian or classical conditioning. Using multiple learning paradigms, we examine brain function across four primary structures: the amygdala, cerebellum, hippocampus, and prefrontal cortex.
In one line of research, we are investigating how amygdala-dependent emotional regulation modulates the acquisition, consolidation, and retrieval of a simple form of associative learning called classical eyeblink conditioning. Just like Pavlov's dogs, if an organism is presented with a neutral or conditioned stimulus (e.g., a light or tone) followed by an aversive unconditioned stimulus (e.g., an electrical shock near the eye), the subject will learn to blink (a conditioned response) in anticipation of the shock. The behavior and neural circuitry of this simple form of motor learning, which relies on the brainstem and cerebellum, is arguably better understood than any other form learning. Yet, it is still unclear exactly how the emotional attributes of the shock modify the learning process. The amygdala is proposed to amplify responsiveness to the conditioned and unconditioned stimuli in structures both upstream and downstream of the cerebellum, resulting in faster acquisition of the conditioned blink. As we move forward, we are particularly interested in characterizing how and when several feedforward- and feedback-loops between the amygdala, cerebellum, and hippocampus are engaged as a function of eyeblink conditioning.
In a second line of research, alcohol is administered to rat pups in an animal model of fetal alcohol syndrome (FAS). Previously we have examined the adverse effects of early ethanol exposure on the cerebellum and eyeblink conditioning. More recently, our focus has shifted to alcohol's effects within the forebrain, particularly the hippocampus and prefrontal cortex. As adults, the FAS rats are impaired in a variety of hippocampal-dependent learning tasks, including trace fear conditioning and a particular variant of context fear conditioning called the context pre-exposure facilitation effect (CPFE). Based on the observed ethanol-induced learning deficits we are now studying the underlying neurodevelopmental changes in forebrain function that are responsible. We hypothesize that early ethanol exposure may disrupt normal developmental changes in NMDA receptor subunit composition and function, leading to impaired synaptic plasticity and learning. These changes may be particularly pronounced in learning tasks that require the bridging of two stimuli across time (trace conditioning) or the conjunctive encoding of contextual memories, both of which are thought to rely on NMDA receptors within the recurrent collateral circuitry of the hippocampus and prefrontal cortex.