JOHN T. GREEN
My research interests are within the neurobiology of learning and memory. One line of current research involves examining the impact of voluntary exercise on different forms of learning and the neural substrates that support these different forms of learning. A second line of current research involves examining some of the fundamental neural mechanisms underlying learning and memory, using a cerebellum-dependent form of learning, eyeblink classical conditioning. A third line of current research involves examining the role of the cerebellum in human clinical conditions, particularly attention-deficit/hyperactivity disorder.
Physical Activity and Learning
Numerous studies in rodents have shown that voluntary exercise facilitates hippocampus-dependent learning and hippocampal plasticity. Few studies have examined the impact of voluntary exercise on other brain areas and on forms of learning and memory that require these brain areas. We have recently shown that running wheel exercise in rats facilitates cerebellum-dependent motor learning (eyeblink conditioning) and striatum-dependent discrimination learning (cross-maze task). We are currently examining the neural mechanisms that underlie these enhancements of non-hippocampus dependent learning, with a focus on catecholamine systems.
Neural Mechanisms of Learning
Eyeblink conditioning is one of the most well-understood forms of mammalian learning and memory, at both a behavioral and a neural level. The simplicity of the stimuli used and the response measured in eyeblink conditioning have aided greatly in the delineation of the necessary and sufficient neural circuitry in the brainstem and cerebellum, and the identification of key sites of plasticity in the cerebellum. Nevertheless, neither the exact mechanisms of neural plasticity, nor the interaction between sites of plasticity in cerebellar cortex and sites of plasticity in the deep cerebellar nuclei is completely understood. Answering these fundamental questions will provide clues as to how the mammalian brain supports learning and memory in general. We approach these questions by combining behavior with single-unit recording and intracranial infusions.
The Cerebellum and ADHD
Attention-deficit/hyperactivity disorder (ADHD) is a neurobehavioral disorder with core symptoms of inattention and hyperactivity/impulsivity that must be present by age 7 and cause impairment in two or more settings. It has been known for some time that abnormalities in prefrontal cortex and striatum contribute to ADHD. More recently, the cerebellum has been associated with the pathophysiology of ADHD. In particular, aberrant temporal information processing by the cerebellum may play a role in impulsive behavior. We are using eyeblink conditioning as a means to tap into cerebellar temporal information processing. We have shown that two different rat models of ADHD, the spontaneously hypertensive rat (SHR) and the Wistar-Kyoto Hyperactive rat (WKHA), exhibit shortened latencies of learned eyeblinks. These shortened learned eyeblinks are strongly indicative of abnormal cerebellar cortical processing. The same abnormalities may be present in people with ADHD.
Zelaznik, H. N., Vaughn, A. J., Green, J. T., Smith, A. L., Hoza, B., & Linnea, K. (2011). Motor timing deficits in children with Attention-Deficit/Hyperactivity Disorder. Human Movement Science.
Thanellou, A., & Green, J. T. (2011). Spontaneous recovery but not reinstatement of the extinguished conditioned eyeblink response in the rat. Behavioral Neuroscience, 125,
Chess, A. C., Raymond, B. E., Gardner-Morse, I. G., Stefani, M. R., & Green, J. T. (2011). Set shifting in a rodent model of Attention-Deficit/Hyperactivity Disorder. Behavioral Neuroscience, 125, 372-382.
Green, J. T., Chess, A. C., Burns, M., Schachinger, K. M., & Thanellou, A. (2011). The effects of two forms of physical activity on eyeblink classical conditioning. Behavioural Brain Research, 219, 165-174.
Thanellou, A., Schachinger, K. M., & Green, J. T. (2009). Shortened conditioned eyeblink response latency in male but not female Wistar-Kyoto Hyperactive rats. Behavioral Neuroscience, 123, 650-664.
Chess, A. C., & Green, J. T. (2008). Abnormal topography and altered acquisition of conditioned eyeblink responses in a rodent model of Attention-Deficit/Hyperactivity Disorder. Behavioral Neuroscience, 122, 63-74.
Green, J. T., & Arenos, J. D. (2007). Hippocampal and cerebellar single-unit activity during delay and trace eyeblink conditioning in the rat. Neurobiology of Learning and Memory, 87, 269-284.
Green, J. T., Arenos, J. D., & Dillon, C. J. (2006). The effects of moderate neonatal ethanol exposure on eyeblink conditioning and deep cerebellar nuclei neuron numbers in the rat. Alcohol, 39, 135-150.
Woodruff-Pak, D. S., Green, J. T., Levin, S. I., & Meisler, M. H. (2006). Inactivation of sodium channel Scn8A (Nav1.6) in Purkinje neurons impairs learning in Morris water maze and delay but not trace eyeblink classical conditioning. Behavioral Neuroscience, 120, 229-240.
Green, J. T., & Steinmetz, J. E. (2005). Purkinje cell activity in the cerebellar anterior lobe after rabbit eyeblink conditioning. Learning and Memory, 12, 260-269.
Last modified July 19 2012 11:32 AM