Molecular through behavioral approaches are used across multiple species to assess both the effects of injury and the potential for plasticity and recovery following spinal cord injury.  Main emphases are on axonal growth, new circuitry, recovery of locomotor function, biomarkers, and extracellular matrix proteins.   

We are interested in elucidating the molecular and cellular mechanisms involved in the pathogenesis of Alzheimer's disease. We are trying to identify the regulatory mechanisms of assembly and intracellular trafficking of gamma-secretase, the enzyme complex responsible for the generation of neurotoxic amyloid beta peptides.

Our research focus is to understand and manage peripheral nerve development, pathology, regeneration, and repair. We are also working to develop nerve tumor therapeutics and engineer extracellular matrix based (decellularized) nerve grafts.

We investigate how alterations in subcellular protein homeostatic mechanisms contribute to the pathogenesis of demyelinating diseases and to aging-associated decline in neural function. We are also interested in understanding the cellular and molecular pathways underlying the development of peripheral nerves.

We study the biophysics and pharmacology of brain nicotine receptors by either expressing cloned forms of those receptors or by studying the nature receptors in fresh brain slices. Our goals are to understand the underpinnings of nicotine addiction and also to understand how to target specific nicotine receptor subtypes for the treatment of neurological diseases such as Alzheimer's or schizophrenia.

We study the development of the cerebral cortex and its pathogenesis which frequently is associated with epilepsy, mental retardation and autism. Primarily, we approach this in mice by introducing new or mutated genes into neural progenitors in the embryonic cerebral cortex which enables us to examine subsequent anatomical, physiological and behavioral changes during brain development.  

We study the cell biology of normal and diseased retinal photoreceptors and develop viral-based gene therapies for treatment of diseased photoreceptors. We also develop viral-based gene delivery systems for use in studies of neural diseases.

We use cell culture and in vivo models to define the roles for adult stem and progenitor cells in neural development and repair, and in brain tumorigenesis.

We use mouse models to study both neurodevelopment and neurodegeneration with particular emphasis on inherited neurological diseases including fragile X associated tremor/ataxia syndrome, the
spinocerebellar ataxias and myotonic dystrophy.

We study the chemical basis of communication and defense. Our primary laboratory model is Caenorhabditis elegans and other nematodes.

Our research focuses on understanding brain mechanisms for modifying synaptic transmission and their relationship to memory, particularly in the context of cognitive decline during aging. We use a combination of behavioral, biochemical, molecular, and electrophysiological techniques to obtain a vertically integrated perspective on neural aging, from the molecular to the cognitive level.

We use electrophysiological and optical techniques to study neurophysiological mechanisms implicated in aging, epilepsy, and drug abuse.

Our research revolves around identifying the role of neural circuits and neurotransmitters involved in integrating cardiovascular and respiratory control in both health and disease. Current interests are specifically focused on the role of orexin and monoamines in modulating cardiorespiratory function during sleep or wakefulness in adolescent and adult rodents.

Our research focuses on the stereotyped or inflexible repetitive behavior diagnostic of autism and commonly seen in many neurodevelopmental disorders. We use both clinical and animal models, the latter involving examination of the genetics and neurobiology underlying the development and expression of repetitive behavior in two different mouse models.

Our research focus is to understand and manage peripheral nerve development, pathology, regeneration, and repair. We are also working to develop nerve tumor therapeutics and engineer extracellular matrix based (decellularized) nerve grafts.

We study the development of the cerebral cortex and its pathogenesis which frequently is associated with epilepsy, mental retardation and autism. Primarily, we approach this in mice by introducing new or mutated genes into neural progenitors in the embryonic cerebral cortex which enables us to examine subsequent anatomical, physiological and behavioral changes during brain development.  

Our research is focused on the mechanisms controlling the responses to stress (hypoxia and hypotension) in the fetus in utero and on the mechanisms controlling the timing of birth.

Several research projects in my lab focus on the use of viral vectors to rescue specific developmental defects of a mouse model of Fragile X syndrome (FXS). Key questions to be answered include the role of Fragile X Mental Retardation Protein in FXS, and the mechanism of how this protein can rescue behavioral defects post-developmentally in the FXS knock-out mouse.

We use the central pattern generating networks found in the crustacean stomatogastric nervous system to study plasticity and homeostasis of network function, motor pattern generation, and dopamine modulation of motor axons. The techniques employed to conduct this research include electrophysiology, biophysics, high-resolution microscopy, and gene expression studies.

We study the basic mechanisms of pain transmission focusing on the interactions of neuropeptide and excitatory amino acid receptors. A second line of research involves probing the molecular physiology of central sensitization in the nucleus caudalis.

Our research is aimed at understanding how neuroplasticity in the brain and spinal cord influences the control of breathing. Current projects focus on 1) mechanisms of spinal plasticity induced by cellular replacement therapy and rehabilitative training following cervical spinal cord injury; 2) mechanisms underlying spontaneous respiratory motor recovery following cervical spinal cord injury, and 3) gene delivery to respiratory motoneurons as a tool for improving breathing in certain disease states.

We study translational models of declining physical and cognitive performance to investigate the role of the renin-angiotensin system, exercise, and nutrition in physical/cognitive decline and sarcopenia using genetic, pharmaceutical, nutritional and behavioral interventions. We also study pain, aging, and disability.

In one project, we use rodent models to investigate the biochemical basis of stress-induced psychopathology (e.g. major depression), with an emphasis on plasticity in limbic brain regions. In a second project, we use rodents to investigate the biochemical basis of self-injurious behavior (e.g. head banging in autism).

Students and faculty affiliated with our laboratory engage in a variety of basic scientific endeavors with a primary goal to understand the mechanisms of epilepsy and to apply this knowledge toward developing new treatments and cures.

We use whole cell patch clamp methods to classify and characterize nociceptor phenotypes of the dorsal root ganglion.

We study the neural control and regulation of cellular cation homeostasis and intracellular/intercellular calcium signaling pathways, under neurotransmitter stimulation and mechanical perturbation.

Our major research focus is to develop animal or laboratory models of addiction and bring them from concept to therapy.