Paul D Shepard
 

Paul D Shepard Ph.D.

Academic Title: Associate Professor
Primary Appointment: Psychiatry
Secondary Appointments: Pharmacology and Experimental Therapeutics
pshepard@mprc.umaryland.edu
Location: 701 W. Pratt St., 388 (MPRC)
Phone: (410) 402-7753

Personal History

Ph.D. 1986, University of Texas Southwestern Medical School in Dallas, Texas

Postdoctoral Fellowship in Neuropsychopharmacology 1986-1989, Yale University School of Medicine in New Haven, Conn.

Research Interests

Our laboratory is investigating the physiological mechanisms through which dopamine-containing neurons in the ventral midbrain encode information. Located in the pars compacta of the substantia nigra and in the adjacent ventral tegmental area, these cells form reciprocal connections with neurons in the basal ganglia, cortex and limbic forebrain. Dopamine neurons and their circuits are critically involved in the regulation of motor activity and in the motivational processes underlying learning and execution of goal-directed behaviors. Understanding the basic mechanisms involved in regulating the electrical activity of these cells and their neuronal targets is an essential step in the development of new strategies for treating a variety of clinical syndromes including Parkinson's disease, schizophrenia and drug abuse.
Much of our current research is focused on study of the ionic currents that produce the complex firing patterns exhibited by dopamine neurons with an emphasis on those responsible for generating bursting activity. To accomplish this, we use a variety of contemporary electrophysiological and pharmacological techniques including intracellular and extracellular recording, in vitro brain slice techniques, microstimulation and microiontophoresis. Our research has shown that bursts of action potentials are generated intrinsically by a repetitive oscillation in membrane potential driven by voltage dependent calcium channels expressed in the dopamine neurons themselves. Currently, we are examining the interplay between these intrinsic mechanisms and the influence of afferents that contain neurotransmitters and modulators capable of modifying dopamine cell activity. Future studies are aimed at identifying the cellular mechanisms responsible for switching the firing pattern of dopamine neurons between bursting and nonbursting modalities and applying this knowledge to advance our current understanding of the influence of dopamine on target neurons throughout the forebrain.

Publications

Canavier CC, Perla SR and Shepard PD  (2004) Scaling of prediction error does not confirm chaotic dynamics underlying irregular firing using interspike intervals from midbrain dopamine neurons. Neuroscience 129:491-502.
 
Sarpal D, Koenig JI, Adelman JP, Brady D, Clerkin L and Shepard PD (2004) Regional distribution of SK3 mRNA-containing neurons in the adult and adolescent rat ventral midbrain and their relationship to dopamine-containing cells. Synapse 53:104-113.
 
Joy B, McMahon RP and Shepard PD (2004) Effects of acute and chronic clozapine on D-amphetamine-induced disruption of auditory gating in the rat. Psychopharmacology 174:274-282.
 
Kitai ST, Shepard PD, Callaway, JC and Scroggs R (1999)  Afferent modulation of dopamine neuron firing patterns.  Current Opinion in Neurobiology 9:690-697.
 
Ping H and Shepard PD (1999) Blockade of SK-Type Ca2+-Activated K+ Channels Uncovers a Ca2+-Dependent Slow Afterdepolarization in Nigral Dopamine Neurons. Journal of Neurophysiology 81: 977-984
 
Shepard PD and Stump D (1999) Nifedipine blocks apamin-induced bursting activity in nigral dopamine-containing neurons. Brain Research 817:104-109.



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