Gerald J. LaHoste, Ph.D.
Villere Chair for
Research in Neuroscience
Associate Professor
Research Interests
Dr. LaHoste's research program is unique in that it seeks to understand the biological bases of behavior at several levels of organization from molecular genetics to behavior as well as many of the levels in between (gene and protein expression, chemical neuroanatomy and physiology).The goal of this strategy is to obtain a comprehensive view of the complexity of normal and pathological human behavior. This strategy and the techniques involved have been applied mostly to behaviors that are profoundly influenced by the neurotransmitter dopamine. Not only are the effects of dopamine profound, but they extend to a remarkably wide range of behaviors including cognition, attention, motivation, drug addiction, and the translation of thought into movement.
Dr. LaHoste's research is "translational," or applied, in nature.
His most recent findings promise to lead directly to a novel, superior
treatment for schizophrenia and late-stage Parkinson's disease. These
findings were prompted by behavioral results that led to the use of
molecular genetics by which Dr. LaHoste co-discovered a novel gene. The function of this gene was, in turn, tested in behavioral models
(genetically engineered mice). Thus, although molecular techniques
are used, behavior represents the start-point and the end-point of all
of Dr. LaHoste's research.
In earlier work, Dr. LaHoste was the first to discover the link between a dopamine-related gene and Attention Deficit Hyperactivity Disorder (ADHD). This finding has been replicated in many laboratories world-wide, and the two original papers describing this discovery have been cited over 500 times in scientific journals. The previously unknown link between this gene and ADHD has had an important impact on current theories and represents a major new avenue for the development of better drugs in the treatment of this childhood disorder.
Selected Publications
Nola EB, Harrison LM, LaHoste GJ & Ruskin DN. Behavioral synergism between D1 and D2 dopamine receptors in mice does not depend on gap junctions. (2007) Synapse 61:279-287.
Harrison LM & LaHoste GJ. (2006) Rhes, the Ras Homolog Enriched in Striatum, is reduced under conditions of dopamine supersensitivity. Neuroscience 137: 483-492.
Ruskin DN, Anand R & LaHoste GJ. (2006) Menthol and nicotine oppositely modulate body temperature in the rat. Eur J Pharmacol 559:161-164.
Chen C, Hardy M, Ruskin DN, Zhang J, LaHoste GJ & Bazan NG. (2006) Altered NMDA receptor trafficking contributes to sleep deprivation-induced hippocampal synaptic and cognitive impairments, submitted. Biochem Biophys Res Commun. 340: 435-40.
LaHoste GJ, Henry BL & Marshall JF. (2000) Dopamine D1 receptors synergize with D2 but not D3 or D4 receptors in the striatum without involvement of action potentials. J Neurosci 20: 6666-6671.
LaHoste GJ, Swanson JM, Wigal S, Glabe C, Wigal T, King N & Kennedy JL. (1996) Dopamine D4 receptor gene polymorphism is associated with attention deficit-hyperactivity disorder. Molecular Psychiatry 1: 128-131.
LaHoste GJ, Yu J & Marshall JF. (1993) Striatal Fos expression is indicative of dopamine D1/D2 synergism and receptor supersensitivity. Proc Natl Acad Sci USA 90: 7451-7455.
LaHoste GJ & Marshall JF. (1992) Dopamine supersensitivity and D1/D2 synergism are unrelated to changes in striatal receptor density. Synapse 12: 14-26.
LaHoste, G.J., Swanson, J.M., Wigal, S., Glabe, C., Wigal, T., King, N. and Kennedy, J.L. (1996) Dopamine D4 receptor gene polymorphism is associated with attention deficit-hyperactivity disorder. Molecular Psychiatry 1: 128-131.
LaHoste, G.J., Ruskin, D.N. and Marshall, J.F. (1996) Cerebrocortical Fos expression following dopamine agonist stimulation: D1/D2 synergism and its breakdown. Brain Research 728: 97-104.
LaHoste, G.J. and Marshall, J.F. (1996) Dopamine receptor interactions in the brain. In T.W. Stone (editor), CNS Neurotransmitters and Neuromodulators: Dopamine, Boca Raton FL, CRC Press, p.107-119
LaHoste, G.J. and Marshall, J.F. (1994) Rapid development of D1 and D2 dopamine receptor supersensitivity as indicated by striatal and pallidal Fos expression. Neuroscience Letters 179: 153-156.
LaHoste, G.J. and Marshall, J.F. (1993) New concepts in dopamine receptor plasticity. Annals of the New York Academy of Sciences 702: 183-196.
LaHoste, G.J., Yu, J. and Marshall, J.F. (1993) Striatal Fos expression is indicative of dopamine D1/D2 synergism and receptor supersensitivity. Proceedings of the National Academy of Sciences of the United States of America 90: 7451-7455.
LaHoste, G.J. and Marshall, J.F. (1993) The role of dopamine in the maintenance and breakdown of D1/D2 synergism. Brain Research 611: 108-116.
LaHoste, G.J. and Marshall, J.F. (1992) Dopamine supersensitivity and D1/D2 synergism are unrelated to changes in striatal receptor density. Synapse 12:14-26.
LaHoste, G.J. and Marshall, J.F. (1991) Chronic eticlopride and dopamine denervation induce equal nonadditive increases in striatal D2 receptor density: Autoradiographic evidence against the dual mechanism hypothesis. Neuroscience 41: 473-481.
LaHoste, G.J., O'Dell, S.J., Widmark, C.B., Shapiro, R.M., Potkin, S.G. and Marshall, J.F. (1991) Differential changes in dopamine and serotonin receptors induced by clozapine and haloperidol. In C. Tamminga and S.C. Schulz (Eds.), Advances in Neuropsychiatry and Psychopharmacology, Vol 1: Schizophrenia Research, New York, Raven Press, pp. 351-361.
LaHoste,G.J.
and Marshall, J.F. (1990) Nigral D1 and striatal D2 receptors mediate
the behavioral effects of dopamine agonists. Behavioural Brain Research
38: 233-242.
last modified 07/15/08.
