The neuromodulator dopamine is implicated in mechanisms of attention and reinforcement of learning. Many brain disorders (schizophrenia, attention deficit, Parkinson disease, alcohol and drug addition) involve the disruption of dopaninergic function, and cause different forms of memory impairment. Long-term potentiation (LTP) in the CA1 region of the hippocampus is a convenient model for studies of cellular mechanisms of memory. Our data with field potential recordings indicate that D1 dopamine modulations enhances early LTP by a cAMP- dependent mechanism. This proposal deals with the intracellular targets of dopamine and cAMP action. Two fundamental possibilities for the enhancement of LTP by dopamine will be addressed: D1 activation could increase depolarization during the tetanus or it could affect the enzymatic mechanisms of plasticity. The first possibility, D1 action on electrical properties of pyramidal cells, will be accessed by whole-cell recording methods (Aim 1). The second possibility, that D1 and cAMP affects the enzymatic machinery of LPT, will be analyzed by voltage clamp with intracellular perfusion of substances in interest (Aim 2).

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
1F32MH011720-01
Application #
2033412
Study Section
Neuropharmacology and Neurochemistry Review Committee (NPNC)
Program Officer
Oliver, Eugene J
Project Start
1997-09-20
Project End
Budget Start
1997-05-01
Budget End
1998-04-30
Support Year
1
Fiscal Year
1997
Total Cost
Indirect Cost
Name
Brandeis University
Department
Biology
Type
Schools of Arts and Sciences
DUNS #
616845814
City
Waltham
State
MA
Country
United States
Zip Code
02454