title: The neuronal death protein par-4 mediates dopaminergic synaptic plasticity.
abstract: Par-4, discovered in a screen for genes whose expression is increased in prostate tumor cells undergoing apoptosis, participates in physiological and pathological nerve cell death. A new study, however, provides evidence for an unexpected role for Par-4 in regulating synaptic transmission in the brain: Par-4 binds to the D2 dopamine receptor (D2DR) and modulates its activity. Mice in which the function of Par-4 is disrupted exhibit impaired dopaminergic neurotransmission, resulting in a depression-like syndrome. Several other cell death-related proteins also appear to function in regulating synaptic plasticity, suggesting that a better understanding of the functions of these proteins may lead to novel therapeutic approaches for a psychiatric and neurodegenerative disorders.
authors.affiliation: Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA. mattsonm@grc.nia.nih.gov
authors.forename: Mark P
authors.initials: MP
authors.lastname: Mattson
authors.forename: Marc
authors.initials: M
authors.lastname: Gleichmann
mesh_terms: D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism / Q000502:physiology*; D004298:Dopamine; D006801:Humans; D009473:Neuronal Plasticity; D017448:Receptors, Dopamine D2 / Q000819:agonists; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission
chemical_list: D051017:Apoptosis Regulatory Proteins; D017448:Receptors, Dopamine D2; C101296:prostate apoptosis response-4 protein; D004298:Dopamine