Asset Details
Do you wish to reserve the book?
Selective Deletion of GRK2 Alters Psychostimulant-Induced Behaviors and Dopamine Neurotransmission
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Selective Deletion of GRK2 Alters Psychostimulant-Induced Behaviors and Dopamine Neurotransmission
Do you wish to request the book?
Selective Deletion of GRK2 Alters Psychostimulant-Induced Behaviors and Dopamine Neurotransmission
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Selective Deletion of GRK2 Alters Psychostimulant-Induced Behaviors and Dopamine Neurotransmission
2014
Overview
GRK2 is a G protein-coupled receptor kinase (GRK) that is broadly expressed and is known to regulate diverse types of receptors. GRK2 null animals exhibit embryonic lethality due to a severe developmental heart defect, which has precluded the study of this kinase in the adult brain. To elucidate the specific role of GRK2 in the brain dopamine (DA) system, we used a conditional gene knockout approach to selectively delete GRK2 in DA D1 receptor (D1R)-, DA D2 receptor (D2R)-, adenosine 2A receptor (A2AR)-, or DA transporter (DAT)-expressing neurons. Here we show that select GRK2-deficient mice display hyperactivity, hyposensitivity, or hypersensitivity to the psychomotor effects of cocaine, altered striatal signaling, and DA release and uptake. Mice with GRK2 deficiency in D2R-expressing neurons also exhibited increased D2 autoreceptor activity. These findings reveal a cell-type-specific role for GRK2 in the regulation of normal motor behavior, sensitivity to psychostimulants, dopamine neurotransmission, and D2 autoreceptor function.
Publisher
Nature Publishing Group
Subject
/ Behavior
/ Biology
/ Central Nervous System Stimulants - pharmacology
/ Cocaine
/ Conditioning (Psychology) - drug effects
/ Conditioning (Psychology) - physiology
/ Dopamine
/ Dopamine Plasma Membrane Transport Proteins - genetics
/ Dopamine Plasma Membrane Transport Proteins - metabolism
/ G-Protein-Coupled Receptor Kinase 2 - genetics
/ G-Protein-Coupled Receptor Kinase 2 - metabolism
/ Kinases
/ Motor Activity - drug effects
/ Original
/ Proteins
/ Receptor, Adenosine A2A - genetics
/ Receptor, Adenosine A2A - metabolism
/ Receptors, Dopamine D1 - genetics
/ Receptors, Dopamine D1 - metabolism
/ Receptors, Dopamine D2 - genetics
/ Receptors, Dopamine D2 - metabolism
/ Space Perception - drug effects
