GPR55, a G-Protein Coupled Receptor for Lysophosphatidylinositol, Plays a Role in Motor Coordination

Autor: Chris P. Jew, Hongmei Chen, Hui-Chen Lu, Heather B. Bradshaw, James Wager-Miller, Corinne M. Spencer, Alex Straiker, Jie Zhu, Chia Shan Wu, Ken Mackie, Hao Sun
Rok vydání: 2013
Předmět:
Central Nervous System
Male
Cerebellum
Mouse
lcsh:Medicine
Hippocampus
Biochemistry
Mice
Behavioral Neuroscience
Learning and Memory
0302 clinical medicine
Conditioning
Psychological
Receptors
Cannabinoid
lcsh:Science
Mice
Knockout
Neurons
0303 health sciences
Neuronal Plasticity
Multidisciplinary
Behavior
Animal
Neurochemistry
Animal Models
Endocannabinoid system
Motor coordination
medicine.anatomical_structure
Knockout mouse
Female
Neurochemicals
Motor learning
Research Article
Histology
Motor Activity
Biology
03 medical and health sciences
Model Organisms
Neuropsychology
medicine
Animals
030304 developmental biology
Motor Systems
lcsh:R
nervous system
GPR55
Cellular Neuroscience
Synapses
Synaptic plasticity
lcsh:Q
Lysophospholipids
Molecular Neuroscience
Neuroscience
Psychomotor Performance
030217 neurology & neurosurgery
Endocannabinoids
Zdroj: PLoS ONE, Vol 8, Iss 4, p e60314 (2013)
PLoS ONE
ISSN: 1932-6203
Popis: The G-protein coupled receptor 55 (GPR55) is activated by lysophosphatidylinositols and some cannabinoids. Recent studies found prominent roles for GPR55 in neuropathic/inflammatory pain, cancer and bone physiology. However, little is known about the role of GPR55 in CNS development and function. To address this question, we performed a detailed characterization of GPR55 knockout mice using molecular, anatomical, electrophysiological, and behavioral assays. Quantitative PCR studies found that GPR55 mRNA was expressed (in order of decreasing abundance) in the striatum, hippocampus, forebrain, cortex, and cerebellum. GPR55 deficiency did not affect the concentrations of endocannabinoids and related lipids or mRNA levels for several components of the endocannabinoid system in the hippocampus. Normal synaptic transmission and short-term as well as long-term synaptic plasticity were found in GPR55 knockout CA1 pyramidal neurons. Deleting GPR55 function did not affect behavioral assays assessing muscle strength, gross motor skills, sensory-motor integration, motor learning, anxiety or depressive behaviors. In addition, GPR55 null mutant mice exhibited normal contextual and auditory-cue conditioned fear learning and memory in a Pavlovian conditioned fear test. In contrast, when presented with tasks requiring more challenging motor responses, GPR55 knockout mice showed impaired movement coordination. Taken together, these results suggest that GPR55 plays a role in motor coordination, but does not strongly regulate CNS development, gross motor movement or several types of learned behavior.
Databáze: OpenAIRE
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