Stress-Evoked Tyrosine Phosphorylation of Signal Regulatory Protein α Regulates Behavioral Immobility in the Forced Swim Test

Ohnishi, Hiroshi; Murata, Takaaki; Kusakari, Shinya; Hayashi, Yuriko; Takao, Keizo; Maruyama, Toshi; Ago, Yukio; Koda, Ken; Jin, Feng; Okawa, Katsuya; Oldenborg, Per Arne; Okazawa, Hideki; Murata, Yoji; Furuya, Nobuhiko; Matsuda, Takehisa; Miyakawa, Tsuyoshi; Matozaki, Takashi

doi:10.1523/jneurosci.0257-10.2010

Cited by 40 publications

(45 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In our previous study, we revealed that forced swimming stress, but not tail suspension stress, led to CD47-dependent tyrosine phosphorylation of SIRPα in the brain of mice [21]. In an earlier study, both CD47 KO mice and SIRPα mutant mice displayed increased depression-like behaviors in the forced swimming test, while there were no changes in depression-like behavior of SIRPα mutant mice in the tail suspension test (Table S1) [21].…”

Section: Discussionmentioning

confidence: 91%

Comprehensive Behavioral Analysis of Cluster of Differentiation 47 Knockout Mice

et al. 2014

View full text Add to dashboard Cite

Cluster of differentiation 47 (CD47) is a member of the immunoglobulin superfamily which functions as a ligand for the extracellular region of signal regulatory protein α (SIRPα), a protein which is abundantly expressed in the brain. Previous studies, including ours, have demonstrated that both CD47 and SIRPα fulfill various functions in the central nervous system (CNS), such as the modulation of synaptic transmission and neuronal cell survival. We previously reported that CD47 is involved in the regulation of depression-like behavior of mice in the forced swim test through its modulation of tyrosine phosphorylation of SIRPα. However, other potential behavioral functions of CD47 remain largely unknown. In this study, in an effort to further investigate functional roles of CD47 in the CNS, CD47 knockout (KO) mice and their wild-type littermates were subjected to a battery of behavioral tests. CD47 KO mice displayed decreased prepulse inhibition, while the startle response did not differ between genotypes. The mutants exhibited slightly but significantly decreased sociability and social novelty preference in Crawley’s three-chamber social approach test, whereas in social interaction tests in which experimental and stimulus mice have direct contact with each other in a freely moving setting in a novel environment or home cage, there were no significant differences between the genotypes. While previous studies suggested that CD47 regulates fear memory in the inhibitory avoidance test in rodents, our CD47 KO mice exhibited normal fear and spatial memory in the fear conditioning and the Barnes maze tests, respectively. These findings suggest that CD47 is potentially involved in the regulation of sensorimotor gating and social behavior in mice.

show abstract

Section: Discussionmentioning

confidence: 91%

Comprehensive Behavioral Analysis of Cluster of Differentiation 47 Knockout Mice

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Nicotine exposure may also have impact on negative affective symptoms of schizophrenia, as the SFK-induced upregulation of GluN2B-NMDAR function is implicated in the regulation of depression-like behavior in animals (Ohnishi et al, 2010). Thus, it is possible that the nicotine-initiated signaling cascade also converges with the schizophrenia-linked signaling for mood regulation, counteracting negative affective symptoms of schizophrenia.…”

Section: Discussionmentioning

confidence: 99%

Nicotine-induced neuroplasticity counteracts the effect of schizophrenia-linked neuregulin 1 signaling on NMDAR function in the rat hippocampus

Yamazaki

Sumikawa

2017

Neuropharmacology

View full text Add to dashboard Cite

A high rate of heavy tobacco smoking among people with schizophrenia has been suggested to reflect self-medication and amelioration of cognitive dysfunction, a core feature of schizophrenia. NMDAR hypofunction is hypothesized to be a mechanism of cognitive dysfunction, and excessive schizophrenia-linked neuregulin 1 (NRG1) signaling through its receptor ErbB4 can suppress NMDAR function by preventing Src-mediated enhancement of NMDAR responses. Here we investigated whether chronic nicotine exposure in rats by subcutaneous injection of nicotine (0.5–1 mg/kg, twice daily for 10 to 15 days) counteracts the suppressive effect of NRG1β on NMDAR-mediated responses recorded from CA1 pyramidal cells in acute hippocampal slices. We found that NRG1β, which prevents the enhancement of NMDAR responses by the Src-family-kinase-activating peptide pYEEI in naive rats, failed to block the effect of pYEEI in nicotine-exposed rats. In naive rats, NRG1β acts only on GluN2B-NMDARs by blocking their Src-mediated upregulation. Chronic nicotine exposure causes enhanced GluN2B-NMDAR responses via Src upregulation and recruits Fyn for the enhancement of GluN2A-NMDAR responses. NRG1β has no effect on both enhanced basal GluN2B-NMDAR responses and Fyn-mediated enhancement of GluN2A-NMDAR responses. Src-mediated enhancement of GluN2B-NMDAR responses and Fyn-mediated enhancement of GluN2A-NMDAR responses initiate long-term potentiation (LTP) of AMPAR synaptic responses in naive and nicotine-exposed CA1 pyramidal cells, respectively. These results suggest that NRG1β suppresses LTP by blocking Src-mediated enhancement of GluN2B-NMDAR responses, but has no effect on LTP in nicotine-exposed rats. These effects of chronic nicotine exposure may counteract the negative effect of increased NRG1-ErbB4 signaling on the cellular mechanisms of learning and memory in individuals with schizophrenia, and therefore may motivate heavy smoking.

show abstract

“…In addition to GluN2A, GluN2B is sensitive to stress that causes depression. Forced swim induced tyrosine phosphorylation of GluN2B [45] , which may contribute to a metabasis leading to NMDAR plasticity and depression behavior. Of note, anxiety-like behavior that is usually associated with depression-like behavior seems to involve a different NMDAR response.…”

Section: Tyrosine Phosphorylation Of Glutamate Receptors In Major Depmentioning

confidence: 99%

Tyrosine phosphorylation of glutamate receptors by non-receptor tyrosine kinases: roles in depression-like behavior

Mao

Wang

2016

Neurotransmitter

View full text Add to dashboard Cite

Several key members of the non-receptor tyrosine kinase (nRTK) family are abundantly present within excitatory synapses in the mammalian brain. These neuron-enriched nRTKs interact with glutamate receptors and phosphorylate the receptors at tyrosine sites. The N-methyl-D-aspartate receptor is a direct substrate of nRTKs and has been extensively investigated in its phosphorylation responses to nRTKs. The -amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor is the other glutamate receptor subtype that is subject to nRTK-mediated tyrosine phosphorylation. Recently, group I metabotropic glutamate receptors (mGluR1/5) were found to be sensitive to nRTKs. Robust tyrosine phosphorylation may occur in C-terminal tails of mGluR5. Tyrosine phosphorylation of glutamate receptors is either constitutive or induced activity-dependently by changing cellular and/or synaptic input. Through inducing tyrosine phosphorylation, nRTKs regulate trafficking, subcellular distribution, and function of modified receptors. Available data show that nRTK-glutamate receptor interactions and tyrosine phosphorylation of the receptors undergo drastic adaptations in mood disorders such as major depressive disorder. The remodeling of the nRTK-glutamate receptor interplay contributes to the long-lasting pathophysiology and symptomology of depression. This review summarizes the recent progress in tyrosine phosphorylation of glutamate receptors and analyzes the role of nRTKs in regulating glutamate receptors and depression-like behavior.

show abstract

Stress-Evoked Tyrosine Phosphorylation of Signal Regulatory Protein α Regulates Behavioral Immobility in the Forced Swim Test

Cited by 40 publications

References 55 publications

Comprehensive Behavioral Analysis of Cluster of Differentiation 47 Knockout Mice

Comprehensive Behavioral Analysis of Cluster of Differentiation 47 Knockout Mice

Nicotine-induced neuroplasticity counteracts the effect of schizophrenia-linked neuregulin 1 signaling on NMDAR function in the rat hippocampus

Tyrosine phosphorylation of glutamate receptors by non-receptor tyrosine kinases: roles in depression-like behavior

Contact Info

Product

Resources

About