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Article ; Online: Aversive Stress Reduces Mu Opioid Receptor Expression in the Intercalated Nuclei of the Rat Amygdala.

Gouty, Shawn / Silveira, Julia Tomoyasu / Cote, Thomas E / Cox, Brian M

2021 Volume 41, Issue 5, Page(s) 1119–1129

Abstract: The amygdala plays an important role in the integration of responses to noxious and fearful stimuli. Sensory information from many systems is integrated in the lateral and basolateral amygdala and transmitted to the central amygdala, the major output ... ...

Abstract	The amygdala plays an important role in the integration of responses to noxious and fearful stimuli. Sensory information from many systems is integrated in the lateral and basolateral amygdala and transmitted to the central amygdala, the major output nucleus of the amygdala regulating both motor and emotional responses. The network of intercalated cells (ITC) which surrounds the lateral and basolateral amygdala and serves to modulate information flow from the lateral amygdala to the central nucleus, express a very high local concentration of mu-type opioid receptors. Loss of the ITC neurons impairs fear extinction. We demonstrate here that exposure of rats to a severe stress experience resulted in a marked downregulation of the level of expression of mu opioid receptors in the ITC nuclei over a period of at least 24 h after the end of the stress exposure. The endogenous opioid dynorphin is also expressed in the central and ITC nuclei of the amygdala. Following stress exposure, we also observed an increase in the expression in the more lateral regions of the central amygdala of pro-dynorphin mRNA and a peptide product of pro-dynorphin with known affinity for mu opioid receptors. It is possible that the downregulation of mu receptors in ITC neurons after stress may result from sustained activation and internalization of mu receptors following a stress-induced increase in the release of endogenous opioid peptides.
MeSH term(s)	Amygdala/metabolism ; Animals ; Avoidance Learning/physiology ; Down-Regulation/physiology ; Gene Expression ; Male ; Rats ; Rats, Sprague-Dawley ; Receptors, Opioid, mu/antagonists & inhibitors ; Receptors, Opioid, mu/biosynthesis ; Receptors, Opioid, mu/genetics ; Stress, Psychological/genetics ; Stress, Psychological/metabolism ; Stress, Psychological/psychology
Chemical Substances	Oprm1 protein, rat ; Receptors, Opioid, mu
Language	English
Publishing date	2021-01-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	283404-2
ISSN	1573-6830 ; 0272-4340
ISSN (online)	1573-6830
ISSN	0272-4340
DOI	10.1007/s10571-020-01026-7
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Zs.A 1727: Show issues

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Article ; Online: Repetitive mild traumatic brain injury induces persistent alterations in spontaneous synaptic activity of hippocampal CA1 pyramidal neurons.

Langlois, Ludovic D / Selvaraj, Prabhuanand / Simmons, Sarah C / Gouty, Shawn / Zhang, Yumin / Nugent, Fereshteh S

IBRO neuroscience reports

2022 Volume 12, Page(s) 157–162

Abstract: Mild traumatic brain injury (mTBI) or concussion is the most common form of TBI which frequently results in persistent cognitive impairments and memory deficits in affected individuals [1]. Although most studies have investigated the role of hippocampal ... ...

Abstract	Mild traumatic brain injury (mTBI) or concussion is the most common form of TBI which frequently results in persistent cognitive impairments and memory deficits in affected individuals [1]. Although most studies have investigated the role of hippocampal synaptic dysfunction in earlier time points following a single injury, the long-lasting effects of mTBI on hippocampal synaptic transmission following multiple brain concussions have not been well-elucidated. Using a repetitive closed head injury (3XCHI) mouse model of mTBI, we examined the alteration of spontaneous synaptic transmission onto hippocampal CA1 pyramidal neurons by recording spontaneous excitatory AMPA receptor (AMPAR)- and inhibitory GABA
Language	English
Publishing date	2022-02-09
Publishing country	Netherlands
Document type	Journal Article
ISSN	2667-2421
ISSN (online)	2667-2421
DOI	10.1016/j.ibneur.2022.02.002
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Article: Blast-Induced Mild Traumatic Brain Injury Alterations of Corticotropin-Releasing Factor Neuronal Activity in the Mouse Hypothalamic Paraventricular Nucleus.

Simmons, Sarah / Langlois, Ludovic D / Oyola, Mario G / Gouty, Shawn / Wu, T John / Nugent, Fereshteh S

Frontiers in synaptic neuroscience

2022 Volume 13, Page(s) 804898

Abstract: Blast-induced mild traumatic brain injury (mbTBI) is the most common cause of TBI in US service members and veterans. Those exposed to TBI are at greater risk of developing neuropsychiatric disorders such as posttraumatic stress disorder, anxiety and ... ...

Abstract	Blast-induced mild traumatic brain injury (mbTBI) is the most common cause of TBI in US service members and veterans. Those exposed to TBI are at greater risk of developing neuropsychiatric disorders such as posttraumatic stress disorder, anxiety and depressive disorders, and substance use disorders following TBI. Previously, we have demonstrated that mbTBI increases anxiety-like behaviors in mice and dysregulates stress at the level of corticotropin-releasing factor (CRF) neurons in the paraventricular nucleus (PVN). To expand on how mTBI may dysregulate the stress axis centrally, here PVN CRF neuronal activity was evaluated using whole cell-patch clamp recordings in hypothalamic slices from sham and mbTBI adult male CRF:tdTomato mice 7 days post-injury. We found that mbTBI generally did not affect the neuronal excitability and intrinsic membrane properties of PVN CRF neurons; this injury selectively increased the frequency of spontaneous neuronal firing of PVN CRF neurons localized to the dorsal PVN (dPVN) but not ventral PVN (vPVN). Consistently, mbTBI-induced dPVN CRF hyperactivity was associated with pre- and post-synaptic depression of spontaneous GABAergic transmission onto dPVN CRF neurons suggesting that mbTBI-induced GABAergic synaptic dysfunction may underlie dPVN CRF neuronal hyperactivity and increases in dPVN CRF signaling. The present results provide the first evidence for mbTBI-induced alterations in PVN CRF neuronal activity and GABAergic synaptic function that could mediate hypothalamic CRF dysregulation following mbTBI contributing to stress psychopathology associated with blast injury.
Language	English
Publishing date	2022-01-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2592086-8
ISSN	1663-3563
ISSN	1663-3563
DOI	10.3389/fnsyn.2021.804898
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Article ; Online: AKAP150-anchored PKA regulates synaptic transmission and plasticity, neuronal excitability and CRF neuromodulation in the mouse lateral habenula.

Simmons, Sarah C / Flerlage, William J / Langlois, Ludovic D / Shepard, Ryan D / Bouslog, Christopher / Thomas, Emily H / Gouty, Kaitlyn M / Sanderson, Jennifer L / Gouty, Shawn / Cox, Brian M / Dell'Acqua, Mark L / Nugent, Fereshteh S

Communications biology

2024 Volume 7, Issue 1, Page(s) 345

Abstract: The scaffolding A-kinase anchoring protein 150 (AKAP150) is critically involved in kinase and phosphatase regulation of synaptic transmission/plasticity, and neuronal excitability. Emerging evidence also suggests that AKAP150 signaling may play a key ... ...

Abstract	The scaffolding A-kinase anchoring protein 150 (AKAP150) is critically involved in kinase and phosphatase regulation of synaptic transmission/plasticity, and neuronal excitability. Emerging evidence also suggests that AKAP150 signaling may play a key role in brain's processing of rewarding/aversive experiences, however its role in the lateral habenula (LHb, as an important brain reward circuitry) is completely unknown. Using whole cell patch clamp recordings in LHb of male wildtype and ΔPKA knockin mice (with deficiency in AKAP-anchoring of PKA), here we show that the genetic disruption of PKA anchoring to AKAP150 significantly reduces AMPA receptor-mediated glutamatergic transmission and prevents the induction of presynaptic endocannabinoid-mediated long-term depression in LHb neurons. Moreover, ΔPKA mutation potentiates GABA
MeSH term(s)	Animals ; Male ; Mice ; A Kinase Anchor Proteins/genetics ; A Kinase Anchor Proteins/metabolism ; Corticotropin-Releasing Hormone/metabolism ; Endocannabinoids ; Habenula/metabolism ; Neuronal Plasticity/physiology ; Neurons/physiology ; Receptors, AMPA/genetics ; Receptors, AMPA/metabolism ; Receptors, GABA-A/metabolism ; Synaptic Transmission/physiology
Chemical Substances	A Kinase Anchor Proteins ; Corticotropin-Releasing Hormone (9015-71-8) ; Endocannabinoids ; Receptors, AMPA ; Receptors, GABA-A ; Akap5 protein, mouse
Language	English
Publishing date	2024-03-20
Publishing country	England
Document type	Journal Article
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-024-06041-8
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Article ; Online: Potentiation of glutamatergic synaptic transmission onto lateral habenula neurons following early life stress and intravenous morphine self-administration in rats.

Langlois, Ludovic D / Berman, Rina Y / Shepard, Ryan D / Simmons, Sarah C / Tsuda, Mumeko C / Gouty, Shawn / Choi, Kwang H / Nugent, Fereshteh S

Addiction biology

2021 Volume 27, Issue 1, Page(s) e13064

Abstract: Early life stress presents an important risk factor for drug addiction and comorbid depression and anxiety through persistent effects on the mesolimbic dopamine pathways. Using an early life stress model for child neglect (a single 24 h episode of ... ...

Abstract	Early life stress presents an important risk factor for drug addiction and comorbid depression and anxiety through persistent effects on the mesolimbic dopamine pathways. Using an early life stress model for child neglect (a single 24 h episode of maternal deprivation, MD) in rats, recent published works from our lab show that MD induces dysfunction in the ventral tegmental area and its negative controller, the lateral habenula (LHb). MD-induced potentiation of glutamatergic synaptic transmission onto LHb neurons shifts the coordination of excitation/inhibition (E/I) balance towards excitation, resulting in an increase in the overall spontaneous neuronal activity with elevation in bursting and tonic firing, and in the intrinsic excitability of LHb neurons in early adolescent male rats. Here, we explored how MD affects intravenous morphine self-administration (MSA) acquisition and sucrose preference as well as glutamatergic synaptic function in LHb neurons of adult male rats self-administering morphine. We found that MD-induced increases in LHb neuronal and glutamatergic synaptic activity and E/I ratio persisted into adulthood. Moreover, MD significantly reduced morphine intake, triggered anhedonia-like behaviour in the sucrose preference test and was associated with persistent glutamatergic potentiation 24 h after the last MSA session. MSA also altered the decay time kinetics of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor (AMPAR) currents in LHb neurons of control rats during this time period. Our data highlight that early life stress-induced glutamatergic plasticity in LHb may dampen the positive reinforcing and motivational properties of both natural rewards and opioids, and may contribute to the development of anhedonia and dysphoric states associated with opioids.
MeSH term(s)	Animals ; Male ; Rats ; Dopamine/metabolism ; gamma-Aminobutyric Acid/metabolism ; Glutamic Acid/metabolism ; Habenula/drug effects ; Morphine/pharmacology ; Neurons/drug effects ; Receptors, AMPA/metabolism ; Self Administration ; Synaptic Transmission/drug effects ; Ventral Tegmental Area/metabolism ; Stress, Psychological
Chemical Substances	Dopamine (VTD58H1Z2X) ; gamma-Aminobutyric Acid (56-12-2) ; Glutamic Acid (3KX376GY7L) ; Morphine (76I7G6D29C) ; Receptors, AMPA
Language	English
Publishing date	2021-05-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1324314-7
ISSN	1369-1600 ; 1355-6215
ISSN (online)	1369-1600
ISSN	1355-6215
DOI	10.1111/adb.13064
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Zs.A 4586: Show issues

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Article ; Online: Involvement of Lateral Habenula Dysfunction in Repetitive Mild Traumatic Brain Injury-Induced Motivational Deficits.

Flerlage, William J / Langlois, Ludovic D / Rusnak, Milan / Simmons, Sarah C / Gouty, Shawn / Armstrong, Regina C / Cox, Brian M / Symes, Aviva J / Tsuda, Mumeko C / Nugent, Fereshteh S

Journal of neurotrauma

2022 Volume 40, Issue 1-2, Page(s) 125–140

Abstract: Affective disorders including depression (characterized by reduced motivation, social withdrawal, and anhedonia), anxiety, and irritability are frequently reported as long-term consequences of mild traumatic brain injury (mTBI) in addition to cognitive ... ...

Abstract	Affective disorders including depression (characterized by reduced motivation, social withdrawal, and anhedonia), anxiety, and irritability are frequently reported as long-term consequences of mild traumatic brain injury (mTBI) in addition to cognitive deficits, suggesting a possible dysregulation within mood/motivational neural circuits. One of the important brain regions that control motivation and mood is the lateral habenula (LHb), whose hyperactivity is associated with depression. Here, we used a repetitive closed-head injury mTBI model that is associated with social deficits in adult male mice and explored the possible long-term alterations in LHb activity and motivated behavior 10-18 days post-injury. We found that mTBI increased the proportion of spontaneous tonically active LHb neurons yet decreased the proportion of LHb neurons displaying bursting activity. Additionally, mTBI diminished spontaneous glutamatergic and GABAergic synaptic activity onto LHb neurons, while synaptic excitation and inhibition (E/I) balance was shifted toward excitation through a greater suppression of GABAergic transmission. Behaviorally, mTBI increased the latency in grooming behavior in the sucrose splash test suggesting reduced self-care motivated behavior following mTBI. To show whether limiting LHb hyperactivity could restore motivational deficits in grooming behavior, we then tested the effects of Gi (hM4Di)-DREADD-mediated inhibition of LHb activity in the sucrose splash test. We found that chemogenetic inhibition of LHb glutamatergic neurons was sufficient to reverse mTBI-induced delays in grooming behavior. Overall, our study provides the first evidence for persistent LHb neuronal dysfunction due to an altered synaptic integration as causal neural correlates of dysregulated motivational states by mTBI.
MeSH term(s)	Mice ; Male ; Animals ; Habenula/physiology ; Brain Concussion/complications ; Neurons ; Motivation ; Sucrose/pharmacology
Chemical Substances	Sucrose (57-50-1)
Language	English
Publishing date	2022-09-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	645092-1
ISSN	1557-9042 ; 0897-7151
ISSN (online)	1557-9042
ISSN	0897-7151
DOI	10.1089/neu.2022.0224
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Zs.A 2016: Show issues

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Article ; Online: Biased signaling by endogenous opioid peptides.

Gomes, Ivone / Sierra, Salvador / Lueptow, Lindsay / Gupta, Achla / Gouty, Shawn / Margolis, Elyssa B / Cox, Brian M / Devi, Lakshmi A

Proceedings of the National Academy of Sciences of the United States of America

2020 Volume 117, Issue 21, Page(s) 11820–11828

Abstract: Opioids, such as morphine and fentanyl, are widely used for the treatment of severe pain; however, prolonged treatment with these drugs leads to the development of tolerance and can lead to opioid use disorder. The "Opioid Epidemic" has generated a drive ...

Abstract	Opioids, such as morphine and fentanyl, are widely used for the treatment of severe pain; however, prolonged treatment with these drugs leads to the development of tolerance and can lead to opioid use disorder. The "Opioid Epidemic" has generated a drive for a deeper understanding of the fundamental signaling mechanisms of opioid receptors. It is generally thought that the three types of opioid receptors (μ, δ, κ) are activated by endogenous peptides derived from three different precursors: Proopiomelanocortin, proenkephalin, and prodynorphin. Posttranslational processing of these precursors generates >20 peptides with opioid receptor activity, leading to a long-standing question of the significance of this repertoire of peptides. Here, we address some aspects of this question using a technical tour de force approach to systematically evaluate ligand binding and signaling properties ([
MeSH term(s)	Animals ; Cell Line, Tumor ; Humans ; Male ; Opioid Peptides/agonists ; Opioid Peptides/metabolism ; Pro-Opiomelanocortin/metabolism ; Protein Binding ; Rats ; Rats, Sprague-Dawley ; Receptors, Opioid/metabolism ; Signal Transduction/physiology
Chemical Substances	Opioid Peptides ; Receptors, Opioid ; Pro-Opiomelanocortin (66796-54-1)
Language	English
Publishing date	2020-05-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2000712117
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Zs.A 1148: Show issues

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Article: Early life stress dysregulates kappa opioid receptor signaling within the lateral habenula.

Simmons, Sarah C / Shepard, Ryan D / Gouty, Shawn / Langlois, Ludovic D / Flerlage, William J / Cox, Brian M / Nugent, Fereshteh S

Neurobiology of stress

2020 Volume 13, Page(s) 100267

Abstract: The lateral habenula (LHb) is an epithalamic brain region associated with value-based decision making and stress evasion through its modulation of dopamine (DA)-mediated reward circuitry. Specifically, increased activity of the LHb is associated with ... ...

Abstract	The lateral habenula (LHb) is an epithalamic brain region associated with value-based decision making and stress evasion through its modulation of dopamine (DA)-mediated reward circuitry. Specifically, increased activity of the LHb is associated with drug addiction, schizophrenia and stress-related disorders such as depression, anxiety and posttraumatic stress disorder. Dynorphin (Dyn)/Kappa opioid receptor (KOR) signaling is a mediator of stress response in reward circuitry. Previously, we have shown that maternal deprivation (MD), a severe early life stress, increases LHb spontaneous neuronal activity and intrinsic excitability while blunting the response of LHb neurons to extrahypothalamic corticotropin-releasing factor (CRF) signaling, another stress mediator. CRF pathways also interact with Dyn/KOR signaling. Surprisingly, there has been little study of direct KOR regulation of the LHb despite its distinct role in stress, reward and aversion processing. To test the functional role of Dyn/KOR signaling in the LHb, we utilized ex-vivo electrophysiology combined with pharmacological tools in rat LHb slices. We show that activation of KORs by a KOR agonist (U50,488) exerted differential effects on the excitability of two distinct sub-populations of LHb neurons that differed in their expression of hyperpolarization-activated cation currents (HCN, Ih). Specifically, KOR stimulation increased neuronal excitability in LHb neurons with large Ih currents (Ih+) while decreasing neuronal excitability in small/negative Ih (Ih-) neurons. We found that an intact fast-synaptic transmission was required for the effects of U50,488 on the excitability of both Ih- and Ih+ LHb neuronal subpopulations. While AMPAR-, GABA
Language	English
Publishing date	2020-11-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	2816500-7
ISSN	2352-2895
ISSN	2352-2895
DOI	10.1016/j.ynstr.2020.100267
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Article ; Online: Targeting histone deacetylation for recovery of maternal deprivation-induced changes in BDNF and AKAP150 expression in the VTA.

Shepard, Ryan D / Gouty, Shawn / Kassis, Haifa / Berenji, Aylar / Zhu, William / Cox, Brian M / Nugent, Fereshteh S

Experimental neurology

2018 Volume 309, Page(s) 160–168

Abstract: Severe early life stressors increase the probability of developing psychiatric disorders later in life through modifications in neuronal circuits controlling brain monoaminergic signaling. Our previous work demonstrated that 24 h maternal deprivation (MD) ...

Abstract	Severe early life stressors increase the probability of developing psychiatric disorders later in life through modifications in neuronal circuits controlling brain monoaminergic signaling. Our previous work demonstrated that 24 h maternal deprivation (MD) in male Sprague Dawley rats modifies dopamine (DA) signaling from the ventral tegmental area (VTA) through changes at GABAergic synapses that were reversible by in vitro histone deacetylase (HDAC) inhibition which led to restoration of the scaffold A-kinase anchoring protein (AKAP150) signaling and subsequently recovered GABAergic plasticity (Authement et al., 2015). Using a combination of in situ hybridization, Western blots and immunohistochemistry, we confirmed that MD-induced epigenetic modifications at the level of histone acetylation were associated with an upregulation of HDAC2. MD also increased Akap5 mRNA levels in the VTA. Western blot analysis of AKAP150 protein expression showed an increase in synaptic levels of AKAP150 protein in the VTA with an accompanying decrease in synaptic levels of protein kinase A (PKA). Moreover, the abundance of mature brain-derived neurotrophic factor (BDNF) protein of VTA tissues from MD rats was significantly lower than in control groups. In vivo systemic injection with a selective class I HDAC inhibitor (CI-994) was sufficient to reverse MD-induced histone hypoacetylation in the VTA for 24 h after the injection. Furthermore, HDAC inhibition normalized the levels of mBDNF and AKAP150 proteins at 24 h. Our data suggest that HDAC-mediated targeting of BDNF and AKAP-dependent local signaling within VTA could provide novel therapeutics for prevention of later-life psychopathology.
MeSH term(s)	A Kinase Anchor Proteins/metabolism ; Acetylation/drug effects ; Animals ; Brain-Derived Neurotrophic Factor/metabolism ; Dopamine/metabolism ; Enzyme Inhibitors/pharmacology ; Gene Expression Regulation/physiology ; Histone Deacetylase 2/genetics ; Histone Deacetylase 2/metabolism ; Histones/metabolism ; In Vitro Techniques ; Male ; Maternal Deprivation ; RNA, Messenger/metabolism ; Rats ; Rats, Sprague-Dawley ; Subcellular Fractions/drug effects ; Subcellular Fractions/metabolism ; Tyrosine 3-Monooxygenase/metabolism ; Ventral Tegmental Area/drug effects ; Ventral Tegmental Area/metabolism
Chemical Substances	A Kinase Anchor Proteins ; Akap5 protein, rat ; Brain-Derived Neurotrophic Factor ; Enzyme Inhibitors ; Histones ; RNA, Messenger ; Tyrosine 3-Monooxygenase (EC 1.14.16.2) ; Hdac2 protein, rat (EC 3.5.1.98) ; Histone Deacetylase 2 (EC 3.5.1.98) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2018-08-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2018.08.002
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Zs.A 184: Show issues

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Article ; Online: Mu opioid receptor activation enhances regulator of G protein signaling 4 association with the mu opioid receptor/G protein complex in a GTP-dependent manner.

Santhappan, Rema / Crowder, Alicia Tamara / Gouty, Shawn / Cox, Brian M / Côté, Thomas E

Journal of neurochemistry

2015 Volume 135, Issue 1, Page(s) 76–87

Abstract: The interaction of Regulator of G protein Signaling 4 (RGS4) with the rat mu opioid receptor (MOR)/G protein complex was investigated. Solubilized MOR from rat brain membranes was immunoprecipitated in the presence of RGS4 with antibodies against the N- ... ...

Abstract	The interaction of Regulator of G protein Signaling 4 (RGS4) with the rat mu opioid receptor (MOR)/G protein complex was investigated. Solubilized MOR from rat brain membranes was immunoprecipitated in the presence of RGS4 with antibodies against the N-terminus of MOR (anti-MOR10-70 ). Activation of MOR with [D-Ala(2) , N-Me-Phe(4) , Gly(5) -ol] enkephalin (DAMGO) during immunoprecipitation caused a 150% increase in Goα and a 50% increase in RGS4 in the pellet. When 10 μM GTP was included with DAMGO, there was an additional 72% increase in RGS4 co-immunoprecipitating with MOR (p = 0.003). Guanosine 5'-O-(3-thiotriphosphate) (GTPγS) increased the amount of co-precipitating RGS4 by 93% (compared to DAMGO alone, p = 0.008), and the inclusion of GTPγS caused the ratio of MOR to RGS4 to be 1 : 1 (31 fmoles : 28 fmoles, respectively). GTPγS also increased the association of endogenous RGS4 with MOR. In His6 RGS4/Ni(2+) -NTA agarose pull down experiments, 0.3 μM GTPγS tripled the binding of Goα to His6 RGS4, whereas the addition of 100 μM GDP blocked this effect. Importantly, activation of solubilized MOR with DAMGO in the presence of 100 μM GDP and 0.3 μM GTPγS increased Goα binding to His6 RGS4/Ni(2+) -NTA agarose (p = 0.001). Regulators of G protein Signaling (RGS) shorten the time that G proteins are active. Activation of the mu opioid receptor (MOR) causes GTP to bind to and to activate Go (αoβγ). RGS4 then binds to the activated αo-GTP/MOR complex and accelerates the intrinsic GTPase of αo. After αo dissociates from MOR, RGS4 remains bound to the C-terminal region of MOR.
MeSH term(s)	Analgesics, Opioid/pharmacology ; Animals ; Cell Line, Tumor ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-/pharmacology ; Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology ; Guanosine Triphosphate/metabolism ; Humans ; Immunoprecipitation/methods ; RGS Proteins/metabolism ; Rats ; Receptors, Opioid, mu/metabolism ; Signal Transduction/drug effects
Chemical Substances	Analgesics, Opioid ; OPRM1 protein, human ; Oprm1 protein, rat ; RGS Proteins ; Receptors, Opioid, mu ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)- (100929-53-1) ; RGS4 protein (175335-35-0) ; Guanosine 5'-O-(3-Thiotriphosphate) (37589-80-3) ; Guanosine Triphosphate (86-01-1)
Language	English
Publishing date	2015-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.13222
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