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Role of 5-hydroxytryptamine type 3 receptors in the regulation of anxiety reactions

Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2024年第1期25卷 23-37页

作者： Yinan DU Zhiwei LI Yukui ZHAO Jing HAN Weiping HU Zhiqiang LIU MOE Key Laboratory of Modern Teaching Technology Shaanxi Normal UniversityXi’an710062China

5-Hydroxytryptamine(5-HT)type 3 receptor(5-HT_(3)R)is the only type of ligand-gated ion channel in the 5-HT receptor family.Through the high permeability of Na+,K+,and Ca2+and activation of subsequent voltage-gated calcium channels(VGCCs),5-HT_(3)R induces a rapid increase of neuronal excitability or the release of neurotransmitters from axon terminals in the central nervous system(CNS).5-HT_(3)Rs are widely expressed in the medial prefrontal cortex(mPFC),amygdala(AMYG),hippocampus(HIP),periaqueductal gray(PAG),and other brain regions closely associated with anxiety reactions.They have a bidirectional regulatory effect on anxiety reactions by acting on different types of cells in different brain regions.5-HT_(3)Rs mediate the activation of the cholecystokinin(CCK)system in the AMYG,and theγ-aminobutyric acid(GABA)“disinhibition”mechanism in the prelimbic area of the mPFC promotes anxiety by the activation of GABAergic intermediate inhibitory neurons(IINs).In contrast,a 5-HT_(3)R-induced GABA“disinhibition”mechanism in the infralimbic area of the mPFC and the ventral HIP produces anxiolytic effects.5-HT_(2)R-mediated regulation of anxiety reactions are also activated by 5-HT_(3)R-activated 5-HT release in the HIP and PAG.This provides a theoretical basis for the treatment of anxiety disorders or the production of anxiolytic drugs by targeting 5-HT_(3)Rs.However,given the circuit specific modulation of 5-HT_(3)Rs on emotion,systemic use of 5-HT_(3)R agonism or antagonism alone seems unlikely to remedy anxiety,which deeply hinders the current clinical application of 5-HT_(3)R drugs.Therefore,the exploitation of circuit targeting methods or a combined drug strategy might be a useful developmental approach in the future.

关键词： 5-Hydroxytryptamine type 3 receptor(5-HT_(3)R) Anxiety Medial prefrontal cortex Amygdala Hippocampus periaqueductal gray

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The periaqueductal gray and Its Extended Participation in Drug Addiction Phenomena

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Neuroscience Bulletin 2021年第10期37卷 1493-1509页

作者： Priscila Vazquez-Leon Abraham Miranda-Paez Jesus Chavez-Reyes Gonzalo Allende Paulino Barragan-Iglesias Bruno A.Marichal-Cancino Departamento de Fisiologia y Farmacologia Centro de Ciencias BasicasUniversidad Autonoma de AguascalientesCiudad Universitaria20131 AguascalientesAgs.Mexico Departamento de Fisiologia Escuela Nacional de Ciencias BiologicasInstituto Politecnico NacionalWilfrido Massieu esq.Manuel Stampa s/n Col.Nueva Industrial Vallejo07738 Gustavo A.MaderoMexico CityMexico

The periaqueductal gray(PAG)is a complex mesencephalic structure involved in the integration and execution of active and passive self-protective behaviors against imminent threats,such as immobility or flight from a predator.PAG activity is also associated with the integration of responses against physical discomfort(e.g.,anxiety,fear,pain,and disgust)which occurs prior an imminent attack,but also during withdrawal from drugs such as morphine and cocaine.The PAG sends and receives projections to and from other well-documented nuclei linked to the phenomenon of drug addiction including:(i)the ventral tegmental area;(ii)extended amygdala;(iii)medial prefrontal cortex;(iv)pontine nucleus;(v)bed nucleus of the stria terminalis;and(vi)hypothalamus.Preclinical models have suggested that the PAG contributes to the modulation of anxiety,fear,and nociception(all of which may produce physical discomfort)linked with chronic exposure to drugs of abuse.Withdrawal produced by the major pharmacological classes of drugs of abuse is mediated through actions that include participation of the PAG.In support of this,there is evidence of functional,pharmacological,molecular.And/or genetic alterations in the PAG during the impulsive/compulsive intake or withdrawal from a drug.Due to its small size,it is difficult to assess the anatomical participation of the PAG when using classical neuroimaging techniques,so its phys-iopathology in drug addiction has been underestimated and poorly documented.In this theoretical review,we discuss the involvement of the PAG in drug addiction mainly via its role as an integrator of responses to the physical discomfort associated with drug withdrawal.

关键词： periaqueductal gray Reward circuit Antireward circuit Alcohol Caffeine Cannabis Opioids Stimulants

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Switching from morphine to fentanyl attenuates the decline of μ-opioid receptor expression in periaqueductal gray of rats with morphine tolerance

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Chinese Medical Journal 2013年第19期126卷 3712-3716页

作者： DONG Yan-peng SUN Li LIU Xiao-yan LIU Ruo-shan Department of Anesthesiology Cancer Hospital and Institute PekingUnion Medical College and Chinese Academy of Medical SciencesBeijing 100021 China

Background Opioid switching is a therapeutic maneuver to improve analgesic response and/or reduce adverse side effects although the underlying mechanisms remain unknown.The μ-opioid receptor （MOR） has an important role in mediating the actions of morphine and other analgesic agents.This study is aimed at exploring the changes of MOR in the periaqueductal gray （PAG） in rats when morphine is substituted for equianalgesic fentanyl.Methods Forty rats were randomly assigned to five treatment groups：7 days normal saline group （N group）,7 days fentanyl group （F group）,7 days morphine group （M group）,7 days morphine and 7 days fentanyl-switching group （MF group）,and 14 days morphine group （MM group）.Rats repeatedly received subcutaneous injections of morphine sulfate （10 mg/kg） or equianalgesic fentanyl sulfate （0.1 mg/kg） twice daily.Rats＇ antinociceptive response to thermal pain was evaluated by the tail flick latency assay.MOR mRNA and protein expression in the PAG were measured using RT-PCR and Western blotting analyses respectively.Results This study showed that after morphine was substituted with fentanyl on day 8,the tail flick latency （TFL） increased from （3.9±0.4） seconds to （11.4±0.4） seconds.The results also demonstrated that both MOR mRNA and protein expression in the PAG of rats in the MF group were less than that in the M group （P〈0.05） but more than that in MM group （P〈0.05）.Conclusions Equianalgesic fentanyl was still antinociceptive effective in rats with morphine tolerance,which may be due to the switching from morphine to fentanyl attenuating the decline of MOR expression in the PAG of rats.

关键词： morphine Jentanyl tolerance switching μ-opioid receptor periaqueductal gray

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Preoperative Acute Sleep Deprivation Causes Postoperative Pain Hypersensitivity and Abnormal Cerebral Function

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Neuroscience Bulletin 2022年第12期38卷 1491-1507页

作者： Meimei Guo Yuxiang Wu Danhao Zheng Lei Chen Bingrui Xiong Jinfeng Wu Ke Li Li Wang Kangguang Lin Zongze Zhang Anne Manyande Fuqiang Xu Jie Wang Mian Peng Department of Anesthesiology Zhongnan Hospital of Wuhan UniversityWuhan 430071China Department of Health and Kinesiology School of Physical EducationJianghan UniversityWuhan 430056China State Key Laboratory of Magnetic Resonance and Atomic and Molecular Physics National Center for Magnetic Resonance in WuhanWuhan Institute of Physics and MathematicsInnovation Academy for Precision Measurement Science and TechnologyChinese Academy of Sciences-Wuhan National Laboratory for OptoelectronicsWuhan 430071China Department of Anesthesiology Peking University Third HospitalBeijing 100191China Department of Afective Disorders The Afliated Brain Hospital of Guangzhou Medical UniversityGuangzhou 510000China School of Human and Social Sciences University of West LondonLondon W1S 3PRUK Institute of Neuroscience and Brain Disease Xiangyang Central HospitalAfliated Hospital of Hubei University of Arts and ScienceXiangyang 441000China University of Chinese Academy of Sciences Beijing 100049China

Preoperative sleep loss can amplify post-operative mechanical hyperalgesia.However,the underlying mechanisms are still largely unknown.In the current study,rats were randomly allocated to a control group and an acute sleep deprivation(ASD)group which experienced 6 h ASD before surgery.Then the variations in cerebral function and activity were investigated with multi-modal techniques,such as nuclear magnetic resonance,functional magnetic resonance imaging,c-Fos immunofluorescence,and electrophysiology.The results indicated that ASD induced hyperalgesia,and the metabolic kinetics were remarkably decreased in the striatum and midbrain.The functional connectivity(FC)between the nucleus accumbens(NAc,a subregion of the ventral striatum)and the ventrolateral periaqueductal gray(vLPAG)was significantly reduced,and the c-Fos expression in the NAc and the vLPAG was suppressed.Furthermore,the electrophysiological recordings demonstrated that both the neuronal activity in the NAc and the vLPAG,and the coherence of the NAc-vLPAG were suppressed in both resting and task states.This study showed that neuronal activity in the NAc and the vLPAG were weakened and the FC between the NAc and the vLPAG was also suppressed in rats with ASD-induced hyperalgesia.This study highlights the importance of preoperative sleep management for surgical patients.

关键词： Acute sleep deprivation Incisional pain Nucleus accumbens periaqueductal gray Functional connectivity

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Functional interaction between orexin and CB1 receptors in the periaqueductal gray matter on antinociceptive responses induced by stimulation of the lateral hypothalamus

Functional interaction between orexin and CB1 receptors in t...

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中国神经科学学会第十二届全国学术会议

作者： Leila Zarepour Abbas Haghparast Department of Physiology Iran University of Medical Sciences Neuroscience Research Center School of Medicine Shahid Beheshti University of Medical Sciences

Orexin receptors are found at high density in the ventrolateral periaqueductal gray matter（vl PAG）. Chemical stimulation of the lateral hypothalamus（LH） with carbachol induces antinociception in the tail-flick test, a model of acute pain. In the current study, we tried to examine the effect of TCS OX2 29 as an Ox2 r antagonist（5, 15, 50, 150 and 500 n M） microinjected into the vl PAG on LH-induced antinociception by carbachol administration（125 n M）. TCS OX2 29 dose dependently reduced carbacholinduced antinociception. In our previous study, we showed that the vl PAG CB1 receptors are involved in mediation of antinociceptive effect of carbachol. In the second set of experiments, animals were treated with carbachol 5 min after intra-vl PAG administration of 15 n M TCS OX2 29 and 1 n M AM251（as a selective CB1 receptor antagonist）, or 150 n M TCS OX2 29 and 10 n M AM251. The findings showed that the antinociceptive effect of orexin is partially mediated by activation of vl PAG Ox2 receptors. Furthermore, the administration of ineffective doses of Ox2 and CB1 receptor antagonists reduced the LHinduced antinociception. It seems that the orexinergic and cannabinoid systems in the PAG cooperate in the mediation of LH-induced antinociception.

关键词： Pain Lateral hypothalamus periaqueductal gray Orexin-2 receptor CB1 receptor Tail-flick test

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The role of HCN channels within the periaqueductal gray in neuropathic pain

The role of HCN channels within the periaqueductal gray in n...

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中国神经科学学会第十届全国学术会议

作者： Lu Du Huai-Zhen Ruan Department of Neurobiology Chongqing Key Laboratory of NeurobiologyThird Military Medical University

Background:Peripheral and spinal hyperpolarization-activated cyclic nucleotide-gated（HCN） channels play a key role in neuropathic pain by regulating neuronal *** channels are expressed in the ventral-lateral periaqueductal gray（vlPAG）,a region that is important for pain modulation.However,the role of vlPAG HCN channels in neuropathic pain remains poorly understood.In the present study,we investigated the impact of changes to vlPAG HCN channels on neural activity in neuropathic pain.Methods:First,sciatic nerve chronic constriction injury（CCI） was established as a neuropathic pain model.Then,changes in HCN channels and their influence on vlPAG neuronal activity were detected.Finally,role of the channels alteration was verified by the intra-vlPAG infusion of ZD7288,a specific HCN blocker.Results:After CCI surgery the following changes occur in vlPAG neurons:the expression of HCN1 and HCN2 channels is increased,the amplitude of the \h is augmented and its activation curve is shifted to more positive potentials and there is an increase in the frequency of AP firing and spontaneous EPSCs that is attenuated by ZD7288,a HCN channel blocker.In addition,forskolin,which can elevate intracellular cAMP,mimics the CCI induced changes in neuronal excitability in the vlPAG.The effects of forskolin were also reversed by ZD7288.Intra-vlPAG infusion of ZD7288 significantly relieved mechanical allodyma and thermal hyperalgesia in CCI animals.Conclusion:Taken together,HCN channels in the vlPAG play an important role in neuropathic pain by modulating neural activity and impact the facilitation role of vlPAG.

关键词： neuropathic pain hyperpolarization-activated cyclic nucleotide-gated cation channel periaqueductal gray ZD7288

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PVT-CeA-PAG pathway facilitating neuropathic pain information transmission

PVT-CeA-PAG pathway facilitating neuropathic pain informatio...

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中国神经科学学会第十二届全国学术会议

作者： Shao-Hua Liang Yu-Lin Dong Yun-Qing Li Department of Anatomy and K.K.Leung Brain Research Centre The Fourth Military Medical University Collaborative Innovation Center for Brain Science Fudan University

Objective The paraventricular thalamic nucleus（PVT） is considered to be a critical site for the integration of neural signals and to modulate both visceral information and negative emotions. The aim of the present study was attempted to investigate the activation of PVT neurons involved in modulation of the mechanical allodynia induced by neuropathic pain and the PVT-central amygdaloid nucleus（Ce A）-periaqueductal gray（PAG） pathway might underlie the descending facilitative effects on the nociceptive transmission. Methods The connections of the PVT-Ce A-PAG pathway was confirmed by morphological tract tracing techniques. The facilitating effects of this pathway for the neuropathic pain information transmission were demonstrated with patch-clamp recording, behavior observation and optogenetic approach. Results（1） It was found that paw withdrawal threshold（PWT） was increased significantly（P ＜0.01） after the inhibition of PVT neuronal activations by chemical or pharmacogenetic lesion in spared nerve injury（SNI） rats.（2） The frequency, but not amplitude of the spontaneous excitatory postsynaptic currents（s EPSCs） of PVT neurons which sent projection fibers to Ce A was significantly increased in the SNI rats. Selective activation of PVT-Ce A pathway by optogenetic approach induced obvious mechanical allodynia in the naive rats.（3） After injection of biotinylated dextran amine（BDA） into PVT and fluoro-gold（FG） into the ventrolateral subregion of the PAG, respectively, BDA-labeled fibers and terminals originated from PVT were found to make asymmetric synapses with FGlabeled neurons in Ce A which projected to PAG.（4）It was demonstrated that the Ce APAG connection was GABAergic in nature. Conclusion The present results suggest that there is a novel PVT-Ce A-PAG pathway which is essential for descending facilitation on neuropathic pain information transmission.

关键词： paraventricular thalamic nucleus central amygdaloid nucleus periaqueductal gray pathway neuropathic pain facilitation

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Modulation of pain by activating circuit of thalamic nucleus submediusventrolateral orbital cortex-periaqueductal gay

Modulation of pain by activating circuit of thalamic nucleus...

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Jing-Shi TANG~*,Fu-Quan HUO,Chao-Ling QU Department of Physiology and Pathophysiology,Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education,Xi’an Jiaotong University School of Medicine,Xi’an 710061,China

In view of the anatomical and electrophysiological studies,we propose that the thalamic submedius nucleus (Sm) and the ventrolateral orbital cortex(VLO) are involved in modulation of nociception such that activation of ascending nociceceptive pathway through Sm to VLO leads to activation of the periaqueductal gray(PAG) brainstem descending inhibitory system and depression of nociceptive inputs at the spinal and trigeminal levels.To provide support for this hypothesis,we carried out a series of experiments using animal behavioral,electrophysiological,neuropharmacological and immunohistochemical methods.The results are summarized as follows.(1).Bilateral electrolytic lesions or GABAinduced inhibition of Sm or VLO facilitated the rat tail-flick(TF) reflex(shortened TF latency) and eliminated the analgesia induced by high intensity(5 mA) electroacupuncture(EA) stimulation but not by low intensity(0.5 mA) EA stimulation as assessed by the TF test and the nociceptive responses of neurons in the spinal dorsal horn.(2).Electrically or chemically evoked-activation of Sm or VLO depressed the TF reflex,jaw-opening reflex and nociceptive responses of the spinal dorsal horn neurons,and that these antinociceptive effects were blocked by electrolytic lesions of or GABA-induced depression of VLO or PAG.(3).Microinjection of opioid agents into Sm or VLO depressed the TF reflex,formalin or bee venom-induced nociceptive behaviors and Fos expression in the spinal dorsal horn as well as the allodynia induced in a neuropathic pain model,and that these effects were antagonized byμ-opioid receptor antagonist,but not by 8- and K-opioid receptor antagonists.Systemic morphine inhibited the activity of On-cells and excited the activity of Off-cells in Sm,the interaction of two classes of pain modulatory neurons may be the cellular mechanism of opioid-induced descending antinociception. (4).Microinjection of 5-HT receptor agonists into Sm or VLO depressed the TF reflex,formalin-induced nociceptive behaviors and Fos expression in the spinal d

关键词： thalamic submedius nucleus ventrolateral orbital cortex periaqueductal gray nociceptive modulation opioid serotonin dopamine glutamate GABA

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