Bio


QiLiang “Q” Chen, MD, PhD, is a Pain Medicine Fellow and a postdoctoral researcher at Stanford University. He is also part of the Stanford Fellowship in Anesthesia Research (FARM) program. His research focuses on delineating the basic mechanism of chronic pain and characterizing the physiological changes in the descending pain-modulating circuits after head injury and other forms of trauma, a topic especially relevant to chronic posttraumatic pain sufferers. Clinically, his interests include integrating advanced image guidance in pain procedures and exploring novel pharmacological and minimally invasive interventions for complex headaches and craniofacial pain conditions.

Academic Appointments


Professional Education


  • Fellowship, Stanford School of Medicine, Pain Medicine
  • Residency, Stanford School of Medicine, Anesthesiology (2022)
  • Internship, Stanford School of Medicine, General Surgery (2019)
  • MD, Oregon Health & Science University, Medicine (2018)
  • PhD, Oregon Health & Science University, Neuroscience (2016)
  • MT, University of Wisconsin - Madison, Clinical Laboratory Science (2010)
  • BS, University of Wisconsin - Madison, Chemistry (2010)

All Publications


  • Shifting the Balance: How Top-Down and Bottom-Up Input Modulate Pain via the Rostral Ventromedial Medulla. Frontiers in pain research (Lausanne, Switzerland) Chen, Q., Heinricher, M. M. 2022; 3: 932476

    Abstract

    The sensory experience of pain depends not only on the transmission of noxious information (nociception), but on the state of the body in a biological, psychological, and social milieu. A brainstem pain-modulating system with its output node in the rostral ventromedial medulla (RVM) can regulate the threshold and gain for nociceptive transmission. This review considers the current understanding of how RVM pain-modulating neurons, namely ON-cells and OFF-cells, are engaged by "top-down" cognitive and emotional factors, as well as by "bottom-up" sensory inputs, to enhance or suppress pain.

    View details for DOI 10.3389/fpain.2022.932476

    View details for PubMedID 35836737

    View details for PubMedCentralID PMC9274196

  • The Molecular Basis and Pathophysiology of Trigeminal Neuralgia. International journal of molecular sciences Chen, Q., Yi, D. I., Perez, J. N., Liu, M., Chang, S. D., Barad, M. J., Lim, M., Qian, X. 2022; 23 (7)

    Abstract

    Trigeminal neuralgia (TN) is a complex orofacial pain syndrome characterized by the paroxysmal onset of pain attacks in the trigeminal distribution. The underlying mechanism for this debilitating condition is still not clearly understood. Decades of basic and clinical evidence support the demyelination hypothesis, where demyelination along the trigeminal afferent pathway is a major driver for TN pathogenesis and pathophysiology. Such pathological demyelination can be triggered by physical compression of the trigeminal ganglion or another primary demyelinating disease, such as multiple sclerosis. Further examination of TN patients and animal models has revealed significant molecular changes, channelopathies, and electrophysiological abnormalities in the affected trigeminal nerve. Interestingly, recent electrophysiological recordings and advanced functional neuroimaging data have shed new light on the global structural changes and the altered connectivity in the central pain-related circuits in TN patients. The current article aims to review the latest findings on the pathophysiology of TN and cross-examining them with the current surgical and pharmacologic management for TN patients. Understanding the underlying biology of TN could help scientists and clinicians to identify novel targets and improve treatments for this complex, debilitating disease.

    View details for DOI 10.3390/ijms23073604

    View details for PubMedID 35408959

  • Enhanced recovery pathways and patient-reported outcome measures in gynaecological oncology. Anaesthesia Chen, Q., Mariano, E. R., Lu, A. C. 2021; 76 Suppl 4: 131–38

    Abstract

    Comprehensive peri-operative care for women with gynaecological malignancy is essential to ensure optimal clinical outcomes and maximise patient experience through the continuum of care. Implementation of peri-operative enhanced recovery pathways in gynaecological oncology have been repeatedly shown to improve postoperative recovery, decrease complications and reduce healthcare costs. With increasing emphasis being placed on patient-centred care in the current healthcare environment, incorporation of patient-reported outcome data collection and analysis within the enhanced recovery pathway as part of quality measurement is not only useful, but necessary. Inclusion of patient-reported outcome enhanced recovery pathway evaluation enables clinicians to capture authentic patient-reported parameters such as subtle symptoms, changes in function and multiple dimensions of well-being, directly from the source. These data guide the treatment course by encouraging shared decision-making between the patient and clinicians and provide the necessary foundation for ongoing peri-operative quality improvement efforts. Elements of the gynaecological oncology enhanced recovery pathway are divided into five phases of care: pre-admission; pre-operative; intra-operative; postoperative; and post-discharge. The development process starts with detailing each step of the patient's journey in all five phases, then identifying stakeholder groups responsible for care at each of these phases and assembling a multidisciplinary team including: gynaecologists; anaesthetists; nurses; nutritionists; physical therapists; and others, to provide input into the institutional pathway. To practically integrate patient-reported outcomes into an enhanced recovery pathway, a validated measurement tool should be incorporated into the peri-operative workflow. The ideal tool should be concise to facilitate longitudinal assessments by the clinical staff.

    View details for DOI 10.1111/anae.15422

    View details for PubMedID 33682089

  • Awake CT-guided percutaneous stylomastoid foramen puncture and radiofrequency ablation of facial nerve for treatment of hemifacial spasm. Journal of neurosurgery Huang, B. n., Yao, M. n., Chen, Q. n., Lin, H. n., Du, X. n., Huang, H. n., Zhao, X. n., Do, H. n., Qian, X. n. 2021: 1–7

    Abstract

    Hemifacial spasm (HFS) is a debilitating neuromuscular disorder with limited treatment options. The current study describes a novel minimally invasive procedure that provided effective and sustained relief for patients with HFS. The authors provide a detailed description of the awake CT-guided percutaneous radiofrequency ablation (RFA) of the facial nerve for treatment of HFS, and they examine its clinical efficacy. This is the first time in the literature that this procedure has been applied and systematically analyzed for HFS.Patients with a history of HFS were recruited between August 2018 and April 2020. Those with a history of cerebellopontine lesions, coagulopathy, ongoing pregnancy, cardiac pacemaker or defibrillator implants, or who declined the procedure were excluded from the study. Fifty-three patients who met the study criteria were included and underwent awake CT-guided RFA. Under minimal sedation, a radiofrequency (RF) needle was used to reach the stylomastoid foramen on the affected side under CT guidance, and the facial nerve was localized using a low-frequency stimulation current. Patients were instructed to engage facial muscles as a proxy for motor monitoring during RFA. Ablation stopped when the patients' hemifacial contracture resolved. Patients were kept for inpatient monitoring for 24 hours postoperatively and were followed up monthly to monitor resolution of HFS and complications for up to 19 months.The average duration of the procedure was 32-34 minutes. Postoperatively, 91% of the patients (48/53) had complete resolution of HFS, whereas the remaining individuals had partial resolution. A total of 48 patients reported mild to moderate facial paralysis immediately post-RFA, but most resolved within 1 month. No other significant complication was observed during the study period. By the end of the study period, 5 patients had recurrence of mild HFS symptoms, whereas only 2 patients reported dissatisfaction with the treatment results.The authors report for the first time that awake CT-guided RFA of the facial nerve at the stylomastoid foramen is a minimally invasive procedure and can be an effective treatment option for HFS.

    View details for DOI 10.3171/2020.10.JNS203209

    View details for PubMedID 33862595

  • A Narrative Review on Perioperative Pain Management Strategies in Enhanced Recovery Pathways-The Past, Present and Future. Journal of clinical medicine Chen, Q., Chen, E., Qian, X. 2021; 10 (12)

    Abstract

    Effective pain management is a key component in the continuum of perioperative care to ensure optimal outcomes for surgical patients. The overutilization of opioids in the past few decades for postoperative pain control has been a major contributor to the current opioid epidemic. Multimodal analgesia (MMA) and enhanced recovery after surgery (ERAS) pathways have been repeatedly shown to significantly improve postoperative outcomes such as pain, function and satisfaction. The current review aims to examine the history of perioperative MMA strategies in ERAS and provide an update with recent evidence. Furthermore, this review details recent advancements in personalized pain medicine. We speculate that the next important step for improving perioperative pain management could be through incorporating these personalized metrics, such as clinical pharmacogenomic testing and patient-reported outcome measurements, into ERAS program.

    View details for DOI 10.3390/jcm10122568

    View details for PubMedID 34200695

  • Efficacy and Safety of Awake CT-guided Percutaneous Balloon Compression of Trigeminal Ganglion for Trigeminal Neuralgia. Pain medicine (Malden, Mass.) Huang, B., Yao, M., Chen, Q., Du, X., Li, Z., Xie, K., Fei, Y., Do, H., Qian, X. 2021

    Abstract

    To describe the method and clinical efficacy of awake CT-guided percutaneous balloon compression (PBC) as a treatment for trigeminal neuralgia (TN).In this case-series, TN patients were treated with awake CT-guided PBC and followed for treatment efficacy and complications for 12 months.A single-center study.66 patients with medical treatment-refractory TN were recruited for the study.The procedure was performed under moderate sedation. A balloon catheter was inserted through a trocar needle to reach Meckel's cavity under CT-guidance. The position and optimal shape of the contrast-filled balloon was confirmed with CT 3-dimension reconstruction. Compression of the TG was considered completed when the patient notified operators about facial hypoesthesia or the resolution of TN symptoms. All patients were followed up monthly for 12 months to monitor treatment efficacy and complications.The average TG compression time was 272±81 seconds, at which point the patients reported significant facial hypoesthesia comparing to the contralateral side or resolution of triggered pain in the affected area. All patients had resolution of TN symptoms for 6 months, with a 1-year recurrent rate of 13%. Overall safety profile is improved with the current technique. Side effects, such as hypoesthesia, and mastication weakness, were overall mild, and did not impact patients' quality-of-life. Some complications that were historically associated with PBC, such as diplopia and keratitis, were not present.This new awake CT-guided PBC technique produces better outcomes than the traditional PBC under fluoroscopy-guidance and general anesthesia.

    View details for DOI 10.1093/pm/pnab228

    View details for PubMedID 34320638

  • Perioperative Care and Airway Management for a Patient With Sagliker Syndrome CUREUS Chen, Q., Lorenzo, J., Lu, A. 2020; 12 (9)
  • Follow-Up Phone Interviews and Attendance Motivation From A Free Head and Neck Cancer Screening. Ear, nose, & throat journal Urdang, Z. D., Rosales, D. H., Chen, Q. n., Li, R. J., Andersen, P. E., Gross, N. D., Clayburgh, D. R. 2020: 145561320940866

    Abstract

    Head and Neck Cancer Awareness and Screening Programs (HNCASP) are popular community outreach events hosted by academic and community otolaryngology departments. However, long-term follow-up of participants is lacking.Participants of a HNCASP held at an academic cancer center prospectively filled out demographic and risk factor surveys followed by HNC screening examination. A phone interview was conducted for participants between 2012 and 2016 with suspicious findings to assess outcomes.Participants were largely Caucasian, female, and had health insurance, reflecting the setting at an academic medical center. Despite this, there were 156 (16.8%) positive screenings; 47 of these completed follow up interviews. Twelve (1.1% of all participants) cancer cases were confirmed.A significant proportion of HNCASP participants benefited from this screening opportunity. Education regarding HNC is the primary benefit and motivational factor for attendance of HNCASPs, although a significant subset of patients was identified that needed follow-up, and several cancers were detected.

    View details for DOI 10.1177/0145561320940866

    View details for PubMedID 32703031

  • Role of fragile X mental retardation protein in chronic pain Molecular pain Mei, X., Yang, Y., Zhao, J., Wang, Y., Chen, Q., Qian, X., Li, X., Feng, Z. 2020; 16 (1744806920928619)

    View details for DOI 10.1177/1744806920928619

  • Descending Control Mechanisms and Chronic Pain CURRENT RHEUMATOLOGY REPORTS Chen, Q., Heinricher, M. M. 2019; 21 (5)
  • Plasticity in the Link between Pain-Transmitting and Pain-Modulating Systems in Acute and Persistent Inflammation JOURNAL OF NEUROSCIENCE Chen, Q., Heinricher, M. M. 2019; 39 (11): 2065–79

    Abstract

    There is strong evidence that spinoparabrachial neurons in the superficial dorsal horn contribute to persistent pain states, and that the lateral parabrachial complex (PB) conveys relevant nociceptive information to higher structures. The role of PB itself in hyperalgesia and how it recruits descending facilitation has nevertheless received significantly less attention. The current study is a first step toward delineating the functional dynamics of PB and its link to descending control in acute and persistent inflammatory pain. In lightly anesthetized rats, we recorded behavioral withdrawal evoked by mechanical stimulation of the hindpaw and, simultaneously, the activity of identified pain-modulating neurons, "ON-cells" and "OFF-cells," in the rostral ventromedial medulla (RVM). This was done before and after the inactivation of PB, contralateral or ipsilateral to an inflamed paw [1 h, 1 d, or 5-6 d after intraplantar injection of Complete Freund's Adjuvant (CFA)]. The inactivation of contralateral, but not ipsilateral, PB interfered with nociceptive input to RVM under basal conditions, as well as in acute inflammation. By contrast, blocking ipsilateral, but not contralateral, PB in established inflammation interfered with behavioral hyperalgesia and ON-cell and OFF-cell responses. The lesioning of contralateral PB before CFA injection prevented this recruitment of ipsilateral PB in persistent inflammation. These experiments show that contralateral PB is required to initiate hyperalgesia, which is then maintained by ipsilateral PB, most likely in both cases via the engagement of pain-modulating neurons of the RVM.SIGNIFICANCE STATEMENT The lateral parabrachial complex (PB) relays nociceptive information to brain circuits that are important for the transmission and modulation of pain, but its specific role in persistent pain and engagement of descending control mechanisms has received relatively little attention. We show here that PB contralateral and ipsilateral to an inflammatory insult demonstrate different functions as inflammation persists, likely by engaging pain-facilitating neurons of the rostral ventromedial medulla. While the contralateral PB, the target of the major spinoparabrachial pathway, relays acute nociceptive information, the ipsilateral PB is recruited or unmasked in persistent inflammation to maintain hyperalgesia. These data point to plasticity in the PB itself or its direct and indirect connections with pain-modulating systems as central to the development and maintenance of persistent pain.

    View details for PubMedID 30651329

  • Descending Control Mechanisms and Chronic Pain. Current rheumatology reports Chen, Q., Heinricher, M. M. 2019; 21 (5): 13

    Abstract

    PURPOSE OF REVIEW: The goal of the review was to highlight recent advances in our understanding of descending pain-modulating systems and how these contribute to persistent pain states, with an emphasis on the current state of knowledge around "bottom-up" (sensory) and "top-down" (higher structures mediating cognitive and emotional processing) influences on pain-modulating circuits.RECENT FINDINGS: The connectivity, physiology, and function of these systems have been characterized extensively over the last 30years. The field is now beginning to ask how and when these systems are engaged to modulate pain. A recent focus is on the parabrachial complex, now recognized as the major relay of nociceptive information to pain-modulating circuits, and plasticity in this circuit and its connections to the RVM is marked in persistent inflammatory pain. Top-down influences from higher structures, including hypothalamus, amygdala, and medial prefrontal areas, are also considered. The challenge will be to tease out mechanisms through which a particular behavioral context engages distinct circuits to enhance or suppress pain, and to understand how these mechanisms contribute to chronic pain.

    View details for PubMedID 30830471

  • Efficacy of Dextromethorphan/Quinidine for Patients With Psychosis-Related Aggression: A Retrospective Case Series. The primary care companion for CNS disorders Chen, Q., Calcagno, H. E., Shad, M. 2018; 20 (3)

    Abstract

    Treatment-resistant aggressive behavior is a complex psychoneurological phenomenon with high health care and societal costs commonly observed in mental illnesses involving psychosis. Here, we report a preliminary evaluation of treatment with dextromethorphan/quinidine in 4 adult patients with significant history of psychosis-related aggression and impulsive behaviors.The files of 4 inpatients with DSM-5-defined psychotic disorder and treatment-resistant aggression treated at the Oregon State Hospital (Salem, Oregon) between June and November of 2017 were retrospectively analyzed. The patients (age: mean ± SD = 59.8 ± 7.6) received open-label treatment with dextromethorphan/quinidine (final dose 20 mg/10 mg twice daily) for at least 12 weeks. Outcome was measured on the basis of patient self-report, treatment team evaluation, and physical examination by psychiatrists and primary care physicians.Three of the 4 patients were considered responders to dextromethorphan/quinidine based on clinical impressions of reduction in aggression and impulsive behavior. The nonresponder, who had a history of multiple traumatic brain injuries, showed mild improvement in agitation but continued to display impulsive self-harm behavior despite treatment. Dextromethorphan/quinidine was generally well-tolerated. No metabolic, gastrointestinal, or cardiovascular side effects were observed.These preliminary findings support dextromethorphan/quinidine as a potential alternative to conventional regimens for treating aggression and impulsive behavior in patients with psychotic disorder. These results should be interpreted cautiously, as extended, double-blinded, placebo-controlled studies with a larger sample size are needed to validate findings from this retrospective case series.

    View details for DOI 10.4088/PCC.18m02284

    View details for PubMedID 29985567

  • Unmasking the Pain in Latent Sensitization. Neuroscience Chen, Q., Heinricher, M. M. 2018; 381: 159-160

    View details for DOI 10.1016/j.neuroscience.2018.04.007

    View details for PubMedID 29776485

  • Effectiveness of Dextromethorphan/Quinidine in Frontotemporal Dementia. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry Chen, Q., Ermann, A., Shad, M. U. 2018; 26 (4): 506

    View details for DOI 10.1016/j.jagp.2017.10.008

    View details for PubMedID 29132987

  • Optogenetic Evidence for a Direct Circuit Linking Nociceptive Transmission through the Parabrachial Complex with Pain-Modulating Neurons of the Rostral Ventromedial Medulla (RVM). eNeuro Chen, Q., Roeder, Z., Li, M. H., Zhang, Y., Ingram, S. L., Heinricher, M. M. 2017; 4 (3)

    Abstract

    The parabrachial complex (PB) is a functionally and anatomically complex structure involved in a range of homeostatic and sensory functions, including nociceptive transmission. There is also evidence that PB can engage descending pain-modulating systems, the best characterized of which is the rostral ventromedial medulla (RVM). Two distinct classes of RVM neurons, "ON-cells" and "OFF-cells," exert net pronociceptive and anti-nociceptive effects, respectively. PB was recently shown to be a relay of nociceptive information to RVM ON- and OFF-cells. The present experiments used optogenetic methods in a lightly anesthetized rat and an adult RVM slice to determine whether there are direct, functionally relevant inputs to RVM pain-modulating neurons from PB. Whole-cell patch-clamp recordings demonstrated that PB conveys direct glutamatergic and GABAergic inputs to RVM neurons. Consistent with this, in vivo recording showed that nociceptive-evoked responses of ON- and OFF-cells were suppressed by optogenetic inactivation of archaerhodopsin (ArchT)-expressing PB terminals in RVM, demonstrating that a net inhibitory input to OFF-cells and net excitatory input to ON-cells are engaged by acute noxious stimulation. Further, the majority of ON- and OFF-cells responded to optogenetic activation of channelrhodopsin (ChR2)-expressing terminals in the RVM, confirming a direct PB influence on RVM pain-modulating neurons. These data show that a direct connection from the PB to the RVM conveys nociceptive information to the pain-modulating neurons of RVM under basal conditions. They also reveal additional inputs from PB with the capacity to activate both classes of RVM pain-modulating neurons and the potential to be recruited under different physiological and pathophysiological conditions.

    View details for DOI 10.1523/ENEURO.0202-17.2017

    View details for PubMedID 28660248

    View details for PubMedCentralID PMC5483601

  • Parabrachial complex links pain transmission to descending pain modulation. Pain Roeder, Z., Chen, Q., Davis, S., Carlson, J. D., Tupone, D., Heinricher, M. M. 2016; 157 (12): 2697-2708

    Abstract

    The rostral ventromedial medulla (RVM) has a well-documented role in pain modulation and exerts antinociceptive and pronociceptive influences mediated by 2 distinct classes of neurons, OFF-cells and ON-cells. OFF-cells are defined by a sudden pause in firing in response to nociceptive inputs, whereas ON-cells are characterized by a "burst" of activity. Although these reflex-related changes in ON- and OFF-cell firing are critical to their pain-modulating function, the pathways mediating these responses have not been identified. The present experiments were designed to test the hypothesis that nociceptive input to the RVM is relayed through the parabrachial complex (PB). In electrophysiological studies, ON- and OFF-cells were recorded in the RVM of lightly anesthetized male rats before and after an infusion of lidocaine or muscimol into PB. The ON-cell burst and OFF-cell pause evoked by noxious heat or mechanical probing were substantially attenuated by inactivation of the lateral, but not medial, parabrachial area. Retrograde tracing studies showed that neurons projecting to the RVM were scattered throughout PB. Few of these neurons expressed calcitonin gene-related peptide, suggesting that the RVM projection from PB is distinct from that to the amygdala. These data show that a substantial component of "bottom-up" nociceptive drive to RVM pain-modulating neurons is relayed through the PB. While the PB is well known as an important relay for ascending nociceptive information, its functional connection with the RVM allows the spinoparabrachial pathway to access descending control systems as part of a recurrent circuit.

    View details for DOI 10.1097/j.pain.0000000000000688

    View details for PubMedID 27657698

    View details for PubMedCentralID PMC5113739

  • Contribution of adenylyl cyclase modulation of pre- and postsynaptic GABA neurotransmission to morphine antinociception and tolerance. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology Bobeck, E. N., Chen, Q., Morgan, M. M., Ingram, S. L. 2014; 39 (9): 2142-52

    Abstract

    Opioid inhibition of presynaptic GABA release in the ventrolateral periaqueductal gray (vlPAG) activates the descending antinociception pathway. Tolerance to repeated opioid administration is associated with upregulation of adenylyl cyclase activity. The objective of these studies was to test the hypothesis that adenylyl cyclase contributes to opioid tolerance by modulating GABA neurotransmission. Repeated microinjections of morphine or the adenylyl cyclase activator NKH477 into the vlPAG decreased morphine antinociception as would be expected with the development of tolerance. Conversely, microinjection of the adenylyl cyclase inhibitor SQ22536 reversed both the development and expression of morphine tolerance. These behavioral results indicate that morphine tolerance is dependent on adenylyl cyclase activation. Electrophysiological experiments revealed that acute activation of adenylyl cyclase with forskolin increased the frequency of presynaptic GABA release. However, recordings from rats treated with repeated morphine administration did not exhibit increased basal miniature inhibitory postsynaptic current (mIPSC) frequency but showed a decrease in mean amplitude of mIPSCs indicating that repeated morphine administration modulates postsynaptic GABAA receptors without affecting the probability of presynaptic GABA release. SQ22536 reversed this change in mIPSC amplitude and inhibited mIPSC frequency selectively in morphine tolerant rats. Repeated morphine or NKH477 administration also decreased antinociception induced by microinjection of the GABAA receptor antagonist bicuculline, further demonstrating changes in GABA neurotransmission with morphine tolerance. These results show that the upregulation of adenylyl cyclase caused by repeated vlPAG morphine administration produces antinociceptive tolerance by modulating both pre- and postsynaptic GABA neurotransmission.

    View details for DOI 10.1038/npp.2014.62

    View details for PubMedID 24622471

    View details for PubMedCentralID PMC4104331

  • Empathy is moderated by genetic background in mice. PloS one Chen, Q., Panksepp, J. B., Lahvis, G. P. 2009; 4 (2): e4387

    Abstract

    Empathy, as originally defined, refers to an emotional experience that is shared among individuals. When discomfort or alarm is detected in another, a variety of behavioral responses can follow, including greater levels of nurturing, consolation or increased vigilance towards a threat. Moreover, changes in systemic physiology often accompany the recognition of distressed states in others. Employing a mouse model of cue-conditioned fear, we asked whether exposure to conspecific distress influences how a mouse subsequently responds to environmental cues that predict this distress. We found that mice are responsive to environmental cues that predict social distress, that their heart rate changes when distress vocalizations are emitted from conspecifics, and that genetic background substantially influences the magnitude of these responses. Specifically, during a series of pre-exposure sessions, repeated experiences of object mice that were exposed to a tone-shock (CS-UCS) contingency resulted in heart rate deceleration in subjects from the gregarious C57BL/6J (B6) strain, but not in subjects from the less social BALB/cJ (BALB) strain. Following the pre-exposure sessions, subjects were individually presented with the CS-only for 5 consecutive trials followed by 5 consecutive pairings of the CS with the UCS. Pre-exposure to object distress increased the freezing responses of B6 mice, but not BALB mice, on both the CS-only and the CS-UCS trials. These physiological and behavioral responses of B6 mice to social distress parallel features of human empathy. Our paradigm thus has construct and face validity with contemporary views of empathy, and provides unequivocal evidence for a genetic contribution to the expression of empathic behavior.

    View details for DOI 10.1371/journal.pone.0004387

    View details for PubMedID 19209221

    View details for PubMedCentralID PMC2633046

  • Affiliative behavior, ultrasonic communication and social reward are influenced by genetic variation in adolescent mice. PloS one Panksepp, J. B., Jochman, K. A., Kim, J. U., Koy, J. J., Wilson, E. D., Chen, Q., Wilson, C. R., Lahvis, G. P. 2007; 2 (4): e351

    Abstract

    Social approach is crucial for establishing relationships among individuals. In rodents, social approach has been studied primarily within the context of behavioral phenomena related to sexual reproduction, such as mating, territory defense and parental care. However, many forms of social interaction occur before the onset of reproductive maturity, which suggests that some processes underlying social approach among juvenile animals are probably distinct from those in adults. We conducted a longitudinal study of social investigation (SI) in mice from two inbred strains to assess the extent to which genetic factors influence the motivation for young mice to approach one another. Early-adolescent C57BL/6J (B6) mice, tested 4-6 days after weaning, investigated former cage mates to a greater degree than BALB/cJ (BALB) mice, irrespective of the sex composition within an interacting pair. This strain difference was not due to variation in maternal care, the phenotypic characteristics of stimulus mice or sensitivity to the length of isolation prior to testing, nor was it attributable to a general difference in appetitive motivation. Ultrasonic vocalization (USV) production was positively correlated with the SI responses of mice from both strains. Interestingly, several USV characteristics segregated with the genetic background of young mice, including a higher average frequency and shorter duration for the USVs emitted by B6 mice. An assessment of conditioned place preference responses indicated that there was a strain-dependent difference in the rewarding nature of social contact. As adolescent mice aged, SI responses gradually became less sensitive to genetic background and more responsive to the particular sex of individuals within an interacting pair. We have thus identified a specific, genetic influence on the motivation of early-adolescent mice to approach one another. Consistent with classical theories of motivation, which propose a functional relationship between behavioral approach and reward, our findings indicate that reward is a proximal mechanism through which genetic factors affect social motivation during early adolescence.

    View details for DOI 10.1371/journal.pone.0000351

    View details for PubMedID 17406675

    View details for PubMedCentralID PMC1831495

  • Role of fragile X mental retardation protein in chronic pain. Molecular pain Mei, X. n., Yang, Y. n., Zhao, J. n., Wang, Y. n., Chen, Q. n., Qian, X. n., Li, X. n., Feng, Z. n. ; 16: 1744806920928619

    Abstract

    Chronic pain has detrimental effects on one's quality of life. However, its treatment options are very limited, and its underlying pathogenesis remains unclear. Recent research has suggested that fragile X mental retardation protein is involved in the development of chronic pain, making it a potential target for prevention and treatment. The current review of literature will examine the function of fragile X mental retardation protein and its associated pathways, through which we hope to gain insight into how fragile X mental retardation protein may contribute to nociceptive sensitization and chronic pain.

    View details for DOI 10.1177/1744806920928619

    View details for PubMedID 32496847