scholarly journals Role of astrocytes and altered regulation of spinal glutamatergic neurotransmission in stress-induced visceral hyperalgesia in rats

2011 ◽  
Vol 301 (3) ◽  
pp. G580-G589 ◽  
Author(s):  
Sylvie Bradesi ◽  
Viktoriya Golovatscka ◽  
Helena S. Ennes ◽  
James A. McRoberts ◽  
Iordanes Karagiannidis ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Critical Role ◽  
Nociceptive Response ◽  
Control Mechanisms ◽  
Glutamatergic Neurotransmission ◽  
Visceral Hyperalgesia ◽  
Excitatory Neurotransmitter ◽  
Pharmacological Inhibition ◽  
Male Wistar Rats

Glutamate (Glu) is the primary excitatory neurotransmitter in the central nervous system and plays a critical role in the neuroplasticity of nociceptive networks. We aimed to examine the role of spinal astroglia in the modulation of glutamatergic neurotransmission in a model of chronic psychological stress-induced visceral hyperalgesia in male Wistar rats. We assessed the effect of chronic stress on different glial Glu control mechanisms in the spinal cord including N-methyl-d-aspartate receptors (NMDARs), glial Glu transporters (GLT1 and GLAST), the Glu conversion enzyme glutamine synthetase (GS), and glial fibrillary acidic protein (GFAP). We also tested the effect of pharmacological inhibition of NMDAR activation, of extracellular Glu reuptake, and of astrocyte function on visceral nociceptive response in naive and stressed rats. We observed stress-induced decreased expression of spinal GLT1, GFAP, and GS, whereas GLAST expression was upregulated. Although visceral hyperalgesia was blocked by pharmacological inhibition of spinal NMDARs, we observed no stress effects on NMDAR subunit expression or phosphorylation. The glial modulating agent propentofylline blocked stress-induced visceral hyperalgesia, and blockade of GLT1 function in control rats resulted in enhanced visceral nociceptive response. These findings provide evidence for stress-induced modulation of glia-controlled spinal Glu-ergic neurotransmission and its involvement in chronic stress-induced visceral hyperalgesia. The findings reported in this study demonstrate a unique pattern of stress-induced changes in spinal Glu signaling and metabolism associated with enhanced responses to visceral distension.

The Main Sequence of Human Optokinetic Afternystagmus (OKAN)

2009 ◽  
Vol 101 (6) ◽  
pp. 2889-2897 ◽  
Author(s):  
Andre Kaminiarz ◽  
Kerstin Königs ◽  
Frank Bremmer
Keyword(s):  
Neural Networks ◽  
Eye Movements ◽  
Main Sequence ◽  
Critical Role ◽  
Saccade Target ◽  
Control Mechanisms ◽  
Visually Guided ◽  
Background Characteristics ◽  
Optokinetic Afternystagmus

Different types of fast eye movements, including saccades and fast phases of optokinetic nystagmus (OKN) and optokinetic afternystagmus (OKAN), are coded by only partially overlapping neural networks. This is a likely cause for the differences that have been reported for the dynamic parameters of fast eye movements. The dependence of two of these parameters—peak velocity and duration—on saccadic amplitude has been termed “main sequence.” The main sequence of OKAN fast phases has not yet been analyzed. These eye movements are unique in that they are generated by purely subcortical control mechanisms and that they occur in complete darkness. In this study, we recorded fast phases of OKAN and OKN as well as visually guided and spontaneous saccades under identical background conditions because background characteristics have been reported to influence the main sequence of saccades. Our data clearly show that fast phases of OKAN and OKN differ with respect to their main sequence. OKAN fast phases were characterized by their lower peak velocities and longer durations compared with those of OKN fast phases. Furthermore we found that the main sequence of spontaneous saccades depends heavily on background characteristics, with saccades in darkness being slower and lasting longer. On the contrary, the main sequence of visually guided saccades depended on background characteristics only very slightly. This implies that the existence of a visual saccade target largely cancels out the effect of background luminance. Our data underline the critical role of environmental conditions (light vs. darkness), behavioral tasks (e.g., spontaneous vs. visually guided), and the underlying neural networks for the exact spatiotemporal characteristics of fast eye movements.

scholarly journals Chronic Pain and Chronic Stress: Two Sides of the Same Coin?

2017 ◽  
Vol 1 ◽  
pp. 247054701770476 ◽  
Author(s):  
Chadi G Abdallah ◽  
Paul Geha
Keyword(s):  
Decision Making ◽  
Posttraumatic Stress Disorder ◽  
Chronic Pain ◽  
Posttraumatic Stress ◽  
Chronic Stress ◽  
Stress Disorder ◽  
Internal State ◽  
Critical Role ◽  
Well Being

Pain and stress share significant conceptual and physiological overlaps. Both phenomena challenge the body’s homeostasis and necessitate decision-making to help animals adapt to their environment. In addition, chronic stress and chronic pain share a common behavioral model of failure to extinguish negative memories. Yet, they also have discrepancies such that the final brain endophenotype of posttraumatic stress disorder, depression, and chronic pain appears to be different among the three conditions, and the role of the hypothalamic-pituitary-adrenal axis remains unclear in the physiology of pain. Persistence of either stress or pain is maladaptive and could lead to compromised well-being. In this brief review, we highlight the commonalities and differences between chronic stress and chronic pain, while focusing particularly on the central role of the limbic brain. We assess the current attempts in the field to conceptualize and understand chronic pain, within the context of knowledge gained from the stress literature. The limbic brain—including hippocampus, amygdala, and ventromedial prefrontal cortex—plays a critical role in learning. These brain areas integrate incoming nociceptive or stress signals with internal state, and generate learning signals necessary for decision-making. Therefore, the physiological and structural remodeling of this learning circuitry is observed in conditions such as chronic pain, depression, and posttraumatic stress disorder, and is also linked to the risk of onset of these conditions.

The influence of contextual faces on bilingual language control

2019 ◽  
Vol 72 (9) ◽  
pp. 2313-2327 ◽  
Author(s):  
Cong Liu ◽  
Kalinka Timmer ◽  
Lu Jiao ◽  
Yuan Yuan ◽  
Ruiming Wang
Keyword(s):  
Cultural Identity ◽  
Switch Cost ◽  
Dominance Effect ◽  
Critical Role ◽  
Control Mechanisms ◽  
Language Dominance ◽  
The Face ◽  
Language Control ◽  
Global Language

How do faces with social-cultural identity affect bilingual language control? We approach this question by looking at the switch cost patterns and reversed language dominance effect, which are suggested to reflect bilingual language control mechanisms, in the absence (i.e., baseline context) or presence of faces with socio-cultural identity (Asian or Caucasian). In separate blocks, the face matched (i.e., congruent context) or mismatched (i.e., incongruent context) the language to be spoken. In addition, cue preparation time was manipulated to be long (Experiment 1) or short (Experiment 2). In both experiments, a unique asymmetric switch cost with larger costs for L2 was observed in the congruent context as compared with the baseline and incongruent contexts. Furthermore, the reversed language dominance effect was not modulated across contexts. These results suggest a critical role of contextual faces in modulating local but not global language control. Thus, bilingual language control changes flexibly within an environment that includes faces with socio-cultural identity.

scholarly journals Rho/Rho-associated Kinase-II Signaling Mediates Disassembly of Epithelial Apical Junctions

2007 ◽  
Vol 18 (9) ◽  
pp. 3429-3439 ◽  
Author(s):  
Stanislav N. Samarin ◽  
Andrei I. Ivanov ◽  
Gilles Flatau ◽  
Charles A. Parkos ◽  
Asma Nusrat
Keyword(s):  
Epithelial Cells ◽  
Rho Gtpase ◽  
Critical Role ◽  
Junctional Complex ◽  
Nucleotide Exchange ◽  
Calcium Depletion ◽  
Pharmacological Inhibition ◽  
Apical Junctional Complex ◽  
Apical Junctions

Apical junctional complex (AJC) plays a vital role in regulation of epithelial barrier function. Disassembly of the AJC is observed in diverse physiological and pathological states; however, mechanisms governing this process are not well understood. We previously reported that the AJC disassembly is driven by the formation of apical contractile acto-myosin rings. In the present study, we analyzed the signaling pathways regulating acto-myosin–dependent disruption of AJC by using a model of extracellular calcium depletion. Pharmacological inhibition analysis revealed a critical role of Rho-associated kinase (ROCK) in AJC disassembly in calcium-depleted epithelial cells. Furthermore, small interfering RNA (siRNA)-mediated knockdown of ROCK-II, but not ROCK-I, attenuated the disruption of the AJC. Interestingly, AJC disassembly was not dependent on myosin light chain kinase and myosin phosphatase. Calcium depletion resulted in activation of Rho GTPase and transient colocalization of Rho with internalized AJC proteins. Pharmacological inhibition of Rho prevented AJC disassembly. Additionally, Rho guanine nucleotide exchange factor (GEF)-H1 translocated to contractile F-actin rings after calcium depletion, and siRNA-mediated depletion of GEF-H1 inhibited AJC disassembly. Thus, our findings demonstrate a central role of the GEF-H1/Rho/ROCK-II signaling pathway in the disassembly of AJC in epithelial cells.

scholarly journals Role of Spinal Microglia in Visceral Hyperalgesia and NK1R Up-Regulation in a Rat Model of Chronic Stress

2009 ◽  
Vol 136 (4) ◽  
pp. 1339-1348.e2 ◽  
Author(s):  
Sylvie Bradesi ◽  
Camilla I. Svensson ◽  
Joanne Steinauer ◽  
Charalabos Pothoulakis ◽  
Tony L. Yaksh ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Rat Model ◽  
Visceral Hyperalgesia

Corticotropin-releasing factor type 1 receptors mediate the visceral hyperalgesia induced by repeated psychological stress in rats

2008 ◽  
Vol 294 (4) ◽  
pp. G1033-G1040 ◽  
Author(s):  
Muriel Larauche ◽  
Sylvie Bradesi ◽  
Mulugeta Million ◽  
Peter McLean ◽  
Yvette Taché ◽  
...  
Keyword(s):  
Psychological Stress ◽  
Functional Gastrointestinal Disorders ◽  
Visceral Hypersensitivity ◽  
Pathophysiological Mechanism ◽  
Visceral Hyperalgesia ◽  
Before And After ◽  
Visceromotor Response ◽  
Male Wistar Rats ◽  
Factor Type

Visceral hypersensitivity has been implicated as an important pathophysiological mechanism in functional gastrointestinal disorders. In this study, we investigated whether the sustained visceral hyperalgesia induced by repeated psychological stress in rats involves the activation of CRF1 signaling system using two different antagonists. Male Wistar rats were exposed to 10 consecutive days of water avoidance stress (WAS) or sham stress for 1 h/day, and the visceromotor response to phasic colorectal distension (CRD) was assessed before and after the stress period. Animals were injected subcutaneously with the brain penetrant CRF1 antagonist, CP-154,526, acutely (30 min before the final CRD) or chronically (via osmotic minipump implanted subcutaneously, during stress) or with the peripherally restricted, nonselective CRF1 and CRF2 antagonist, astressin, chronically (15 min before each stress session). Repeated WAS induced visceral hypersensitivity to CRD at 40 and 60 mmHg. CP-154,526 injected acutely significantly reduced stress-induced visceral hyperalgesia at 40 mmHg but not at 60 mmHg. Chronic subcutaneous delivery of astressin reduced the stress-induced visceral hyperalgesia to baseline at all distension pressures. Interestingly, chronically administered CP-154,526 eliminated hyperalgesia and produced responses below baseline at 40 mmHg and 60 mmHg, indicating a hypoalgesic effect of the compound. These data support a major role for CRF1 in both the development and maintenance of visceral hyperalgesia induced by repeated stress and indicate a possible role of peripheral CRF receptors in such mechanisms.

scholarly journals Critical role of Tim-3 mediated autophagy in chronic stress induced immunosuppression

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Anna Qin ◽  
Ting Zhong ◽  
Huajiao Zou ◽  
Xiaoya Wan ◽  
Bifeng Yao ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Critical Role

scholarly journals Glutamate Transporter GLT-1 Upregulation Attenuates Visceral Nociception and Hyperalgesia via Spinal Mechanisms Not Related to Anti-Inflammatory or Probiotic Effects

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Y. Lin ◽  
K. Roman ◽  
K. D. Foust ◽  
B. K. Kaspar ◽  
M. T. Bailey ◽  
...  
Keyword(s):  
Visceral Pain ◽  
Glutamate Transporter ◽  
Visceral Hypersensitivity ◽  
Nociceptive Response ◽  
Excitatory Neurotransmitter ◽  
Physician Visits ◽  
Over Expression ◽  
Visceral Nociception ◽  
Virus Serotype

Visceral pain is the most common reason for physician visits in US. Glutamate is the major excitatory neurotransmitter and mediates visceral nociceptive neuro-transmission and hypersensitivity. Removal of extracellular glutamate is predominantly mediated by glial glutamate transporter-1 (GLT-1). The pharmacological approach to up-regulate GLT-1 by 1 week administration of ceftriaxone (CTX) has been successful to mitigate visceral nociception. The present study shows that intrathecal delivery of selective GLT-1 antagonist dihydrokainate reversed CTX-blunted visceral nociceptive response, suggesting a spinal site of action. The role of GLT-1 up-regulation in animal models of colitis was studied. CTX treatment reversed TNBS-induced visceral hypersensitivity. In addition, CTX treatment initiated one week after the onset of DSS-induced visceral inflammation also attenuated visceral hypersensitivity, revealing a potential therapeutic effect. Cephalothin, a cephalosporin antibiotic lacking GLT-1 induction activity, failed to attenuate visceral nociception. CTX-induced changes in fecal microbiota do not support a role of probiotic effects in mitigating visceral nociception/hypersensitivity. Finally, adeno-associated virus serotype 9-mediated GLT-1 over-expression was effective to mitigate visceromotor response to 60 mmHg colo-rectal distension. These studies indicate that GLT-1 over-expression is a novel and effective method to attenuate visceral nociception, and is deserving of further study as a translationally relevant approach to treat visceral pain.

The Role of the SLP in Autism Spectrum Disorder Screening and Assessment

2008 ◽  
Vol 15 (2) ◽  
pp. 50-59 ◽  
Author(s):  
Amy Philofsky
Keyword(s):  
Language Development ◽  
Critical Role ◽  
Children With Autism ◽  
Autism Spectrum ◽  
Children With Asd ◽  
Prevalence Estimates ◽  
Notable Increase ◽  
Screening Assessment ◽  
Critical Components

AbstractRecent prevalence estimates for autism have been alarming as a function of the notable increase. Speech-language pathologists play a critical role in screening, assessment and intervention for children with autism. This article reviews signs that may be indicative of autism at different stages of language development, and discusses the importance of several psychometric properties—sensitivity and specificity—in utilizing screening measures for children with autism. Critical components of assessment for children with autism are reviewed. This article concludes with examples of intervention targets for children with ASD at various levels of language development.

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