Response durations encode nociceptive stimulus intensity in the rat medial prefrontal cortex

Zhang, R; Tomida, Mihoko; Katayama, Yoko; Kawakami, Yukio

doi:10.1016/j.neuroscience.2004.01.055

Cited by 32 publications

(42 citation statements)

References 32 publications

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“…For instance, noxious stimulation induced neuronal excitability in the amygdala [60–62] and PFC [63] and neuronal inhibition in the CA1 hippocampus [64, 65]. In line with the electrophysiological findings, immunohistochemical and fMRI studies also showed similar activation patterns in these brain regions by delivering noxious stimulation on rats [63, 66–69]. These findings confirmed the role of acute pain on brain plasticity.…”

Section: Neural Plasticity In Acute and Chronic Painsupporting

confidence: 55%

“…Consistent observations of acute pain-related functional changes in the corticolimbic system have been reported in animal studies. For instance, noxious stimulation induced neuronal excitability in the amygdala [60–62] and PFC [63] and neuronal inhibition in the CA1 hippocampus [64, 65]. In line with the electrophysiological findings, immunohistochemical and fMRI studies also showed similar activation patterns in these brain regions by delivering noxious stimulation on rats [63, 66–69].…”

Section: Neural Plasticity In Acute and Chronic Painmentioning

confidence: 74%

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The Role of Stress Regulation on Neural Plasticity in Pain Chronification

2016

Neural Plasticity

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Pain, especially chronic pain, is one of the most common clinical symptoms and has been considered as a worldwide healthcare problem. The transition from acute to chronic pain is accompanied by a chain of alterations in physiology, pathology, and psychology. Increasing clinical studies and complementary animal models have elucidated effects of stress regulation on the pain chronification via investigating activations of the hypothalamic-pituitary-adrenal (HPA) axis and changes in some crucial brain regions, including the amygdala, prefrontal cortex, and hippocampus. Although individuals suffer from acute pain benefit from such physiological alterations, chronic pain is commonly associated with maladaptive responses, like the HPA dysfunction and abnormal brain plasticity. However, the causal relationship among pain chronification, stress regulation, and brain alterations is rarely discussed. To call for more attention on this issue, we review recent findings obtained from clinical populations and animal models, propose an integrated stress model of pain chronification based on the existing models in perspectives of environmental influences and genetic predispositions, and discuss the significance of investigating the role of stress regulation on brain alteration in pain chronification for various clinical applications.

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Section: Neural Plasticity In Acute and Chronic Painsupporting

confidence: 55%

Section: Neural Plasticity In Acute and Chronic Painmentioning

confidence: 74%

The Role of Stress Regulation on Neural Plasticity in Pain Chronification

2016

Neural Plasticity

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“…The neurons of the primary somatosensory cortex function to discriminate between nociceptive signals (Libet, 1982) whereas neurons in the medial prefrontal cortex are able to encode stimulus intensity (Zhang et al, 2004). The prefrontal cortex has also been implicated in the recall and extinction of fear-related memory of noxious stimuli (Hugues et al, 2004).…”

Section: Cortexmentioning

confidence: 99%

Stress-induced analgesia

Butler

Finn

2009

Progress in Neurobiology

545

420

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Abbreviations: SIA, stress-induced analgesia; FCA, fear-conditioned analgesia; GABA, Ȗ-aminobutyric acid; HA, high analgesia; LA, low analgesia; fMRI, functional magnetic resonance imaging; DNIC, diffuse noxious inhibitory control; PAG, periaqueductal grey; RVM, rostroventral medulla; 5-HT, 5-hydroxytryptamine; CB 1 , cannabinoid type 1; CB 2 , cannabinoid type 2; NMDA, N-methyl-D-aspartic acid; AMPA, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; mGluR, metabotropic glutamate receptor; NK1, neurokinin 1; SP, substance P; 2-AG, 2-arachidonoylglycerol; FAAH, fatty acid amide hydrolase; MGL, monoacylglycerol lipase; HPA, hypothalamo-pituitary-adrenal; ACTH, adrenocorticotropic hormone 3 ABSTRACT For over 30 years, scientists have been investigating the phenomenon of pain suppression upon exposure to unconditioned or conditioned stressful stimuli, commonly known as stress-induced analgesia. These studies have revealed that individual sensitivity to stressinduced analgesia can vary greatly and that this sensitivity is coupled to many different phenotypes including the degree of opioid sensitivity and startle response. Furthermore, stress-induced analgesia sensitivity can vary a great deal depending on age, gender, and prior experience to stressful, painful, or other environmental stimuli. Stress-induced analgesia is mediated by activation of the descending inhibitory pain pathway.Pharmacological and neurochemical studies have demonstrated involvement of a large number of neurotransmitters and neuropeptides. In particular, there are key roles for the HQGRJHQRXV RSLRLG PRQRDPLQH FDQQDELQRLG Ȗ-aminobutyric acid and glutamate systems. The study of stress-induced analgesia has enhanced our understanding of the fundamental physiology of pain and stress and has been a useful approach for uncovering new therapeutic targets for the treatment of pain and stress-related disorders.4

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“…Molecular and functional studies on humans and animal models have shown that several brain areas, such as the periaqueductal grey (Baliki et al, 2014;Palazzo et al, 2012), the anterior cingulate cortex (Barthas et al, 2015;Rainville et al, 1997), the prefrontal cortex (Metz et al, 2009;Zhang et al, 2004) and the thalamus (Baliki et al, 2014;Henderson et al, 2013) are involved in pain processing.…”

Section: Introductionmentioning

confidence: 99%