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Activation of mitogen-activated protein kinase in descending pain modulatory system.

Imbe H, Senba E, Kimura A, Donishi T, Yokoi I, Kaneoke Y - J Signal Transduct (2010)

Bottom Line: They are involved in pain perception and pain-related emotional responses.In addition, psychophysical stress also activates MAPKs in these brain structures.Greater appreciation of the convergence of mechanisms between noxious stimuli- and psychological stress-induced neuroplasticity is likely to lead to the identification of novel targets for a variety of pain syndromes.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Wakayama Medical University, Kimiidera 811-1, Wakayama City 641-8509, Japan.

ABSTRACT
The descending pain modulatory system is thought to undergo plastic changes following peripheral tissue injury and exerts bidirectional (facilitatory and inhibitory) influence on spinal nociceptive transmission. The mitogen-activated protein kinases (MAPKs) superfamily consists of four main members: the extracellular signal-regulated protein kinase1/2 (ERK1/2), the c-Jun N-terminal kinases (JNKs), the p38 MAPKs, and the ERK5. MAPKs not only regulate cell proliferation and survival but also play important roles in synaptic plasticity and memory formation. Recently, many studies have demonstrated that noxious stimuli activate MAPKs in several brain regions that are components of descending pain modulatory system. They are involved in pain perception and pain-related emotional responses. In addition, psychophysical stress also activates MAPKs in these brain structures. Greater appreciation of the convergence of mechanisms between noxious stimuli- and psychological stress-induced neuroplasticity is likely to lead to the identification of novel targets for a variety of pain syndromes.

No MeSH data available.


Related in: MedlinePlus

Schematic drawing of noxious stimuli-induced MAPKs activations in the descending pain modulatory system. Boxes indicate noxious stimulation, activated MAPK, and function that is related to MAPK activation. PFC, prefrontal cortex; ACC, anterior cingulate cortex; AMY, amygdala; HPT, hypothalamus; PAG, periaqueductal gray; LC, locus coeruleus; RVM, rostral ventromedial medulla; DLF, dorsolateral funiculus; SDH, spinal dorsal horn; PAF, primary afferent fiber; POMC, proopiomelanocortin. Upward and downward arrowheads indicate increase and decrease, respectively.
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fig2: Schematic drawing of noxious stimuli-induced MAPKs activations in the descending pain modulatory system. Boxes indicate noxious stimulation, activated MAPK, and function that is related to MAPK activation. PFC, prefrontal cortex; ACC, anterior cingulate cortex; AMY, amygdala; HPT, hypothalamus; PAG, periaqueductal gray; LC, locus coeruleus; RVM, rostral ventromedial medulla; DLF, dorsolateral funiculus; SDH, spinal dorsal horn; PAF, primary afferent fiber; POMC, proopiomelanocortin. Upward and downward arrowheads indicate increase and decrease, respectively.

Mentions: The noxious stimuli induced activations of MAPKs in the components of descending pain modulatory system. The activations in these components were associated with pain perception and pain-related emotional responses (Figure 2). In addition, psychophysical stress also activated MAPKs in these structures. They seem to be mainly related to depressive-like behavior (Figure 3). MAPKs are involved in both transcription-independent and transcription-dependent forms of central sensitization. Stress-induced neural plasticity in these structures via activations of MAPKs might affect nociceptive processing. In turn, the noxious stimuli-induced neural plasticity might potentiate depressive-like behavior in response to psychological stress. Clinical studies have demonstrated a reciprocal interaction between emotionality and pain perception in chronic pain conditions [93]. Elucidation of their physiological functions might contribute to a better understanding of chronic pain and lead to the development of new treatment to a variety of pain syndromes.


Activation of mitogen-activated protein kinase in descending pain modulatory system.

Imbe H, Senba E, Kimura A, Donishi T, Yokoi I, Kaneoke Y - J Signal Transduct (2010)

Schematic drawing of noxious stimuli-induced MAPKs activations in the descending pain modulatory system. Boxes indicate noxious stimulation, activated MAPK, and function that is related to MAPK activation. PFC, prefrontal cortex; ACC, anterior cingulate cortex; AMY, amygdala; HPT, hypothalamus; PAG, periaqueductal gray; LC, locus coeruleus; RVM, rostral ventromedial medulla; DLF, dorsolateral funiculus; SDH, spinal dorsal horn; PAF, primary afferent fiber; POMC, proopiomelanocortin. Upward and downward arrowheads indicate increase and decrease, respectively.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3101953&req=5

fig2: Schematic drawing of noxious stimuli-induced MAPKs activations in the descending pain modulatory system. Boxes indicate noxious stimulation, activated MAPK, and function that is related to MAPK activation. PFC, prefrontal cortex; ACC, anterior cingulate cortex; AMY, amygdala; HPT, hypothalamus; PAG, periaqueductal gray; LC, locus coeruleus; RVM, rostral ventromedial medulla; DLF, dorsolateral funiculus; SDH, spinal dorsal horn; PAF, primary afferent fiber; POMC, proopiomelanocortin. Upward and downward arrowheads indicate increase and decrease, respectively.
Mentions: The noxious stimuli induced activations of MAPKs in the components of descending pain modulatory system. The activations in these components were associated with pain perception and pain-related emotional responses (Figure 2). In addition, psychophysical stress also activated MAPKs in these structures. They seem to be mainly related to depressive-like behavior (Figure 3). MAPKs are involved in both transcription-independent and transcription-dependent forms of central sensitization. Stress-induced neural plasticity in these structures via activations of MAPKs might affect nociceptive processing. In turn, the noxious stimuli-induced neural plasticity might potentiate depressive-like behavior in response to psychological stress. Clinical studies have demonstrated a reciprocal interaction between emotionality and pain perception in chronic pain conditions [93]. Elucidation of their physiological functions might contribute to a better understanding of chronic pain and lead to the development of new treatment to a variety of pain syndromes.

Bottom Line: They are involved in pain perception and pain-related emotional responses.In addition, psychophysical stress also activates MAPKs in these brain structures.Greater appreciation of the convergence of mechanisms between noxious stimuli- and psychological stress-induced neuroplasticity is likely to lead to the identification of novel targets for a variety of pain syndromes.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Wakayama Medical University, Kimiidera 811-1, Wakayama City 641-8509, Japan.

ABSTRACT
The descending pain modulatory system is thought to undergo plastic changes following peripheral tissue injury and exerts bidirectional (facilitatory and inhibitory) influence on spinal nociceptive transmission. The mitogen-activated protein kinases (MAPKs) superfamily consists of four main members: the extracellular signal-regulated protein kinase1/2 (ERK1/2), the c-Jun N-terminal kinases (JNKs), the p38 MAPKs, and the ERK5. MAPKs not only regulate cell proliferation and survival but also play important roles in synaptic plasticity and memory formation. Recently, many studies have demonstrated that noxious stimuli activate MAPKs in several brain regions that are components of descending pain modulatory system. They are involved in pain perception and pain-related emotional responses. In addition, psychophysical stress also activates MAPKs in these brain structures. Greater appreciation of the convergence of mechanisms between noxious stimuli- and psychological stress-induced neuroplasticity is likely to lead to the identification of novel targets for a variety of pain syndromes.

No MeSH data available.


Related in: MedlinePlus