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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

(a) Time courses of p-ERK1/2 and p-p38 MAPK in the RVM after CFA injection into the hindpaw. (b) Photomicrographs showing p-ERK1/2- and p-p38 MAPK-immunoreactive neurons in the RVM (bregma −11.00 mm) following hindpaw inflammation. Scale  bar = 100 μm.
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fig1: (a) Time courses of p-ERK1/2 and p-p38 MAPK in the RVM after CFA injection into the hindpaw. (b) Photomicrographs showing p-ERK1/2- and p-p38 MAPK-immunoreactive neurons in the RVM (bregma −11.00 mm) following hindpaw inflammation. Scale  bar = 100 μm.

Mentions: Peripheral inflammation induced by CFA injection into the hindpaw activated ERK1/2 and p38 MAPK in the RVM. The activation of ERK1/2 exhibited two characteristic phases. The first phase was a transient small increase at 30 minutes after CFA injection. The second phase was more persistent and pronounced increase from 3 hours to 24 hours, with a peak at 7 hours [15]. On the other hand, the activation of p38 MAPK was more short lived. It peaked at 30 minutes and lasted for 1 hour [16] (Figure 1). Phosphorylated ERK1/2 and p38 MAPK (p-ERK1/2 and p-p38 MAPK) were present predominantly in RVM neurons after CFA injection. About 60% of p-ERK1/2 neurons and 40% of p-p38 MAPK neurons in the RVM were serotonergic neurons [15, 16]. Microglial p-p38 MAPK in the RVM has also been reported to increase following carrageenan-induced inflammation [18].


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)

(a) Time courses of p-ERK1/2 and p-p38 MAPK in the RVM after CFA injection into the hindpaw. (b) Photomicrographs showing p-ERK1/2- and p-p38 MAPK-immunoreactive neurons in the RVM (bregma −11.00 mm) following hindpaw inflammation. Scale  bar = 100 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig1: (a) Time courses of p-ERK1/2 and p-p38 MAPK in the RVM after CFA injection into the hindpaw. (b) Photomicrographs showing p-ERK1/2- and p-p38 MAPK-immunoreactive neurons in the RVM (bregma −11.00 mm) following hindpaw inflammation. Scale  bar = 100 μm.
Mentions: Peripheral inflammation induced by CFA injection into the hindpaw activated ERK1/2 and p38 MAPK in the RVM. The activation of ERK1/2 exhibited two characteristic phases. The first phase was a transient small increase at 30 minutes after CFA injection. The second phase was more persistent and pronounced increase from 3 hours to 24 hours, with a peak at 7 hours [15]. On the other hand, the activation of p38 MAPK was more short lived. It peaked at 30 minutes and lasted for 1 hour [16] (Figure 1). Phosphorylated ERK1/2 and p38 MAPK (p-ERK1/2 and p-p38 MAPK) were present predominantly in RVM neurons after CFA injection. About 60% of p-ERK1/2 neurons and 40% of p-p38 MAPK neurons in the RVM were serotonergic neurons [15, 16]. Microglial p-p38 MAPK in the RVM has also been reported to increase following carrageenan-induced inflammation [18].

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