Limits...
Short-term anesthesia inhibits formalin-induced extracellular signal-regulated kinase (ERK) activation in the rostral anterior cingulate cortex but not in the spinal cord.

Tochiki KK, Maiarù M, Miller JR, Hunt SP, Géranton SM - Mol Pain (2015)

Bottom Line: Furthermore, as numerous studies have demonstrated the importance of spinal ERK signaling in the regulation of nociceptive behaviour, we also examined PERK in the superficial dorsal horn of the spinal cord.However, PERK expression was significantly inhibited across all laminae of the rACC in animals anesthetized during formalin injection.This study is the first to demonstrate that isoflurane anesthesia can inhibit formalin-induced PERK in the rACC and therefore might eliminate the unpleasantness of restraint associated with awake hindpaw injection.

View Article: PubMed Central - PubMed

Affiliation: Department of Cell and Developmental Biology, University College London, London, UK. k.tochiki@ucl.ac.uk.

ABSTRACT

Background: The rostral anterior cingulate cortex (rACC) has been implicated in the negative affective response to injury, and importantly, it has been shown that activation of extracellular signal-regulated kinase (ERK) signaling in the rACC contributes to the full expression of the affective component of pain in rodents. In this study, we investigated whether administration of anesthesia at the time of injury could reduce phosphorylated-ERK (PERK) expression in the rACC, which might eliminate the negative affective component of noxious stimulation. Intraplantar hindpaw formalin stimulation, an aversive event in the awake animal, was given with or without general isoflurane anesthesia, and PERK expression was subsequently quantified in the rACC using immunohistochemistry. Furthermore, as numerous studies have demonstrated the importance of spinal ERK signaling in the regulation of nociceptive behaviour, we also examined PERK in the superficial dorsal horn of the spinal cord.

Findings: Formalin injection with and without short-term (<10 min) general isoflurane anesthesia induced the same level of PERK expression in spinal cord laminae I-II. However, PERK expression was significantly inhibited across all laminae of the rACC in animals anesthetized during formalin injection. The effect of anesthesia was such that levels of PERK were the same in formalin and sham treated anesthesized animals.

Conclusions: This study is the first to demonstrate that isoflurane anesthesia can inhibit formalin-induced PERK in the rACC and therefore might eliminate the unpleasantness of restraint associated with awake hindpaw injection.

No MeSH data available.


Related in: MedlinePlus

Short general anesthesia does not modulate formalin induced spinal PERK expression. a Typical PERK expression in the ipsilateral superficial dorsal horn for each treatment group. Scale bar 50 µm. b PERK counts. LSD post hoc, **P < 0.01, Formalin vs. Sham groups. Data presented as mean ± SEM (n = 3 each group).
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
getmorefigures.php?uid=PMC4536792&req=5

Fig1: Short general anesthesia does not modulate formalin induced spinal PERK expression. a Typical PERK expression in the ipsilateral superficial dorsal horn for each treatment group. Scale bar 50 µm. b PERK counts. LSD post hoc, **P < 0.01, Formalin vs. Sham groups. Data presented as mean ± SEM (n = 3 each group).

Mentions: Acute noxious formalin stimulation is known to induce ERK phosphorylation which persists up to 1 h post-injury in the spinal dorsal horn. PERK expression 30 min after formalin stimulation was significantly greater in formalin vs. sham treated animals (Fig. 1) (main effect of treatment; ANOVA F(1, 16) = 23.4, p < 0.001). However, there was no difference in PERK activation between anesthetized and non-anesthetized animals (Fig. 1).Fig. 1


Short-term anesthesia inhibits formalin-induced extracellular signal-regulated kinase (ERK) activation in the rostral anterior cingulate cortex but not in the spinal cord.

Tochiki KK, Maiarù M, Miller JR, Hunt SP, Géranton SM - Mol Pain (2015)

Short general anesthesia does not modulate formalin induced spinal PERK expression. a Typical PERK expression in the ipsilateral superficial dorsal horn for each treatment group. Scale bar 50 µm. b PERK counts. LSD post hoc, **P < 0.01, Formalin vs. Sham groups. Data presented as mean ± SEM (n = 3 each group).
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4536792&req=5

Fig1: Short general anesthesia does not modulate formalin induced spinal PERK expression. a Typical PERK expression in the ipsilateral superficial dorsal horn for each treatment group. Scale bar 50 µm. b PERK counts. LSD post hoc, **P < 0.01, Formalin vs. Sham groups. Data presented as mean ± SEM (n = 3 each group).
Mentions: Acute noxious formalin stimulation is known to induce ERK phosphorylation which persists up to 1 h post-injury in the spinal dorsal horn. PERK expression 30 min after formalin stimulation was significantly greater in formalin vs. sham treated animals (Fig. 1) (main effect of treatment; ANOVA F(1, 16) = 23.4, p < 0.001). However, there was no difference in PERK activation between anesthetized and non-anesthetized animals (Fig. 1).Fig. 1

Bottom Line: Furthermore, as numerous studies have demonstrated the importance of spinal ERK signaling in the regulation of nociceptive behaviour, we also examined PERK in the superficial dorsal horn of the spinal cord.However, PERK expression was significantly inhibited across all laminae of the rACC in animals anesthetized during formalin injection.This study is the first to demonstrate that isoflurane anesthesia can inhibit formalin-induced PERK in the rACC and therefore might eliminate the unpleasantness of restraint associated with awake hindpaw injection.

View Article: PubMed Central - PubMed

Affiliation: Department of Cell and Developmental Biology, University College London, London, UK. k.tochiki@ucl.ac.uk.

ABSTRACT

Background: The rostral anterior cingulate cortex (rACC) has been implicated in the negative affective response to injury, and importantly, it has been shown that activation of extracellular signal-regulated kinase (ERK) signaling in the rACC contributes to the full expression of the affective component of pain in rodents. In this study, we investigated whether administration of anesthesia at the time of injury could reduce phosphorylated-ERK (PERK) expression in the rACC, which might eliminate the negative affective component of noxious stimulation. Intraplantar hindpaw formalin stimulation, an aversive event in the awake animal, was given with or without general isoflurane anesthesia, and PERK expression was subsequently quantified in the rACC using immunohistochemistry. Furthermore, as numerous studies have demonstrated the importance of spinal ERK signaling in the regulation of nociceptive behaviour, we also examined PERK in the superficial dorsal horn of the spinal cord.

Findings: Formalin injection with and without short-term (<10 min) general isoflurane anesthesia induced the same level of PERK expression in spinal cord laminae I-II. However, PERK expression was significantly inhibited across all laminae of the rACC in animals anesthetized during formalin injection. The effect of anesthesia was such that levels of PERK were the same in formalin and sham treated anesthesized animals.

Conclusions: This study is the first to demonstrate that isoflurane anesthesia can inhibit formalin-induced PERK in the rACC and therefore might eliminate the unpleasantness of restraint associated with awake hindpaw injection.

No MeSH data available.


Related in: MedlinePlus