Sleep is an indispensable part of life−its deficiency has significant implications for overall health and wellbeing[1].In today’s fast-paced society,sleep loss from either stressful or non-stressful origins has becom...Sleep is an indispensable part of life−its deficiency has significant implications for overall health and wellbeing[1].In today’s fast-paced society,sleep loss from either stressful or non-stressful origins has become prevalent.Specifically,active sleep deprivation(ASD),resulting from extended use of smartphones and other recreational activities,has risen as a global health issue.Clinical research has underscored a strong correlation between chronic pain and inadequate sleep[2].The relationship between pain and sleep is reciprocal:pain disturbs sleep,while poor sleep quality,in turn,reduces pain tolerance and exacerbates spontaneous pain sensations[3].While these interplays are well-documented in cases of passive sleep deprivation(PSD)associated with external pressures or illnesses,understanding how and which regions of the brain collaborate to recalibrate the intricate neural circuitry governing pain perception during ASD remains a crucial yet unresolved frontier.展开更多
Ethanol is widely known for its ability to cause dramatic changes in emotion, social cognition, and behavior following systemic administration in humans.Human neuroimaging studies suggest that alcohol dependence and c...Ethanol is widely known for its ability to cause dramatic changes in emotion, social cognition, and behavior following systemic administration in humans.Human neuroimaging studies suggest that alcohol dependence and chronic pain may share common mechanisms through amygdala-medial prefrontal cortex（m PFC） interactions. However, whether acute administration of ethanol in the m PFC can modulate pain perception is unknown.Here we showed that bilateral microinjections of ethanol into the prelimbic and infralimbic areas of the m PFC lowered the bilateral mechanical pain threshold for 48 h without influencing thermal pain sensitivity in adult rats.However, bilateral microinjections of artificial cerebrospinal fluid into the m PFC or bilateral microinjections of ethanol into the dorsolateral PFC（also termed as motor cortex area 1 in Paxinos and Watson＇s atlas of The Rat Brain. Elsevier Academic Press, Amsterdam, 2005） failed to do so, suggesting regional selectivity of the effects of ethanol. Moreover, bilateral microinjections of ethanol didnot change the expression of either pro-apoptotic（caspase-3 and Bax） or anti-apoptotic（Bcl-2） proteins, suggesting that the dose was safe and validating the method used in the current study. To determine whether c-aminobutyric acid A（GABA_A） receptors are involved in mediating the ethanol effects, muscimol, a selective GABA_Areceptor agonist, or bicuculline, a selective GABA_A receptor antagonist, was administered alone or co-administered with ethanol through the same route into the bilateral m PFC. The results showed that muscimol mimicked the effects of ethanol while bicuculline completely reversed the effects of ethanol and muscimol. In conclusion, ethanol increases mechanical pain sensitivity through activation of GABA_A receptors in the m PFC of rats.展开更多
Purpose: Memory has been identified as an important protective feature to prevent future injury, but its role has yet to be ascertained. The current study aimed to determine whether there was a difference in pressure ...Purpose: Memory has been identified as an important protective feature to prevent future injury, but its role has yet to be ascertained. The current study aimed to determine whether there was a difference in pressure pain threshold (PPT) responses between participants with a prior history of injury of lower extremity injury (PSI) and those without (NPSI) when exposed to 1) experimental mechanical pain, 2) short-term memory recall of a painful stimulus, or 3) long-term memory of the pain associated with a prior injury. Subjects and Methods: The study used a pretest-posttest quasi-experimental design. A convenience sample of 59 pain-free participants was recruited from an urban university. Twenty-nine PSI and 30 NPSI were stratified into two groups based on their injury history with PPT values measured at baseline and immediately following each of the three experimental conditions. A repeated measure ANCOVA analysis was conducted for each condition to determine whether there was a difference in PPT responses between the two groups. Results: There was a statistically significant difference in PPT values between the two groups when exposed to experimental pain, F(1,57) = 6.010, p = 0.017, partial η<sup>2</sup> = 0.095 and with long-term pain memory, F(1,57) = 4.886, p = 0.031, partial η<sup>2</sup> = 0.079. There was no statistically significant difference between groups with short-term pain memory, F(1,57) = 3.925, p = 0.052, partial η<sup>2</sup> = 0.064. Conclusions: These findings suggest that pain processing may be altered by pain memory, highlighting the role of experience and memory in the rehabilitation process.展开更多
基金supported by the National Natural Science Foundation of China(U21A20418).
文摘Sleep is an indispensable part of life−its deficiency has significant implications for overall health and wellbeing[1].In today’s fast-paced society,sleep loss from either stressful or non-stressful origins has become prevalent.Specifically,active sleep deprivation(ASD),resulting from extended use of smartphones and other recreational activities,has risen as a global health issue.Clinical research has underscored a strong correlation between chronic pain and inadequate sleep[2].The relationship between pain and sleep is reciprocal:pain disturbs sleep,while poor sleep quality,in turn,reduces pain tolerance and exacerbates spontaneous pain sensations[3].While these interplays are well-documented in cases of passive sleep deprivation(PSD)associated with external pressures or illnesses,understanding how and which regions of the brain collaborate to recalibrate the intricate neural circuitry governing pain perception during ASD remains a crucial yet unresolved frontier.
基金supported by grants from the National Basic Research Development Program of China (2013CB835103)the National Natural Science Foundation of China (81571072 and 31600855)
文摘Ethanol is widely known for its ability to cause dramatic changes in emotion, social cognition, and behavior following systemic administration in humans.Human neuroimaging studies suggest that alcohol dependence and chronic pain may share common mechanisms through amygdala-medial prefrontal cortex（m PFC） interactions. However, whether acute administration of ethanol in the m PFC can modulate pain perception is unknown.Here we showed that bilateral microinjections of ethanol into the prelimbic and infralimbic areas of the m PFC lowered the bilateral mechanical pain threshold for 48 h without influencing thermal pain sensitivity in adult rats.However, bilateral microinjections of artificial cerebrospinal fluid into the m PFC or bilateral microinjections of ethanol into the dorsolateral PFC（also termed as motor cortex area 1 in Paxinos and Watson＇s atlas of The Rat Brain. Elsevier Academic Press, Amsterdam, 2005） failed to do so, suggesting regional selectivity of the effects of ethanol. Moreover, bilateral microinjections of ethanol didnot change the expression of either pro-apoptotic（caspase-3 and Bax） or anti-apoptotic（Bcl-2） proteins, suggesting that the dose was safe and validating the method used in the current study. To determine whether c-aminobutyric acid A（GABA_A） receptors are involved in mediating the ethanol effects, muscimol, a selective GABA_Areceptor agonist, or bicuculline, a selective GABA_A receptor antagonist, was administered alone or co-administered with ethanol through the same route into the bilateral m PFC. The results showed that muscimol mimicked the effects of ethanol while bicuculline completely reversed the effects of ethanol and muscimol. In conclusion, ethanol increases mechanical pain sensitivity through activation of GABA_A receptors in the m PFC of rats.
文摘Purpose: Memory has been identified as an important protective feature to prevent future injury, but its role has yet to be ascertained. The current study aimed to determine whether there was a difference in pressure pain threshold (PPT) responses between participants with a prior history of injury of lower extremity injury (PSI) and those without (NPSI) when exposed to 1) experimental mechanical pain, 2) short-term memory recall of a painful stimulus, or 3) long-term memory of the pain associated with a prior injury. Subjects and Methods: The study used a pretest-posttest quasi-experimental design. A convenience sample of 59 pain-free participants was recruited from an urban university. Twenty-nine PSI and 30 NPSI were stratified into two groups based on their injury history with PPT values measured at baseline and immediately following each of the three experimental conditions. A repeated measure ANCOVA analysis was conducted for each condition to determine whether there was a difference in PPT responses between the two groups. Results: There was a statistically significant difference in PPT values between the two groups when exposed to experimental pain, F(1,57) = 6.010, p = 0.017, partial η<sup>2</sup> = 0.095 and with long-term pain memory, F(1,57) = 4.886, p = 0.031, partial η<sup>2</sup> = 0.079. There was no statistically significant difference between groups with short-term pain memory, F(1,57) = 3.925, p = 0.052, partial η<sup>2</sup> = 0.064. Conclusions: These findings suggest that pain processing may be altered by pain memory, highlighting the role of experience and memory in the rehabilitation process.
