Distinct roles of the anterior cingulate cortex in spinal and supraspinal bee venom–induced pain behaviors

Ren, Liying; Lu, Zhuo-Min; Liu, M.-G.; Yu, Yao-Qing; Li, Z.; Shang, Gang-Wei; Chen, J.

doi:10.1016/j.neuroscience.2008.01.067

Cited by 40 publications

(29 citation statements)

References 64 publications

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“…Surgery was performed as described previously [20,33,34]. Rats were anesthetized with chloralose (0.3 g/kg, i.p.…”

Section: Surgerymentioning

confidence: 99%

Gabapentinoid Insensitivity after Repeated Administration is Associated with Down-Regulation of the α2δ-1 Subunit in Rats with Central Post-Stroke Pain Hypersensitivity

Yang

et al. 2016

Neurosci. Bull.

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The a 2 d-1 subunit of the voltage-gated Ca 2? channel (VGCC) is a molecular target of gabapentin (GBP), which has been used as a first-line drug for the relief of neuropathic pain. GBP exerts its anti-nociceptive effects by disrupting trafficking of the a 2 d-1 subunit to the presynaptic membrane, resulting in decreased neurotransmitter release. We previously showed that GBP has an antiallodynic effect in the first two weeks; but this is followed by insensitivity in the later stage after repeated administration in a rat model of central post-stroke pain (CPSP) hypersensitivity induced by intra-thalamic hemorrhage. To explore the mechanisms underlying GBP insensitivity, the cellular localization and time-course of expression of the a 2 d-1 subunit in both the thalamus and spinal dorsal horn were studied in the same model. We found that the a 2 d-1 subunit was mostly localized in neurons, but not astrocytes and microglia. The level of a 2 d-1 protein increased in the first two weeks after injury but then decreased in the third week, when GBP insensitivity occurred. Furthermore, the a 2 d-1 down-regulation was likely caused by later neuronal loss in the injured thalamus through a mechanism other than apoptosis. In summary, the present results suggest that the GBP receptor a 2 d-1 is mainly expressed in thalamic neurons in which it is up-regulated in the early stage of CPSP but this is followed by dramatic down-regulation, which is likely associated with GBP insensitivity after long-term use.Keywords Central post-stroke pain Á Calcium channel a 2 d subunit Á Gabapentinoid Á Thalamic hemorrhagic stroke Á Thalamus Á Spinal dorsal horn

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“…Surgery was performed as described previously [20,33,34]. Rats were anesthetized with chloralose (0.3 g/kg, i.p.…”

Section: Surgerymentioning

confidence: 99%

Gabapentinoid Insensitivity after Repeated Administration is Associated with Down-Regulation of the α2δ-1 Subunit in Rats with Central Post-Stroke Pain Hypersensitivity

Yang

et al. 2016

Neurosci. Bull.

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“…These procedures were as in our previous report [9]. In brief, after the behavioral tests, rats were fully anesthetized with sodium pentobarbital (50 mg/kg, i.p.)…”

Section: Histological Localization Of Injection Sitesmentioning

confidence: 99%

“…Some human neuroimaging studies have suggested that alcohol-dependence and chronic pain may also share mechanisms through amygdala-medial prefrontal cortex (mPFC) interactions [2]. The mPFC, a cortical structure that includes the prelimbic (PrLC), infralimbic (ILC), and anterior cingulate cortex (ACC) [4][5][6], has been demonstrated to be involved in pain processing [7][8][9][10][11][12][13][14]. More recently, we also demonstrated that the mPFC is involved in the mediation of empathy for pain in rats, a phenomenon in which the mechanical pain sensitivity and spinal nociceptive responses of rats are dramatically increased after social interaction with a cagemate (but not a non-cagemate) in pain [15].…”

Section: Introductionmentioning

confidence: 99%

Ethanol Increases Mechanical Pain Sensitivity in Rats via Activation of GABAA Receptors in Medial Prefrontal Cortex

Geng

Wang

et al. 2016

Neurosci. Bull.

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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 (mPFC) interactions. However, whether acute administration of ethanol in the mPFC can modulate pain perception is unknown. Here we showed that bilateral microinjections of ethanol into the prelimbic and infralimbic areas of the mPFC 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 mPFC 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 did not 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 A receptor agonist, or bicuculline, a selective GABA A receptor antagonist, was administered alone or co-administered with ethanol through the same route into the bilateral mPFC. 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 mPFC of rats.

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“…Kainic acid (KA) monohydrate (Sigma) was dissolved in sterile saline, final concentration 1 mg/ml, and adjusted to pH 7.2–7.4, using 0.1 mol/L NaOH. Microinjection of KA solution was administered into the ACC as described in our previous studies (Li et al., 2012) and other reports (Ren et al., 2008). Briefly, anesthetized rats were fixed on the brain stereotactic apparatus; the skull was exposed, and burr holes were drilled above the ACC.…”

Section: Methodsmentioning

confidence: 99%

Anterior cingulate cortex involved in social food‐foraging decision‐making strategies of rats

Zhong

Deng

et al. 2017

Brain and Behavior

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IntroductionDecision making as a complex cognitive process involves assessing risk, reward, and costs. Typically, it has been studied in nonsocial contexts. We have developed a novel laboratory model used with rodents to detect food‐foraging decision‐making strategies in different social settings. However, the brain regions that mediate these behaviors are not well identified. Substantial evidence shows that the anterior cingulate cortex (ACC) participates in evaluation of social information and in decision making.MethodsIn this study, we investigated the effect of bilateral lesions in the ACC on established behaviors. Kainic acid (KA) was administered bilaterally to induce ACC lesions, and saline microinjection into the ACC was used in the sham group.ResultsIn contrast to the sham‐lesioned animals, when faced with the choice of foraging under a social context, rats with ACC lesions preferred foraging for the less desirable food. Moreover, in these situations, the total amount of food foraged by the ACC‐lesioned group was less than the amount foraged by the sham group. Notably, neither social interactions nor social agonistic behaviors were affected by ACC lesions.ConclusionsThese data suggest that the ACC is a key region underlying neural processing of social decision‐making, specifically tending to compete for foraging high predictive reward food.

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Distinct roles of the anterior cingulate cortex in spinal and supraspinal bee venom–induced pain behaviors

Cited by 40 publications

References 64 publications

Gabapentinoid Insensitivity after Repeated Administration is Associated with Down-Regulation of the α2δ-1 Subunit in Rats with Central Post-Stroke Pain Hypersensitivity

Gabapentinoid Insensitivity after Repeated Administration is Associated with Down-Regulation of the α2δ-1 Subunit in Rats with Central Post-Stroke Pain Hypersensitivity

Ethanol Increases Mechanical Pain Sensitivity in Rats via Activation of GABAA Receptors in Medial Prefrontal Cortex

Anterior cingulate cortex involved in social food‐foraging decision‐making strategies of rats

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