Enhanced excitatory and reduced inhibitory synaptic transmission contribute to persistent pain-induced neuronal hyper-responsiveness in anterior cingulate cortex

Gong, Kan; Cao, Fa-Le; Gao, Chong; Wang, D.-D.; Li, H.; Zhang, F.-K.; An, Yonghui; Lin, Qing; Chen, J.

doi:10.1016/j.neuroscience.2010.10.028

Cited by 33 publications

(36 citation statements)

References 81 publications

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“…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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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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“…and ACC slices were obtained according to previously-published procedures (He et al, 2009; Gong et al, 2010; Jin et al, 2013; Lu et al, 2013). Briefly, after decapitation, the whole brain was carefully removed and quickly transferred to an ice-cold bath of artificial cerebrospinal fluid (ACSF; composition in mM: NaCl 124, KCl 3.3, KH 2 PO 4 1.2, CaCl 2 2H 2 O 2.5, MgSO 4 2.4, NaHCO 3 26, and glucose 10).…”

Section: Methodsmentioning

confidence: 99%

“…A single brain slice was then held down in the recording chamber with an anchor and was kept immersed in circulating oxygenated ACSF at a flow rate of 2.2–2.6 ml/min using a fast perfusion system (World Precision Instruments, USA). Recordings were done at room temperature (23–25 °C)(Zhao et al, 2005a,2009; He et al, 2009; Gong et al, 2010; Jin et al, 2013). …”

Section: Methodsmentioning

confidence: 99%

“…Recording procedures, data acquisition and equipment have been described in previously published work by our and other groups (Zhao et al, 2009; Gong et al, 2010; Jin et al, 2013). Briefly, postsynaptic currents were recorded from layers II-III of pyramidal neurons of the ACC because layers II-III are reported to be the major location of intracortical horizontal pathways (Hess et al, 1994), and the superficial layers of the ACC received nucleus of somatosensory information (Zhuo, 2007).…”

Section: Methodsmentioning

confidence: 99%

“…The doses and injection route of antagonists were chosen based on preliminary experiments and previous reports (Zou et al, 2009a,b; Gong et al, 2010). …”

Section: Methodsmentioning

confidence: 99%

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Neonatal ketamine exposure causes impairment of long-term synaptic plasticity in the anterior cingulate cortex of rats

et al. 2014

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Ketamine, a dissociative anesthetic most commonly used in many pediatric procedures, has been reported in many animal studies to cause widespread neuroapoptosis in the neonatal brain after exposure in high doses and/or for prolonged period. This neurodegenerative change occurs most severely in the forebrain including the anterior cingulated cortex (ACC) that is an important brain structure for mediating a variety of cognitive functions. However, it is still unknown whether such apoptotic neurodegeneration early in life would subsequently impair the synaptic plasticity of the ACC later in life. In this study, we performed whole-cell patch-clamp recordings from the ACC brain slices of young adult rats to examine any alterations in long-term synaptic plasticity caused by neonatal ketamine exposure. Ketamine was administered at postnatal day 4–7 (subcutaneous injections, 20 mg/kg given six times, once every 2 h). At 3–4 weeks of age, long-term potentiation (LTP) was induced and recorded by monitoring excitatory postsynaptic currents from ACC slices. We found that the induction of LTP in the ACC was significantly reduced when compared to the control group. The LTP impairment was accompanied by an increase in the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor-mediated excitatory synaptic transmission and a decrease in GABA inhibitory synaptic transmission in neurons of the ACC. Thus, our present findings show that neonatal ketamine exposure causes a significant LTP impairment in the ACC. We suggest that the imbalanced synaptic transmission is likely to contribute to ketamine-induced LTP impairment in the ACC.

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Bee Venom and Pain

Chen¹,

Guan²

2017

Toxinology

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Enhanced excitatory and reduced inhibitory synaptic transmission contribute to persistent pain-induced neuronal hyper-responsiveness in anterior cingulate cortex

Cited by 33 publications

References 81 publications

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

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

Neonatal ketamine exposure causes impairment of long-term synaptic plasticity in the anterior cingulate cortex of rats

Bee Venom and Pain

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