Spatial and temporal plasticity of synaptic organization in anterior cingulate cortex following peripheral inflammatory pain: multi-electrode array recordings in rats

Lu, Youming; Wang, Yan; Zhang, Fu-Kang; He, Ting; Wang, Ruirui; Chen, Xuefeng; Yang, Fei; Gong, Kan

doi:10.1007/s12264-013-1344-9

Cited by 17 publications

(15 citation statements)

References 83 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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“…Eight and 3 male Sprague-Dawley rats received two unilateral injections of either AAV9.CaMKIIa.hChR2-mCherry, or AAV9.CAG.hChR2-mCherry in diHIPP, resp (coordinates available in ST2), were decapitated 4 to 6 weeks post-injection, under deep isoflurane anesthesia, their brains quickly chilled for 3 min in ice-cold oxygenated (95% O2, 5% CO2) dissection solution [mmol/L: sucrose 110, KCl 2.5, CaCl2 0.5, MgCl2 7, NaHCO3 25, NaH2PO4 1.25, glucose 7 (pH 7.4)], trimmed to a 7 mm block, glued onto the stage of a vibratome (Leica VT1200S) using cyanoacrylate, and sliced in 400 µm thick coronal slices at an angle of 10° to the vertical. Slices were then transferred to a chamber containing oxygenated aCSF at 35°C, for 20-25 min, and then to a storage chamber containing oxygenated aCSF at RT (20-25°C) (based on Lu et al, 2014;Rombo et al, 2014Rombo et al, , 2016.…”

Section: Methodsmentioning

confidence: 99%

“…The expression of the viral construct was verified histologically for each slice. This protocol was based on (Hass and Glickfeld, 2016;Lu et al, 2014).…”

Section: Methodsmentioning

confidence: 99%

A Gradient of Hippocampal Inputs to the Medial Mesocortex

Ferreira-Fernandes

Quintino

Remondes

2019

Preprint

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Running title: Hippocampal inputs to the medial mesocortex Key-wordsHippocampus, anterior cingulate cortex (CG), retrosplenial cortex (RSC), medial mesocortex (MMC), hippocampal inputs, optogenetics, in vitro and awake-behaving multi-electrode recordings, long-range inhibitory neurons HighlightsBoth MMC regions CG and RSC receive monosynaptic connections from the dorsalintermediate CA1 CG receives layer-sparse excitatory projections exclusively originated from stratum piramidale whereas RSC is targeted densely in superficial layers by a mixed excitatory and inhibitory input originating from all CA1 strata CA1 monosynaptic projections correspond to active synapses onto distinct layers of the two MMC regions Diverse synchrony between MMC and HIPP recorded in vivo is consistent with the rostro-caudal diversity of direct HIPP-MMC connections AbstractMemory-guided decisions depend on complex, finely tuned interactions between hippocampus and medial mesocortical regions anterior cingulate and retrosplenial 2 cortices. The functional circuitry underlying these interactions is unclear. Using viral anatomical tracing, in vitro and in vivo electrophysiology, and optogenetics, we show that such circuitry is characterized by a functional-anatomical gradient. While CG receives excitatory projections from dorsal-intermediate CA1 originated exclusively in stratum pyramidale, retrosplenial cortex also receives inputs originating in stratum radiatum and lacunosum-moleculare, including GAD+ neurons providing long-range GABAergic projections. Such hippocampal projections establish bona fide synapses throughout cortical layers, with retrosplenial cortex densely targeted on its layer 3, around which it receives a combination of inhibitory and excitatory synapses. This gradient is reflected in the pattern of spontaneous oscillatory synchronicity found in the awake-behaving animal, compatible with the known functional similarity of hippocampus with retrosplenial cortex, which contrasts with the encoding of actions and "task-space" by cingulate cortex. Katche et al., 2013; Vann and Aggleton, 2005), and the former necessary for flexible choice behaviors and long-term memory (Chudasama et al., 2003;Goshen et al., 2011;Maviel et al., 2004; Teixeira et al., 2006; Vetere et al., 2011; Wang et al., 2012).These findings agree with the few studies recording MMC neural activity in vivo, and with the patterns of HIPP-MMC functional coordination Wilson, 2013, 2015). Neurons in CG encode choice effort (Cowen et al., 2012;Endepols et al., 2010) and task-space by assimilating into motor decisions the spatial-contextual properties of available choices (Remondes and Wilson, 2013;Sul et al., 2010), while RSC joins visual-spatial information such as head-direction and movement in space (Chen et al., 1994a(Chen et al., , 1994bCho and Sharp, 2001) to encode spatial landmarks (Alexander and Nitz, 2015;Auger et al., 2012;Mao et al., 2017). The above findings are supported by the patterns of functional interaction between MMC and HIPP in vivo, namely the d...

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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%

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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Spatial and temporal plasticity of synaptic organization in anterior cingulate cortex following peripheral inflammatory pain: multi-electrode array recordings in rats

Cited by 17 publications

References 83 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

A Gradient of Hippocampal Inputs to the Medial Mesocortex

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

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