Prefrontal cortex and mediodorsal thalamus reduced connectivity is associated with spatial working memory impairment in rats with inflammatory pain

Cardoso‐Cruz, Helder; Sousa, Mafalda; Vieira, Joana B.; Lima, Deolinda; Galhardo, Vasco

doi:10.1016/j.pain.2013.07.020

Cited by 72 publications

(53 citation statements)

References 82 publications

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“…Its projections to the PAG, thalamus and amygdala have been studied in the context of chronic pain (Bushnell et al, 2013; Cardoso-Cruz et al, 2013; Ji and Neugebauer, 2014). There is recent evidence that connections between the PFC and the NAc—an important projection within the reward circuitry (Koob and Volkow, 2010)—are distinctly altered by chronic pain (Baliki et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Corticostriatal Regulation of Acute Pain

Martinez

Lin

Zhou

et al. 2017

Front. Cell. Neurosci.

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The mechanisms for acute pain regulation in the brain are not well understood. The prefrontal cortex (PFC) provides top-down control of emotional processes, and it projects to the nucleus accumbens (NAc). This corticostriatal projection forms an important regulatory pathway within the brain’s reward system. Recently, this projection has been suggested to control both sensory and affective phenotypes specifically associated with chronic pain. As this projection is also known to play a role in the transition from acute to chronic pain, we hypothesized that this corticostriatal circuit can also exert a modulatory function in the acute pain state. Here, we used optogenetics to specifically target the projection from the PFC to the NAc. We tested sensory pain behaviors with Hargreaves’ test and mechanical allodynia, and aversive pain behaviors with conditioned place preference (CPP) test. We found that the activation of this corticostriatal circuit gave rise to bilateral relief from peripheral nociceptive inputs. Activation of this circuit also provided important control for the aversive response to transient noxious stimulations. Hence, our results support a novel role for corticostriatal circuitry in acute pain regulation.

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Section: Discussionmentioning

confidence: 99%

Corticostriatal Regulation of Acute Pain

Martinez

Lin

Zhou

et al. 2017

Front. Cell. Neurosci.

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“…Gamma oscillation was shown to participate in the abnormal working memory of chronic pain (Cardoso-Cruz et al, 2013); however, whether oscillatory gamma oscillations play a role in the pain perception in chronic pain is unknown and of great interest. Unlike acute and tonic pain, chronic pain is a pathological, ongoing, and long-lasting condition (Merskey and Bogduk, 1994), featured by its persistence and maintenance of pain.…”

Section: Introductionmentioning

confidence: 99%

Enhanced Gamma Oscillatory Activity in Rats with Chronic Inflammatory Pain

Wang

Xing²,

et al. 2016

Front. Neurosci.

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It has been reported that oscillatory gamma activity participates in brief acute pain and tonic ongoing pain. It is of great interest to determine whether the gamma activity is involved in chronic pain since chronic pain is a more severe pathological condition characterized by pain persistency. To investigate the oscillatory gamma activity in chronic pain, in the present study, we recorded spontaneous electrocorticogram (ECoG) signals during chronic pain development in rats with chronic inflammatory pain induced by monoarthritis. Power spectrum analysis of ECoG data showed that gamma power increased significantly at the late stage of chronic inflammatory pain. The increased gamma activity occurred mainly at electrodes over primary somatosensory cortices. In rats with chronic pain, the gamma power was positively correlated with the hyperalgesia measured by laser energy that elicited hindpaw withdrawal response. Furthermore, an increased coupling between the amplitude of gamma power and the phase of theta oscillations was observed in chronic inflammatory pain condition. These results indicate an enhanced spontaneous gamma activity in chronic pain and suggest a potential biomarker for the severity of chronic pain.

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“…Some pathological conditions, such as seizures, may alter the cortical network and show a prolonged period of hyperactivity and an aberrant avalanche [20-22]. Simulations have indicated that the dynamic range of inputs is optimized in the critical state [6,7,17,23,24].…”

Section: Introductionmentioning

confidence: 99%

Cingulate seizure-like activity reveals neuronal avalanche regulated by network excitability and thalamic inputs

Chang

Shih

et al. 2014

BMC Neurosci

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BackgroundCortical neurons display network-level dynamics with unique spatiotemporal patterns that construct the backbone of processing information signals and contribute to higher functions. Recent years have seen a wealth of research on the characteristics of neuronal networks that are sufficient conditions to activate or cease network functions. Local field potentials (LFPs) exhibit a scale-free and unique event size distribution (i.e., a neuronal avalanche) that has been proven in the cortex across species, including mice, rats, and humans, and may be used as an index of cortical excitability. In the present study, we induced seizure activity in the anterior cingulate cortex (ACC) with medial thalamic inputs and evaluated the impact of cortical excitability and thalamic inputs on network-level dynamics. We measured LFPs from multi-electrode recordings in mouse cortical slices and isoflurane-anesthetized rats.ResultsThe ACC activity exhibited a neuronal avalanche with regard to avalanche size distribution, and the slope of the power-law distribution of the neuronal avalanche reflected network excitability in vitro and in vivo. We found that the slope of the neuronal avalanche in seizure-like activity significantly correlated with cortical excitability induced by γ-aminobutyric acid system manipulation. The thalamic inputs desynchronized cingulate seizures and affected the level of cortical excitability, the modulation of which could be determined by the slope of the avalanche size.ConclusionsWe propose that the neuronal avalanche may be a tool for analyzing cortical activity through LFPs to determine alterations in network dynamics.

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Prefrontal cortex and mediodorsal thalamus reduced connectivity is associated with spatial working memory impairment in rats with inflammatory pain

Cited by 72 publications

References 82 publications

Corticostriatal Regulation of Acute Pain

Corticostriatal Regulation of Acute Pain

Enhanced Gamma Oscillatory Activity in Rats with Chronic Inflammatory Pain

Cingulate seizure-like activity reveals neuronal avalanche regulated by network excitability and thalamic inputs

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