Stimulating muscarinic M1 receptors in the anterior cingulate cortex reduces mechanical hypersensitivity via GABAergic transmission in nerve injury rats

Koga, Katsumi; Matsuzaki, Yu; Migita, Keisuke; Shimoyama, Shuji; Eto, Fumihiro; Nakagawa, Taro; Matsumoto, Taichi; Terada, Kazuki; Mishima, Kenichi; Furue, Hidemasa; Honda, Kazuo

doi:10.1016/j.brainres.2018.10.013

Cited by 10 publications

(7 citation statements)

References 38 publications

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“…However, in practice, rodent studies of cingulate cortex are obviously not treatednor should they be treatedas an entirely separate research field. To compare and synthesise findings across species, studies have sometimes treated rodent Cg1 and/or Cg2 as directly comparable to human ACC [38][39][40][45][46][47][48][49][50][51][52][53][54][55]; mostly without assigning a direct counterpart to human MCC [39,40,45,46,[56][57][58][59][60][61][62][63]; on other occasions, Cg1 and Cg2 have been equated to MCC [64]; and in still other cases, rodent Cg1 has been treated as the counterpart of human dACC [38,42,[65][66][67] and Cg2 as the counterpart of human vACC [68][69][70]. All of these approaches overlook the fact that the border between Cg1 and Cg2 is defined perpendicularly to both the border between ACC/MCC and between dACC/vACC, so that results gained using the Cg1/ Cg2 nomenclature will necessarily represent a mix of data that would have been studied separately under the ACC/MCC (or dACC/vACC) nomenclature.…”

Section: Trends In Neurosciencesmentioning

confidence: 99%

Where is Cingulate Cortex? A Cross-Species View

Heukelum

Mars

Guthrie

et al. 2020

Trends in Neurosciences

192

147

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To compare findings across species, neuroscience relies on cross-species homologies, particularly in terms of brain areas. For cingulate cortex, a structure implicated in behavioural adaptation and control, a homologous definition across mammals is availablebut currently not employed by most rodent researchers. The standard partitioning of rodent cingulate cortex is inconsistent with that in any other model species, including humans. Reviewing the existing literature, we show that the homologous definition better aligns results of rodent studies with those of other species, and reveals a clearer structural and functional organisation within rodent cingulate cortex itself. Based on these insights, we call for widespread adoption of the homologous nomenclature, and reinterpretation of previous studies originally based on the nonhomologous partitioning of rodent cingulate cortex.

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Section: Trends In Neurosciencesmentioning

confidence: 99%

Where is Cingulate Cortex? A Cross-Species View

Heukelum

Mars

Guthrie

et al. 2020

Trends in Neurosciences

192

147

View full text Add to dashboard Cite

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“…Chemogenetic inhibition of medial septum cholinergic neurons abolishes the hyperexcitability of rostral ACC pyramidal neurons, reduces CPA, and alleviates inflammation-induced mechanical and thermal hypersensitivity, whereas activation of the same medial septum neurons abolishes hypersensitivity by activating the ventral hippocampus [50]. Interestingly, the M1-induced increase in mechanical thresholds observed in injured rats, is also enhancing GABA A mediated transmission in the ACC [303,304]. Although the importance of ACh and cholinergic signaling in the mPFC has been clinically recognized, since for example the anti-depressive effect of the muscarinic antagonist scopolamine is mediated by PrL/IL M1 receptors, neither the (micro-)circuitry of cholinergic control nor the mechanisms underlying the SNI-induced downregulation of muscarinic receptors at PrL pyramidal neurons are fully understood so far [155,293,305].…”

Section: Acetylcholine (Ach)mentioning

confidence: 99%

The Medial Prefrontal Cortex as a Central Hub for Mental Comorbidities Associated with Chronic Pain

Kummer

Mitrić

Kalpachidou

et al. 2020

IJMS

108

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Chronic pain patients frequently develop and suffer from mental comorbidities such as depressive mood, impaired cognition, and other significant constraints of daily life, which can only insufficiently be overcome by medication. The emotional and cognitive components of pain are processed by the medial prefrontal cortex, which comprises the anterior cingulate cortex, the prelimbic, and the infralimbic cortex. All three subregions are significantly affected by chronic pain: magnetic resonance imaging has revealed gray matter loss in all these areas in chronic pain conditions. While the anterior cingulate cortex appears hyperactive, prelimbic, and infralimbic regions show reduced activity. The medial prefrontal cortex receives ascending, nociceptive input, but also exerts important top-down control of pain sensation: its projections are the main cortical input of the periaqueductal gray, which is part of the descending inhibitory pain control system at the spinal level. A multitude of neurotransmitter systems contributes to the fine-tuning of the local circuitry, of which cholinergic and GABAergic signaling are particularly emerging as relevant components of affective pain processing within the prefrontal cortex. Accordingly, factors such as distraction, positive mood, and anticipation of pain relief such as placebo can ameliorate pain by affecting mPFC function, making this cortical area a promising target region for medical as well as psychosocial interventions for pain therapy.

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“…The results of this study show that cholinergic-GABAergic projections of the NBM to the PL serve to enhance PL activity, and could thus counteract deactivation of the PL in chronic pain states. In support, there is evidence from an ex-vivo study showing reduction in synaptic expression of excitatory M1 muscarinic receptors in layer 5 neurons of the PL in neuropathic mice 43 and a study reporting suppression of neuropathic allodynia upon application of a M1-M4 agonist in the anterior cingulate cortex 44 .…”

Section: Discussionmentioning

confidence: 94%

A novel role for the cholinergic basal forebrain nucleus of Meynert in chronic pain via modulation of the prelimbic cortex

Kuner

Oswald

Han

et al. 2022

Preprint

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The basal nucleus of Meynert (NBM) subserves critically important functions in attention, arousal and cognition via its profound modulation of neocortical activity and is emerging as a key target in Alzheimer’s and Parkinson’s dementias. Despite the crucial role of neocortical domains in pain perception, however, the NBM has not been studied in chronic pain. Here, using in vivo tetrode recordings in behaving mice, we report that beta and gamma oscillatory activity is evoked in the NBM by noxious stimuli and is facilitated at peak inflammatory pain. Optogenetic and chemogenetic cell-specific, reversible manipulations of NBM cholinergic-GABAergic neurons reveal their role in endogenous control of nociceptive hypersensitivity, which are manifest via projections to the prelimbic cortex, resulting in layer 5-mediated antinociception. Our data unravel the importance of the NBM in top-down control of neocortical processing of pain and suggest a potential for its therapeutic modulation via neurostimulation strategies in chronic pain disorders.

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Stimulating muscarinic M1 receptors in the anterior cingulate cortex reduces mechanical hypersensitivity via GABAergic transmission in nerve injury rats

Cited by 10 publications

References 38 publications

Where is Cingulate Cortex? A Cross-Species View

Where is Cingulate Cortex? A Cross-Species View

The Medial Prefrontal Cortex as a Central Hub for Mental Comorbidities Associated with Chronic Pain

A novel role for the cholinergic basal forebrain nucleus of Meynert in chronic pain via modulation of the prelimbic cortex

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