Recruitment of Spinoparabrachial Neurons by Dorsal Horn Calretinin Neurons

Petitjean, Hugues; Bourojeni, Farin B.; Tsao, D.; Davidova, Albena; Sotocinal, Susana G.; Mogil, Jeffrey S.; Kania, Artur; Sharif‐Naeini, Reza

doi:10.1016/j.celrep.2019.07.048

Cited by 45 publications

(50 citation statements)

References 36 publications

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“…Of note, an increasing number of dorsal horn interneurons that “gate” mechanical pain have been identified. These include neurochemically distinct excitatory interneuron populations: transient VGLUT3, somatostatin, RORα, calretinin and Tac1 (Bourane, Duan, et al, 2015; Cheng et al, 2017; Duan et al, 2014; Huang et al, 2019; Peirs et al, 2015; Petitjean et al, 2019) and distinct inhibitory interneuron populations: dynorphin, calretinin, parvalbumin and encephalin (Boyle et al, 2019; Duan et al, 2014; Francois et al, 2017; Petitjean et al, 2019; Petitjean et al, 2015). The CGRP-expressing interneurons define yet another population of dorsal horn interneurons that contributes to spinal cord processing of mechanical inputs.…”

Section: Discussionmentioning

confidence: 99%

“…For example, the transiently expressing VGLUT3 population is located ventral to the CGRP interneurons, receives low-threshold mechanoreceptive input and their chemogenetic activation also enhances mechanical sensitivity (Cheng et al, 2017; Peirs et al, 2015). Dorsal to the CGRP interneuron are PKCγ and calretinin excitatory interneurons that contribute to nerve injury induced mechanical allodynia (Malmberg et al, 1997; Neumann et al, 2008; Peirs et al, 2015; Petitjean et al, 2019; Smith et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

“…Most importantly, compared to the lamina II radial cells, we recorded much more extensive ventral axon trajectories of the CGRP interneurons, which suggests that these interneurons engage very different circuits in the dorsal and potentially ventral horn. In this regard, the CGRP interneurons are distinct from the calretinin interneurons that target lamina I projection neurons (Petitjean et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

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Dorsal horn CGRP-expressing interneurons contribute to nerve injury-induced mechanical hypersensitivity

Löken¹,

Etlin²,

Bernstein³

et al. 2020

Preprint

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17 Primary sensory neurons are generally considered the only source of dorsal horn 18 calcitonin gene-related peptide (CGRP), a neuropeptide critical to the transmission of 19 pain messages. Using a tamoxifen-inducible CGRP CreER transgenic mouse, here we 20 identified a distinct population of CGRP-expressing excitatory interneurons in lamina III 21 of the spinal cord dorsal horn and trigeminal nucleus caudalis. These interneurons have 22 spine-laden, dorsally-directed, dendrites and ventrally-directed axons. Neither 23 innocuous nor noxious stimulation provoked significant Fos expression in these 24 neurons. However, synchronous, electrical non-nociceptive Aβ primary afferent 25 stimulation of dorsal roots depolarized the CGRP interneurons, consistent with their 26 receipt of a VGLUT1 innervation. In contrast, chemogenetic activation produced a 27 significant mechanical hypersensitivity. Importantly, the CGRP interneurons could be 28 activated after peripheral nerve injury, but only with concurrent innocuous, brush 29 stimulation. These findings suggest that hyperexcitability of dorsal horn CGRP

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Dorsal horn CGRP-expressing interneurons contribute to nerve injury-induced mechanical hypersensitivity

Löken¹,

Etlin²,

Bernstein³

et al. 2020

Preprint

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show abstract

“…Excitatory interneurons of the deeper dorsal horn engage in circuits that process noxious information and thereby contribute to the development of mechanical hypersensitivity or allodynia (i.e. pain induced by innocuous sensory stimuli) [17][18][19][20].Several lines of evidence support the idea that these circuit changes are based on the loss of inhibition exerted by e.g. glycinergic and/or parvalbumin expressing inhibitory interneurons [19,21].…”

mentioning

confidence: 99%

mentioning

confidence: 99%

Neuron Type-Specific Translatomes in Spinal Cords of Naïve and Neuropathic Mice

Gupta

Scheurer

Pelczar

et al. 2020

Preprint

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The spinal dorsal horn harbors a sophisticated and heterogeneous network of excitatory and inhibitory neurons that process peripheral signals encoding different sensory modalities. Although it has long been recognized that this network is crucial both for the separation and the integration of sensory signals of different modalities, the molecular identity of the underlying neurons and signaling mechanisms are still only partially understood. Here, we have used the translating ribosome affinity purification (TRAP) technique to map the translatomes of excitatory glutamatergic (VGLUT2 + ) and inhibitory GABA and/or glycinergic (VGAT + or Gad67 + ) neurons of the mouse spinal cord. Our analyses demonstrate that inhibitory and excitatory neurons are primarily set apart by the expression of genes encoding transcription factors or genes related to the production, release or re-uptake of their principal neurotransmitters (glutamate, GABA or glycine). Subsequent gene ontology (GO) term analyses revealed that neuropeptide signaling-related GO terms were highly enriched in the excitatory population. Eleven neuropeptide genes displayed largely non-overlapping expression patterns closely adhering to the laminar and hence also functional organization of the spinal cord grey matter, suggesting that they may serve as major determinants of modality-specific processing. Since this modality-specific processing of sensory input is severely compromised in chronic, especially neuropathic, pain, we also investigated whether peripheral nerve damage changes the neuron typespecific translatome. In summary, our results suggest that neuropeptides contribute to modalityspecific sensory processing in the spinal cord but also indicate that altered sensory encoding in neuropathic pain states occurs independent of major translatome changes in the spinal neurons.The ability to sense and discriminate different noxious and innocuous somatosensory stimuli is essential for all higher animals and humans in order to react adequately to external stimuli and internal conditions [1,2]. The spinal dorsal horn, i.e., the sensory part of the spinal cord, constitutes a key element in this process. It receives somatosensory signals from peripheral neurons and processes these signals together with other inputs descending from supraspinal sites in a complex network of inhibitory and excitatory interneurons before relaying these signals via projection neurons to supraspinal centers [3]. Projection neurons make up less than 10% of all dorsal horn neurons, while more than 90% of the neuronal population are interneurons of which, between 60 and 70% are excitatory glutamatergic neurons, and the rest is inhibitory (GABA and/or glycinergic).The spinal cord is organized in a laminar fashion, which has initially been proposed on the basis of differences in cell density and morphology between the different laminae [4, 5] but has later been shown to also reflect functional organization. This is especially reflected for example by the lamina specific innervation pattern by ...

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Channelrhodopsin-2 Assisted Circuit Mapping in the Spinal Cord Dorsal Horn

Smith

Graham²

2022

Neuromethods

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Recruitment of Spinoparabrachial Neurons by Dorsal Horn Calretinin Neurons

Cited by 45 publications

References 36 publications

Dorsal horn CGRP-expressing interneurons contribute to nerve injury-induced mechanical hypersensitivity

Dorsal horn CGRP-expressing interneurons contribute to nerve injury-induced mechanical hypersensitivity

Neuron Type-Specific Translatomes in Spinal Cords of Naïve and Neuropathic Mice

Channelrhodopsin-2 Assisted Circuit Mapping in the Spinal Cord Dorsal Horn

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