Nature Neuroscience, Published online: 09 August 2021; doi:10.1038/s41593-021-00903-8
The authors identify a spinal–parabrachial–mesencephalic circuit that regulates the activity of dopamine neurons during pain.
Nature Neuroscience, Published online: 08 March 2021; doi:10.1038/s41593-021-00811-x
Pain hypersensitivity can result from tissue injury and from depression. This study in mice shows that distinct thalamocortical pathways mediate allodynia associated with injury and a stress-induced depression-like state, respectively.
Nature Neuroscience, Published online: 18 May 2020; doi:10.1038/s41593-020-0645-3
General anesthetics during surgery are presumed to block pain by dampening brain activity and promoting loss-of-consciousness. A new study shows that anesthetics activate an endogenous analgesia neural ensemble in the central nucleus of the amygdala.
Nature Neuroscience, Published online: 18 May 2020; doi:10.1038/s41593-020-0632-8
Hua and Chen et al. show that general anesthesia activates a distinct population of central amygdala neurons and that these neurons can potently suppress pain responses through their widespread projections to many pain-processing centers in the brain.
Nature Neuroscience, Published online: 01 October 2019; doi:10.1038/s41593-019-0522-0
Publisher Correction: A neural circuit for comorbid depressive symptoms in chronic pain
Nature Neuroscience, Published online: 09 September 2019; doi:10.1038/s41593-019-0481-5
Huang and colleagues functionally map a brain circuit connecting the amygdala and the spinal cord that is altered after nerve injury and contributes to chronic pain.
Nature Neuroscience, Published online: 27 August 2019; doi:10.1038/s41593-019-0499-8
Chronic pain is associated with anxio-depressive comorbidities, but the neuroanatomical substrates remain unknown. A specific serotonergic pathway from the dorsal raphe nucleus to the lateral habenula via the central amygdala is now uncovered as a key neural circuit governing comorbid depressive symptoms in chronic pain.
Nature Neuroscience, Published online: 26 August 2019; doi:10.1038/s41593-019-0468-2
Zhou et al. report a novel 5-HT circuit from the dorsal raphe nucleus to somatostatin-expressing neurons in the central nucleus of the amygdala that partially mediates depressive-like behavior in a mouse model of chronic pain.
Author Correction: Circuit dissection of the role of somatostatin in itch and pain
Author Correction: Circuit dissection of the role of somatostatin in itch and pain, Published online: 19 April 2018; doi:10.1038/s41593-018-0149-6
Author Correction: Circuit dissection of the role of somatostatin in itch and pain
Circuit dissection of the role of somatostatin in itch and pain
Circuit dissection of the role of somatostatin in itch and pain, Published online: 19 March 2018; doi:10.1038/s41593-018-0119-z
Huang et al. demonstrate that somatostatin (Sst)-expressing primary afferents are pruriceptors. In spinal cord, they show that Sst potentiates itch by disinhibition involving dynorphin-expressing spinal neurons and that Sst also suppresses pain.
Publisher Correction: A craniofacial–specific monosynaptic circuit enables heightened affective pain
Publisher Correction: A craniofacial–specific monosynaptic circuit enables heightened affective pain, Published online: 16 March 2018; doi:10.1038/s41593-018-0103-7
Publisher Correction: A craniofacial–specific monosynaptic circuit enables heightened affective pain
Generalizable representations of pain, cognitive control, and negative emotion in medial frontal cortex
Generalizable representations of pain, cognitive control, and negative emotion in medial frontal cortex, Published online: 01 January 2018; doi:10.1038/s41593-017-0051-7
Assessing person-level human brain maps across 18 fMRI studies, the authors identify separable representations of pain, cognitive control, and negative emotion in the medial frontal cortex that generalize across different studies and tasks.
A craniofacial-specific monosynaptic circuit enables heightened affective pain
A craniofacial-specific monosynaptic circuit enables heightened affective pain, Published online: 13 November 2017; doi:10.1038/s41593-017-0012-1
NatureArticleSnippet(type=short-summary, markup=The authors show that unlike body sensory neurons, craniofacial nociceptive neurons directly synapse with noxious-stimulus-activated lateral parabrachial neurons (PBL), which in turn project to multiple limbic centers processing emotions and affects. This monosynaptic pathway is both sufficient and necessary for craniofacial-pain-activated aversive behaviors.
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Nature Neuroscience 20, 1037 (2017). doi:10.1038/nn.4609
Authors: Erika K Harding & Michael W Salter
Loss of inhibition in a circuit in the primary somatosensory cortex that controls the activity of layer 5 neurons drives pain hypersensitivity. Restoring this inhibition resets the inhibitory–excitatory balance, producing analgesia.
Nature Neuroscience 20, 897 (2017). doi:10.1038/nn.4586
Authors: Michael Hirth, Jagadeesh Gandla & Rohini Kuner
The checkpoint pathway consisting of programmed death ligand 1 (PD-L1) and its receptor, PD-1, modulates immune function in cancer and infection, but unexpectedly, it also silences pain signals in nerves.
Nature Neuroscience 19, 9 (2016). doi:10.1038/nn.4217
Author: Sébastien Thuault
Nature Neuroscience 18, 1861 (2015). doi:10.1038/nn1215-1861d
Author: Andrew R Segerdahl, Melvin Mezue, Thomas W Okell, John T Farrar & Irene Tracey
Nature Neuroscience 18, 1059 (2015). doi:10.1038/nn.4057
Authors: Victoria E Brings & Mark J Zylka
A study finds that pain hypersensitivity in male and female mice is differentially dependent on microglia and T cells, and describes a sex-specific response to microglia-targeted pain treatments. This sex difference will be important to consider when developing treatments for pain and other neurological disorders involving microglia and immune cells.
