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Ejoh, L. L.

Publications and source records attributed to Ejoh, L. L..

5 recordsLinked to original sources

Differential modulation of aversive signaling by expectation across the cingulate cortex

Pain-related aversion is an affective-motivational state driven by sensory experience that promotes learning and recruits widespread cortical networks, yet how distinct cingulate subregions contribute to its adaptive utility remains poorly understood. Here we used longitudinal one-photon calcium imaging in mice to compare dynamics in the anterior cingulate cortex (ACC) and retrosplenial cortex (RSC) across repeated unsignaled foot-shocks and fear conditioning and extinction paradigm. Both regions contained relatively stable ensembles that responded robustly to shocks, indicating shared encoding of acute nociceptive events. However, only the RSC flexibly re-organized its population activity when shocks were preceded by predictive cues. These anticipatory dynamics in the RSC predicted the rate of fear learning across individuals and subsequent extinction. By contrast, the ACC maintained shock-responsive ensembles with limited cue modulation. Instead, its dynamics encoded decisions to freeze, aligning with its role in encoding ongoing nociception and driving immediate defensive behavior. Together, these results reveal a division of labor in which the ACC emphasizes ongoing nociceptive processing, while the RSC transforms sensory signals into predictive codes that shape learning and memory. This specialization highlights how distributed cortical computations cooperate to generate the adaptive value of aversion. More broadly, our findings suggest that these regions assume complementary roles to address immediate sensory-motivational responses while flexibly reconfiguring to support long-term behavioral adaptation. Significance statementPain engages widespread cortical circuits, yet how distinct cingulate subregions collaborate to shape its experience and utility remains unknown. Using longitudinal calcium imaging in mice, we demonstrate that both the anterior cingulate and retrosplenial cortex contain stable shock-responsive ensembles, but only the retrosplenial cortex flexibly remodels its activity when shocks are predicted by cues. These anticipatory dynamics not only predict fear learning but influence extinction. Our findings uncover a division of labor in which the anterior cingulate encodes ongoing nociception and immediate defensive actions, while the retrosplenial cortex transforms these signals into temporally structured representations that support learning and memory. This work highlights how specialized cortical computations interact to generate the adaptive value of pain.

neuroscience↗

Anatomical and molecular organization of the nociceptive medial thalamus

The medial thalamus (MTh) is a critical hub for integrating the affective and motivational dimensions of pain, yet its cellular and circuit organization remains poorly defined. Here, we combine activity-dependent genetic tagging, whole-brain clearing and light-sheet imaging, single-cell transcriptomics, and viral circuit tracing to build a comprehensive anatomical and molecular atlas of nociceptive and opioidergic neurons within the MTh. We show that acute and chronic pain activate distinct, spatially localized microdomains across multiple MTh subnuclei, including the central medial, interanteromedial, mediodorsal, and xiphoid nuclei. Activity-dependent tagging reveals a stable ensemble of nociceptive neurons that remains engaged across acute and chronic pain states, suggesting persistent thalamic encoding of affective nociception. Using fluorescent in situ hybridization, we find that most nociceptive-activated neurons express Oprm1, and that nearly all Oprm1+ neurons are activated by nociceptive stimuli, identifying a pain-active, {micro}-opioid receptor-expressing population in MTh (MThMOR). Rabies-based tracing demonstrates that MThMOR neurons receive convergent inputs from nociceptive and inhibitory regions including the anterior cingulate cortex, periaqueductal gray, parabrachial nucleus, and habenula, while projecting broadly to cortical, subcortical, and brainstem structures involved in pain, arousal, and motivation. Enkephalinergic inputs to MTh arise from distinct, non-nociceptive populations, suggesting parallel pathways for nociceptive transmission and endogenous opioid modulation. Together, these findings define the anatomical and molecular organization of the nociceptive medial thalamus and highlight MThMOR neurons as a cell-type-specific substrate for the development of targeted opioid-based pain therapies. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=57 SRC="FIGDIR/small/692629v1_ufig1.gif" ALT="Figure 1"> View larger version (48K): org.highwire.dtl.DTLVardef@a1e6b3org.highwire.dtl.DTLVardef@13112eborg.highwire.dtl.DTLVardef@d125caorg.highwire.dtl.DTLVardef@107fd80_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

Mimicking opioid analgesia in cortical pain circuits

The anterior cingulate cortex is a key brain region involved in the affective and motivational dimensions of pain, yet how opioid analgesics modulate this cortical circuit remains unclear. Uncovering how opioids alter nociceptive neural dynamics to produce pain relief is essential for developing safer and more targeted treatments for chronic pain. Here we show that a population of cingulate neurons encodes spontaneous pain-related behaviors and is selectively modulated by morphine. Using deep-learning behavioral analyses combined with longitudinal neural recordings in mice, we identified a persistent shift in cortical activity patterns following nerve injury that reflects the emergence of an unpleasant, affective chronic pain state. Morphine reversed these neuropathic neural dynamics and reduced affective-motivational behaviors without altering sensory detection or reflexive responses, mirroring how opioids alleviate pain unpleasantness in humans. Leveraging these findings, we built a biologically inspired gene therapy that targets opioid-sensitive neurons in the cingulate using a synthetic mu-opioid receptor promoter to drive chemogenetic inhibition. This opioid-mimetic gene therapy recapitulated the analgesic effects of morphine during chronic neuropathic pain, thereby offering a new strategy for precision pain management targeting a key nociceptive cortical opioid circuit with safe, on-demand analgesia. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=40 SRC="FIGDIR/small/591113v2_ufig1.gif" ALT="Figure 1"> View larger version (28K): org.highwire.dtl.DTLVardef@d294c0org.highwire.dtl.DTLVardef@123d4f4org.highwire.dtl.DTLVardef@1720deborg.highwire.dtl.DTLVardef@efc632_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

A nociceptive amygdala-striatal pathway for chronic pain aversion

The basolateral amygdala (BLA) is essential for assigning positive or negative valence to sensory stimuli. Noxious stimuli that cause pain are encoded by an ensemble of nociceptive BLA projection neurons (BLAnoci ensemble). However, the role of the BLAnoci ensemble in mediating behavior changes and the molecular signatures and downstream targets distinguishing this ensemble remain poorly understood. Here, we show that the same BLAnoci ensemble neurons are required for both acute and chronic neuropathic pain behavior. Using single nucleus RNA-sequencing, we characterized the effect of acute and chronic pain on the BLA and identified enrichment for genes with known functions in axonal and synaptic organization and pain perception. We thus examined the brain-wide targets of the BLAnoci ensemble and uncovered a previously undescribed nociceptive hotspot of the nucleus accumbens shell (NAcSh) that mirrors the stability and specificity of the BLAnoci ensemble and is recruited in chronic pain. Notably, BLAnoci ensemble axons transmit acute and neuropathic nociceptive information to the NAcSh, highlighting this nociceptive amygdala-striatal circuit as a unique pathway for affective-motivational responses across pain states.

neuroscience↗

Optogenetic inhibition of colon epithelium reduces hypersensitivity in a mouse model of inflammatory bowel disease

Visceral pain is a prevalent symptom of inflammatory bowel disease (IBD) that can be difficult to treat. Pain and hypersensitivity are mediated by extrinsic primary afferent neurons (ExPANs) that innervate the colon. Recent studies indicate that the colon epithelium contributes to initiating ExPAN firing and nociceptive responses. Based on these findings we hypothesized that the epithelium contributes to inflammation-induced hypersensitivity. A key prediction of this hypothesis is that inhibition of the epithelium would attenuate nociceptive signaling and inflammatory hypersensitivity. To test this hypothesis, the inhibitory yellow light activated protein archaerhodopsin was targeted to the intestinal epithelium (villin-Arch) or the ExPANs (TRPV1-Arch) that innervate the colon. Visceral sensitivity was assessed by measuring the visceromotor response (VMR) to colorectal distension (CRD), with and without yellow light illumination of the colon lumen. Inhibition of the colon epithelium in healthy villin-Arch mice significantly diminished the CRD-induced VMR. Direct inhibition of ExPANs during CRD using TRPV1-Arch mice showed that ExPAN and epithelial inhibition were similarly effective in reducing the VMR to CRD. We then investigated the effect of epithelial and ExPAN inhibition in the dextran sulfate sodium (DSS) model of inflammatory bowel disease (IBD). Inhibition of the colon epithelium significantly decreased DSS-induced hypersensitivity and was comparable to inhibition of ExPANS. Together these results reveal the potential of targeting the colon epithelium for treatment of pain.

neuroscience↗