ArticleACS chemical neuroscience2018
Pathway-Specific Alterations of Cortico-Amygdala Transmission in an Arthritis Pain Model.
Article in ACS chemical neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed.
- Molecular Signatures of Maladaptive Plasticity in the Amygdala in a Rat Model of Chronic Neuropathic Pain.Cells · 2026Article
- Prelimbic cortex-basolateral amygdala glutamatergic circuit drives cancer-induced bone pain in mice.iScience · 2026Article
- Emotional pain in non-human mammals: from neural circuitry and opioid signaling to dysthymia-like states, grief-like behaviors, and physiological dysregulation.Frontiers in veterinary science · 2026Review
- Cells and circuits for amygdala neuroplasticity in the transition to chronic pain.Cell reports · 2024Article
- Unraveling the Prefrontal Cortex-Basolateral Amygdala Pathway's Role on Schizophrenia's Cognitive Impairments: A Multimodal Study in Patients and Mouse Models.Schizophrenia bulletin · 2024Article
- Dysfunction of Small-Conductance CaCells · 2024Article
- Impaired amygdala astrocytic signaling worsens neuropathic pain-associated neuronal functions and behaviors.Frontiers in pharmacology · 2024Article
- Pain-related cortico-limbic plasticity and opioid signaling.Neuropharmacology · 2023Review
- HCN-Channel-Dependent Hyperexcitability of the Layer V Pyramidal Neurons in IL-mPFC Contributes to Fentanyl-Induced Hyperalgesia in Male Rats.Molecular neurobiology · 2023Article
- Topographic organization underlies intrinsic and morphological heterogeneity of central amygdala neurons expressing corticotropin-releasing hormone.The Journal of comparative neurology · 2022Article
- Optogenetic manipulations of CeA-CRF neurons modulate pain- and anxiety-like behaviors in neuropathic pain and control rats.Neuropharmacology · 2022Article
- Medial prefrontal cortex-basolateral amygdala circuit dysfunction in chronic alcohol-exposed male rats.Neuropharmacology · 2022Article
- Glutamatergic Neurons in the Amygdala Are Involved in Paclitaxel-Induced Pain and Anxiety.Frontiers in psychiatry · 2022Article
- Fear Extinction-Based Inter-Individual and Sex Differences in Pain-Related Vocalizations and Anxiety-like Behaviors but Not Nocifensive Reflexes.Brain sciences · 2021Article
- Ethanol modulation of cortico-basolateral amygdala circuits: Neurophysiology and behavior.Neuropharmacology · 2021Review
- Neocortical circuits in pain and pain relief.Nature reviews. Neuroscience · 2021Review
- Neural Plasticity in the Brain during Neuropathic Pain.Biomedicines · 2021Review
- Cognition in the Chronic Pain Experience: Preclinical Insights.Trends in cognitive sciences · 2021Review
- Kappa opioid receptor activation in the amygdala disinhibits CRF neurons to generate pain-like behaviors.Neuropharmacology · 2021Article
- Optogenetic Manipulations of Amygdala Neurons Modulate Spinal Nociceptive Processing and Behavior Under Normal Conditions and in an Arthritis Pain Model.Frontiers in pharmacology · 2021Article
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2 authors.
Funding
Abstract
Medial prefrontal cortex (mPFC) and amygdala are closely interconnected brain areas that play a key role in cognitive-affective aspects of pain through their reciprocal interactions. Clinical and preclinical evidence suggests that dysfunctions in the mPFC-amygdala circuitry underlie pain-related cognitive-affective deficits. However, synaptic mechanisms of pain-related changes in these long-range pathways are largely unknown. Here we used optogenetics and brain slice physiology to analyze synaptic transmission in different types of amygdala neurons driven by inputs from infralimbic (IL) and prelimbic (PL) subdivisions of the mPFC. We found that IL inputs evoked stronger synaptic inhibition of neurons in the latero-capsular division of the central nucleus (CeLC) of the amygdala than PL inputs, and this inhibition was impaired in an arthritis pain model. Furthermore, inhibition-excitation ratio in basolateral amygdala neurons was increased in the pain model in the IL pathway but not in the PL pathway. These results suggest that IL rather than PL controls CeLC activity, and that changes in this acute pain model occur predominantly in the IL-amygdala pathway.
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