Articles: chronic.
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Peripheral nerve injury causes maladaptive plasticity in the central nervous system and induces chronic pain. In addition to the injured limb, abnormal pain sensation can appear in the limb contralateral to the injury, called mirror image pain. Because synaptic remodeling in the primary somatosensory cortex (S1) has critical roles in the induction of chronic pain, cortical reorganization in the S1 ipsilateral to the injured limb may also accompany mirror image pain. ⋯ When local inhibitory circuits were blocked, astrocyte-dependent spine plasticity and allodynia were revealed. Thus, we propose that cortical astrocytes prime the induction of spine plasticity and mirror image pain after peripheral nerve injury. Moreover, this result suggests that cortical synaptic rewiring could be sufficient to cause allodynia on the uninjured periphery.
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Minerva anestesiologica · Aug 2018
Hepatic encephalopathy and cirrhotic cardiomyopathy in Intensive Care Unit.
Acute and chronic liver diseases may escalate to hepatic encephalopathy (HE) and multiple organ failure, requiring admission and organ support in Intensive Care Unit (ICU). Hepatic dysfunction in ICU is a broad and complex topic; unfortunately, up to now, the understanding of its underlying pathophysiology is far from complete. HE and cirrhotic cardiomyopathy (CCM) need timely diagnostic and therapeutic measures aiming at the identification and elimination of causative factors, to improve patients' prognosis. Through this short review, we tried to answer the most asked questions about clinical features of HE and CCM at the ICU stage.
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One specific behavior can be synergistically modulated by different neural pathways. Medial septal (MS) cholinergic system innervates widespread cortical and subcortical regions and participates in pain modulation, but the underlying neural pathways are not fully understood. This study examined the contribution of MS cholinergic neurons and 2 neural pathways: MS-rostral anterior cingulate cortex (rACC) and MS-ventral hippocampal CA1 (vCA1), in modulating perceptual and affective pain behaviors in a mouse model of chronic inflammatory pain. ⋯ By contrast, chemogenetic activation of MS cholinergic neurons also produced analgesia, but by rescuing hypofunctional pyramidal neurons in vCA1. These results clearly demonstrate that the MS cholinergic system differentially modulates chronic inflammatory pain through MS-rACC or MS-vCA1 pathways. More significantly, our research provides evidence for a novel paradigm of neural circuit modulation: MS cholinergic inhibition and activation induce similar analgesia but through distinct neural pathways.