{"id":1305,"date":"2025-06-21T03:54:07","date_gmt":"2025-06-21T03:54:07","guid":{"rendered":"https:\/\/www.europesays.com\/us\/1305\/"},"modified":"2025-06-21T03:54:07","modified_gmt":"2025-06-21T03:54:07","slug":"chronic-pain-linked-to-neuron-overactivity-in-the-brainstem","status":"publish","type":"post","link":"https:\/\/www.europesays.com\/us\/1305\/","title":{"rendered":"Chronic Pain Linked to Neuron Overactivity in the Brainstem"},"content":{"rendered":"<p><strong>Summary: <\/strong>A new study reveals that neurons in the brainstem respond very differently to acute versus chronic pain, potentially explaining why some pain persists long after injury. In acute pain, neurons in the medullary dorsal horn reduce their activity through a natural \u201cbraking\u201d system involving A-type potassium currents, helping limit pain signals.<\/p>\n<p>But in chronic pain, this mechanism fails, and the neurons become overactive, continuing to send pain messages. This discovery provides a clearer biological pathway for how pain becomes chronic and may guide future therapies aimed at restoring this internal regulation system.<\/p>\n<p><strong>Key Facts:<\/strong><\/p>\n<ul class=\"wp-block-list\">\n<li><strong>Brainstem Relay Dysfunction:<\/strong> In chronic pain, neurons in the medullary dorsal horn lose their ability to dampen pain signals.<\/li>\n<li><strong>A-Type Potassium Current (IA):<\/strong> This current acts as a brake in acute pain but fails to activate in chronic pain conditions.<\/li>\n<li><strong>Therapeutic Implication:<\/strong> Targeting IA could be a novel strategy to prevent or treat chronic pain.<\/li>\n<\/ul>\n<p><strong>Source: <\/strong>Hebrew University of Jerusalem<\/p>\n<p><strong>Why does some pain go away while other types linger, turning into chronic suffering? <\/strong><\/p>\n<p>A groundbreaking study from scientists at The Hebrew University of Jerusalem may have uncovered part of the answer \u2014 deep inside the brainstem.<\/p>\n<p>  <img fetchpriority=\"high\" decoding=\"async\" width=\"1200\" height=\"799\" src=\"https:\/\/www.europesays.com\/us\/wp-content\/uploads\/2025\/06\/brainstemy-chronic-pain-neuroscience.jpg\" alt=\"This shows a brain.\"  \/> In acute pain, IA increases \u2014 acting like a natural sedative for the pain pathways. Credit: Neuroscience News<\/p>\n<p>In a study published this week in\u00a0Science Advances, researchers led by\u00a0Doctoral student Ben Title under the guidance of Prof. Alexander M. Binshtok from The Hebrew University-Hadassah School of Medicine and the Center for Brain Sciences (ELSC) at The Hebrew University,\u00a0reveal that our bodies respond to acute (short-term) and chronic (long-lasting) pain in surprisingly different ways at the cellular level.<\/p>\n<p>Their discovery sheds new light on how pain becomes chronic \u2014 and opens the door to better-targeted treatments.<\/p>\n<p><strong>The Brain\u2019s \u201cPain Relays\u201d Behave Differently in Acute vs. Chronic Pain<\/strong><\/p>\n<p>The team studied a small but crucial region in the brainstem called the medullary dorsal horn, home to neurons that act as a relay station for pain signals. These projection neurons help send pain messages from the body to the brain.<\/p>\n<p>The scientists found that during acute inflammatory pain, these neurons actually dial down their own activity. This built-in \u201cbraking system\u201d helps limit the amount of pain-related signals sent to the brain. Once the inflammation and pain subside, the neurons return to their normal state.<\/p>\n<p>However, in chronic pain, this braking system fails. The neurons don\u2019t reduce their activity \u2014 in fact, they become more excitable and fire more signals, potentially contributing to the persistence of pain.<\/p>\n<p><strong>The Key Player: A-Type Potassium Current<\/strong><\/p>\n<p>Using a combination of electrophysiology and computer modeling, the researchers identified a key mechanism: a specific potassium current known as the A-type potassium current (IA). This current helps regulate the excitability of neurons.<\/p>\n<p>In acute pain, IA increases \u2014 acting like a natural sedative for the pain pathways. But in chronic pain, this current doesn\u2019t ramp up, and the neurons become hyperactive. The absence of this regulation may be one of the biological switches that turns temporary pain into a long-lasting condition.<\/p>\n<p><strong>Implications for Chronic Pain Treatment<\/strong><\/p>\n<p>\u201cThis is the first time we\u2019ve seen how the same neurons behave so differently in acute versus chronic pain,\u201d said\u00a0Prof. Binshtok.<\/p>\n<p>\u201cThe fact that this natural \u2018calming\u2019 mechanism is missing in chronic pain suggests a new target for therapy. If we can find a way to restore or mimic that braking system, we might be able to prevent pain from becoming chronic.\u201d<\/p>\n<p><strong>A Step Toward Smarter Pain Therapies<\/strong><\/p>\n<p>Chronic pain affects over 50 million people in the U.S. alone, often with few effective treatment options. This new study adds an important piece to the puzzle by showing how the nervous system\u2019s built-in pain controls are disrupted in long-term pain conditions.<\/p>\n<p>By understanding the brain\u2019s own strategies for limiting pain \u2014 and why they sometimes fail \u2014 scientists are now one step closer to developing smarter, more precise therapies for those who suffer from chronic pain.<\/p>\n<p>About this pain and neuroscience research news<\/p>\n<p class=\"has-background\" style=\"background-color:#ffffe8\"><strong>Author: <\/strong><a href=\"http:\/\/neurosciencenews.com\/cdn-cgi\/l\/email-protection#ec888d828d89818fac9f8d9a858382c284998685c28d8fc28580\" target=\"_blank\" rel=\"noreferrer noopener\">Danae Marx<\/a><br \/><strong>Source: <\/strong><a href=\"https:\/\/huji.ac.il\" target=\"_blank\" rel=\"noreferrer noopener\">Hebrew University of Jerusalem<\/a><br \/><strong>Contact: <\/strong>Danae Marx \u2013 Hebrew University of Jerusalem<br \/><strong>Image: <\/strong>The image is credited to Neuroscience News<\/p>\n<p class=\"has-background\" style=\"background-color:#ffffe8\"><strong>Original Research: <\/strong>Open access.<br \/>\u201c<a href=\"https:\/\/dx.doi.org\/10.1126\/sciadv.adr3467\" target=\"_blank\" rel=\"noreferrer noopener\">Opposite regulation of medullary pain-related projection neuron excitability in acute and chronic pain<\/a>\u201d by Alexander M. Binshtok et al. Science Advances<\/p>\n<p><strong>Abstract<\/strong><\/p>\n<p><strong>Opposite regulation of medullary pain-related projection neuron excitability in acute and chronic pain<\/strong><\/p>\n<p>Pain hypersensitivity is associated with increased activity of peripheral and central neurons along the pain neuroaxis.<\/p>\n<p>We show that at the peak of acute inflammatory pain, superficial medullary dorsal horn projection neurons (PNs) that relay nociceptive information to the parabrachial nucleus reduce their intrinsic excitability and, consequently, action potential firing.<\/p>\n<p>When pain resolves, the excitability of these neurons returns to baseline.<\/p>\n<p>Using electrophysiological and computational approaches, we found that an increase in potassium A-current (IA) underlies the decrease in the excitability of medullary dorsal horn PNs in acute pain conditions.<\/p>\n<p>In chronic pain conditions, no changes of\u00a0IA\u00a0were observed, and medullary dorsal horn PNs exhibit increased intrinsic excitability and firing.<\/p>\n<p>Our results reveal a differential modulation of the excitability of medullary dorsal horn projection neurons in acute and chronic pain conditions, suggesting a regulatory mechanism that, in acute pain conditions, tunes the output of the dorsal horn and, if lacking, could facilitate pain chronification.<\/p>\n","protected":false},"excerpt":{"rendered":"Summary: A new study reveals that neurons in the brainstem respond very differently to acute versus chronic pain,&hellip;\n","protected":false},"author":3,"featured_media":1306,"comment_status":"","ping_status":"","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[11],"tags":[827,1797,1798,210,1799,829,912,831,1800,67,132,68],"class_list":{"0":"post-1305","1":"post","2":"type-post","3":"status-publish","4":"format-standard","5":"has-post-thumbnail","7":"category-health","8":"tag-brain-research","9":"tag-brainstem","10":"tag-chronic-pain","11":"tag-health","12":"tag-hebrew-university-of-jerusalem","13":"tag-neurobiology","14":"tag-neurology","15":"tag-neuroscience","16":"tag-pain","17":"tag-united-states","18":"tag-unitedstates","19":"tag-us"},"share_on_mastodon":{"url":"https:\/\/pubeurope.com\/@us\/114719337109295100","error":""},"_links":{"self":[{"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/posts\/1305","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/users\/3"}],"replies":[{"embeddable":true,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/comments?post=1305"}],"version-history":[{"count":0,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/posts\/1305\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/media\/1306"}],"wp:attachment":[{"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/media?parent=1305"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/categories?post=1305"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/tags?post=1305"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}