Social Neuroscience Advances
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Rescooped by Jocelyn Stoller from Neuroscience_topics
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Opening paths to novel analgesics: the role of potassium channels in chronic pain

Opening paths to novel analgesics: the role of potassium channels in chronic pain | Social Neuroscience Advances | Scoop.it

Highlights- Potassium (K+) channels are crucial determinants of neuronal excitability.- Nerve injury or inflammation alters K+ channel activity in neurons of the pain pathway.- These changes can render neurons hyperexcitable and cause chronic pain.- Therapies targeting K+ channels may provide improved pain relief in these states. (...) - By Tsantoulas C & McMahon SB, Trends in Neurosciences, Volume 37, Issue 3, March 2014, Pages 146–158


Via Julien Hering, PhD
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Julien Hering, PhD's curator insight, May 27, 2014 11:01 AM

The exceptional abundance and breadth of function encountered in K+ channels has complicated efforts to untangle explicit roles in pain syndromes. Owing to advances in molecular, biochemical, electrophysiological, and genetic methods, however, we can now appreciate the involvement of specific subunits in maladaptive pain signaling after injury or inflammation. Nevertheless, there are many potential avenues of K+ involvement that have hardly been explored. It seems likely that unknown mutations in K+channel genes might contribute to inherited pain syndromes. There are many ‘silent’ K+ channel subunits for which we have little idea of whether and how they might affect pain processing. Auxiliary subunits can provide alternative substrates for pharmacological modulation; however, our understanding of these interactions in the PNS is also limited. In many chronic pain models an extensive dysregulation of several K+channels is seen, and it is unknown whether a common epigenetic control exists.

Rescooped by Jocelyn Stoller from Neuroscience_topics
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Drug-evoked synaptic plasticity: beyond metaplasticity

Drug-evoked synaptic plasticity: beyond metaplasticity | Social Neuroscience Advances | Scoop.it
  • Addictive drugs alter synaptic plasticity in the VTA through a common mechanism.
  • Changes in the VTA are permissive for later mesocorticolimbic circuit remodeling.
  • Mesocorticolimbic circuit remodeling may underlie addiction-related behaviors.
  • Reversing drug-induced plasticity may ultimately suppress addiction-related behavior.

by Creed MC & Lüscher C, Current Opinion in Neurobiology, online 6 April 2013


Via Julien Hering, PhD
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Rescooped by Jocelyn Stoller from Neuroscience_topics
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Kv7 channels as targets for anti-epileptic and psychiatric drug-development

Kv7 channels as targets for anti-epileptic and psychiatric drug-development | Social Neuroscience Advances | Scoop.it

The Kv7 channels, a family of voltage-dependent K+ channels (Kv7.1–Kv7.5), have gained much attention in drug discovery especially because four members are genetically linked to diseases. For disorders of the CNS focus was originally on epilepsy and pain, but it is becoming increasingly evident that Kv7 channels can also be valid targets for psychiatric disorders, such as anxiety and mania. The common denominator is probably neuronal hyperexcitability in different brain areas, which can be successfully attenuated by pharmacological increment of Kv7 channel activity. This perspective attempts to review the current status and challenges for CNS drug discovery based on Kv7 channels as targets for neurological and psychiatric indications with special focus on selectivity and mode-of-actions. - by Grunnet M. et al., European Journal of Pharmacology, Volume 726, 5 March 2014, Pages 133–137


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