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Neuroscience_topics
Neuroscience: CNS disease, pain, brain research, ion channels, synaptic transmission, channelopathies, neuronal network
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Neurophysiology of HCN channels: From cellular functions to multiple regulations

Neurophysiology of HCN channels: From cellular functions to multiple regulations | Neuroscience_topics | Scoop.it
Highlights
  • Hyperpolarization-activated cyclic nucleotide-gated (HCN) cation channels are involved in multiple physiological processes.
  • HCN channels are excellent targets of various cellular signals to finely regulate neuronal responses to external stimuli.
  • Dysregulation of HCN channels is involved in a variety of neurological disorders.
by He C et al.Progress in NeurobiologyVolume 112, January 2014, Pages 1–23
Julien Hering, PhD's insight:

An interesting review about HCN these must-known ion channels that are involved in numerous physiological processes and brain diseases.

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Ion channels in genetic and acquired forms of epilepsy

Ion channels in genetic and acquired forms of epilepsy | Neuroscience_topics | Scoop.it
[Abstract] Genetic mutations causing dysfunction of both voltage- and ligand-gated ion channels make a major contribution to the cause of many different types of familial epilepsy. Key mechanisms comprise defective Na+ channels of inhibitory neurons or GABAA receptors affecting pre- or postsynaptic GABAergic inhibition, or a dysfunction of different types of channels at axon initial segments. Many of the mentioned ion channel mutations have been modelled in mice which has largely contributed to the understanding of where and how the ion channel defects lead to neuronal hyperexcitability. Defects of ion channel function are also associated with forms of acquired epilepsies. Animal models of febrile seizures or mesial temporal epilepsy have shown that dendritic K+ channels, hyperpolarization-activated cation channels and T-type Ca2+ channels play important roles in the generation of seizures. For the latter, it has been shown that suppression of their function by pharmacological mechanisms or in knock-out mice can antagonize epileptogenesis. Autoantibodies directed against ion channels or associated proteins, such as K+ channels, LGI1 or NMDA receptors, have been identified in epileptic disorders which are summarized under the term limbic encephalitis comprising limbic seizures, status epilepticus and psychiatric symptoms. We conclude that ion channels and associated proteins are important players for different types of genetic and acquired epilepsies. Nevertheless, the molecular bases for most common forms of epilepsy are not yet clear, and evidence to be discussed indicates just how much more we need to understand about the complex mechanisms that underlie epileptogenesis. - Lerche H et al., The Journal of Physiology, doi:
10.1113/jphysiol.2012.240606
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HCN and KV7 (M-) channels as targets for epilepsy treatment

HCN and KV7 (M-) channels as targets for epilepsy treatment | Neuroscience_topics | Scoop.it

Voltage-gated ion channels are important determinants of cellular excitability. The Hyperpolarization-activated Cyclic Nucleotide-gated (HCN) and KV7 (M-) channels are voltage-gated ion channels. Both channels are activated at sub-threshold potentials and have biophysical properties that mirror each other. KV7 channels inhibit neuronal excitability. Thus, mutations in KV7 channels that are associated with Benign Familial Neonatal Convulsions (BFNC) are likely to be epileptogenic. Mutations in HCN channels have also been associated with idiopathic epilepsies such as GEFS+. In addition, HCN channel expression and function are modulated during symptomatic epilepsies such as temporal lobe epilepsy. It is, though, unclear as to whether the changes in HCN channel expression and function associated with the various forms of epilepsy promote epileptogenesis or are adaptive. In this review, we discuss this as well as the potential for KV7 and HCN channels as drug targets for the treatment of epilepsy. (...) - by Shah MM et al., NeuropharmacologyVolume 69, June 2013, Pages 75–81

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Jose Santos's curator insight, May 23, 2013 10:16 PM

well written.

Janys Venne's curator insight, October 26, 2013 2:01 AM


I'll appreciate your time & help to visit my website on #seizures #epilepsy at http://seizures.dolyan.com/. Thank you :)

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HCN2 ion channels: an emerging role as the pacemakers of pain

HCN2 ion channels: an emerging role as the pacemakers of pain | Neuroscience_topics | Scoop.it

Acute nociceptive pain is caused by the direct action of a noxious stimulus on pain-sensitive nerve endings, whereas inflammatory pain (both acute and chronic) arises from the actions of a wide range of inflammatory mediators released following tissue injury. Neuropathic pain, which is triggered by nerve damage, is often considered to be very different in its origins, and is particularly difficult to treat effectively. Here we review recent evidence showing that members of the hyperpolarization-activated cyclic nucleotide-modulated (HCN) ion channel family – better known for their role in the pacemaker potential of the heart – play important roles in both inflammatory and neuropathic pain. Deletion of the HCN2 isoform from nociceptive neurons abolishes heat-evoked inflammatory pain and all aspects of neuropathic pain, but acute pain sensation is unaffected. This work shows that inflammatory and neuropathic pain have much in common, and suggests that selective blockers of HCN2 may have value as analgesics in the treatment of pain. - Emery EC et al.Trends in Pharmacological Sciences Volume 33, Issue 8, August 2012, Pages 456–463

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