• Port-a-Patch

    Smallest patch clamp setup in the world
  • Port-a-Patch

    Easy to learn - ideal for teaching
  • Port-a-Patch

    Records from cells, organelles and bilayers
  • Port-a-Patch

    First planar patch clamp device on the market
  • Port-a-Patch

    Ideal for internal solution exchange applications

2019 - Abolishing cAMP sensitivity in HCN2 pacemaker channels induces generalized seizures

icon pap   Port-a Patch and Internal Perfusion Publication in JCI Insight (2019)

Authors:
Hammelmann, V., Stieglitz, M.S., Hülle, H., Le Meur, K., Kass, J., Brümmer, M., Gruner, C., Rötzer, R.D., Fenske, S., Hartmann, J., Zott, B., Lüthi, A., Spahn, S., Moser, M,, Isbrandt, D., Ludwig, A., Konnerth, A., Wahl-Schott, C., Biel M.

Journal:
JCI Insight (2019) 4(9): e126418


Abstract:

Hyperpolarization-activated cyclic nucleotide–gated (HCN) channels are dually gated channels that are operated by voltage and by neurotransmitters via the cAMP system. cAMP-dependent HCN regulation has been proposed to play a key role in regulating circuit behavior in the thalamus. By analyzing a knockin mouse model (HCN2EA), in which binding of cAMP to HCN2 was abolished by 2 amino acid exchanges (R591E, T592A), we found that cAMP gating of HCN2 is essential for regulating the transition between the burst and tonic modes of firing in thalamic dorsal-lateral geniculate (dLGN) and ventrobasal (VB) nuclei. HCN2EA mice display impaired visual learning, generalized seizures of thalamic origin, and altered NREM sleep properties. VB-specific deletion of HCN2, but not of HCN4, also induced these generalized seizures of the absence type, corroborating a key role of HCN2 in this particular nucleus for controlling consciousness. Together, our data define distinct pathological phenotypes resulting from the loss of cAMP-mediated gating of a neuronal HCN channel.

Download here

Back to Overview

Cookies make it easier for us to provide you with our services. With the usage of our services you permit us to use cookies.
More information Ok