1,721,096 research outputs found
Activation of AMPA, kainate, and metabotropic receptors at hippocampal mossy fiber synapses: role of glutamate diffusion.
No full textThe fate of glutamate molecules escaping from the synaptic cleft in the hippocampus: evidence for non-local activation of NMDA receptors.
No full textSynaptically realeased glutamate reduces gamma-aminobutyric acid (GABA) ergic inhibition in the hippocampus via kainate receptors.
No full textEvidence for a presynaptic contribution to the expression of pairing-induced LTP at medial perforant path synapses on dentate granule cells.
No full textDifferences between medial and lateral perforant path synapses on dentate granule cells.
No full textEpisodic Ataxia Type 1 Mutations in the KCNA1 Gene Impair the Fast Inactivation Properties of the Human K+ Channels Kv1.4-1.1/Kvbeta1.1 and Kv1.4-1.1/Kvbeta1.2
No full textEpisodic ataxia type 1 (EA1) is an autosomal dominant neurological disorder characterized by constant muscle rippling movements (myokymia) and episodic attacks of ataxia. Several heterozygous point mutations have been found in the coding sequence of the voltage-gated potassium channel gene KCNA1 (hKv1.1), which alter the delayed-rectifier function of the channel. Shaker-like channels of different cell types may be formed by unique hetero-oligomeric complexes comprising Kv1.1, Kv1.4 and Kv beta 1.x subunits. Here we show that the human Kv beta 1.1 and Kv beta 1.2 subunits modulated the functional properties of tandemly linked Kv1.4-1.1 wild-type channels expressed in Xenopus laevis oocytes by (i) increasing the rate and amount of N-type inactivation, (ii) slowing the recovery rate from inactivation, (iii) accelerating the cumulative inactivation of the channel and (iv) negatively shifting the voltage dependence of inactivation. To date, the role of the human Kv1.4-1.1, Kv1.4-1.1/Kv beta 1.1 and Kv1.4-1.1/Kv beta 1.2 channels in the aetiopathogenesis of EA1 has not been investigated. Here we also show that the EA1 mutations E325D, V404I and V408A, which line the ion-conducting pore, and I177N, which resides within the S1 segment, alter the fast inactivation and repriming properties of the channels by decreasing both the rate and degree of N-type inactivation and by accelerating the recovery from fast inactivation. Furthermore, the E325D, V404I and I177N mutations shifted the voltage dependence of the steady-state inactivation to more positive potentials. The results demonstrate that the human Kv beta 1.1 and Kv beta 1.2 subunits regulate the proportion of wild-type Kv1.4-1.1 channels that are available to open. Furthermore, EA1 mutations alter heteromeric channel availability which probably modifies the integration properties and firing patterns of neurones controlling cognitive processes and body movements
Extracellular glutamate diffusion determines the occupancy of glutamate receptors at CA1 synapses in the hippocampus.
No full textRole of the synaptic microenvironment in functional modification of synaptic transmission.
No full textDysfunction of the brain calcium channel CaV2.1 in absence epilepsy and episodic ataxia—authors’ response
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