Excitation of rat cerebellar Golgi cells by ethanol: further characterization of the mechanism.

Background: Studies with rodents suggest that acute ethanol exposure impairs information flow through the cerebellar cortex, in part, by increasing GABAergic input to granule cells. Experiments suggest that an increase in the excitability of specialized GABAergic interneurons that regulate granule cell activity (i.e.

Analysis of distinct short and prolonged components in rebound spiking of deep cerebellar nucleus neurons.

Deep cerebellar nucleus (DCN) neurons show pronounced post-hyperpolarization rebound burst behavior, which may contribute significantly to responses to strong inhibitory inputs from cerebellar cortical Purkinje cells. Thus, rebound behavior could importantly shape the output from the cerebellum. We used whole-cell recordings in brain slices to characterize DCN rebound properties and their dependence on hyperpolarization duration and depth.

Alcohol excites cerebellar Golgi cells by inhibiting the Na+/K+ ATPase.

Alcohol-induced alterations of cerebellar function cause motor coordination impairments that are responsible for millions of injuries and deaths worldwide. Cognitive deficits associated with alcoholism are also a consequence of cerebellar dysfunction. The mechanisms responsible for these effects of ethanol are poorly understood.

Database analysis of simulated and recorded electrophysiological datasets with PANDORA's toolbox.

Neuronal recordings and computer simulations produce ever growing amounts of data, impeding conventional analysis methods from keeping pace. Such large datasets can be automatically analyzed by taking advantage of the well-established relational database paradigm. Raw electrophysiology data can be entered into a database by extracting its interesting characteristics (e.

Metabolic energy cost of action potential velocity.

The action potential of the unmyelinated nerve is metabolically expensive. Using the energetic cost per unit length for the biophysically modeled action potential of the squid giant axon, we analyze this cost and identify one possible optimization. The energetic cost arising from an action potential is divided into three separate components: 1) the depolarization of the rising phase; 2) the hyperpolarization of the falling phase; and 3) the largest component, the overlapping of positive and negative currents, which has no electrical effect.

Analysis of the optimal channel density of the squid giant axon using a reparameterized Hodgkin-Huxley model.

A reparameterized Hodgkin-Huxley-type model is developed that improves the 1952 model's fit to the biological action potential. In addition to altering Na(+) inactivation and K(+) activation kinetics, a voltage-dependent gating-current mechanism has been added to the model. The resulting improved model fits the experimental trace nearly exactly over the rising phase, and it has a propagation velocity that is within 3% of the experimentally measured value of 21.