These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: In vivo 4-aminopyridine treatment alters the neurotoxin 3-acetylpyridine-induced plastic changes in intrinsic electrophysiological properties of rat cerebellar Purkinje neurones.
    Author: Goudarzi I, Kaffashian M, Shabani M, Haghdoost-Yazdi H, Behzadi G, Janahmadi M.
    Journal: Eur J Pharmacol; 2010 Sep 10; 642(1-3):56-65. PubMed ID: 20638947.
    Abstract:
    Electrophysiological dysfunction of Purkinje cells causes cerebellar ataxia. Recent studies indicated that 4-aminopyridine (4-AP) can prevent the attacks in patients with episodic ataxia type 2. However, the cellular mechanism(s) by which 4-AP might be beneficial for the improvement of motor function remain unclear. Here, electrophysiological and behavioural consequences of in vivo co-treatment with 4-AP against 3-acetylpyridine (3-AP)-induced ataxia in rats were assessed. Combined treatment with 4-AP partially improved motor behaviour compared to the ataxic rats. Treatment with 3-AP alone induced plastic alterations in the cells' intrinsic properties, so that the latency of the initial neural spike was significantly increased (Pb 0.001); however, both instantaneous firing frequency and amplitude of calcium spikes were significantly (Pb 0.001) suppressed. 3-AP treatment also resulted in significant decrease in the duration of action potential (Pb 0.05) and the amplitude of afterhyperpolarization ((Pb 0.05) as well as post-stimulus hyperpolarization potentials (Pb 0.001). Purkinje cells in rats co-treated with 4-AP, however, fired predominantly in rhythmic bursts. The mean amplitude of Ca2+ spikes was significantly (Pb 0.001) greater compared to ataxic rats, but similar to control value. As evidenced by a significant decrease (Pb 0.001) in the first spike latency, the cells' intrinsic excitability was also increased. In 4-AP co-treated group, the duration of action potential was also significantly lengthened (Pb 0.001) compared to control and 3-AP group. These results suggest that modulation of intrinsic electrical properties and potentiation of Ca2+ channels function caused by in vivo 4-AP treatment is likely to be partly responsible for its neuroprotective action.
    [Abstract] [Full Text] [Related] [New Search]