4-Aminopyridine

4-Aminopyridine is a BBB-penetrant and orally active antagonist of voltage-gated potassium channels. 4-Aminopyridine antagonizes the neuromuscular block caused by D-tubocurarine. 4-Aminopyridine is a substance that blocks the voltage-dependent potassium channels in squid giant axons. 4-Aminopyridine strongly potentiates transmitter release from the unmyelinated terminals of rat motor nerves. 4-Aminopyridine prolongs action potentials of demyelinated and unmyelinated fibres. 4-Aminopyridine acts by enhancing the release of acetylcholine from motor nerve terminals. 4-Aminopyridine inhibits the inflammatory responses in microglia. 4-Aminopyridine can be studied in research for neurological diseases^{[1][2][3][4][5]}. In Vitro:4-Aminopyridine (Compound 4-AP) (5 mM) increases the peak higher of the C component ranged from 4% to 550% in rat dorsal root^[1].
4-Aminopyridine (130 μM, 1 h) causes a slow increase in mepp frequency which progresses over a time course of 1 h in some fibres of frog muscle^[2].
4-Aminopyridine (0-128 μM) results in a dose-dependent increase in the epp amplitude of rat muscle^[2].
4-Aminopyridine (130 μM) increases endplate potential amplitude during repetitive nerve stimulation in rat muscle^[2].
4-Aminopyridine (10 μM) restores neuro-muscular transmission^[2].
4-Aminopyridine (2 mM, 48 h) significantly reduces the amount of Aβ_1-42-induced microglial neurotoxicity by 54%^[4]. In Vivo:4-Aminopyridine (Compound 4-AP) (1 mg/kg, i.p., daily for 7 d) is effective in protecting neurons from Aβ_1-42-induced damage in SD rats^[4].
4-Aminopyridine (0-300 mg/kg, administered in diet, 35 days post-immunization) results in less severe lowering of compound muscle action potential in Lewis rats compared to control groups^[5].