- 1To investigate the role of actin in vertebrate nerve terminals, nerve-muscle preparations from garter snake (Thamnophis sirtalis) were treated with the actin-depolymerizing agent latrunculin A. Immunostaining revealed that actin filaments within presynaptic motor terminal boutons were disrupted by the drug.
- 2In preparations loaded with the optical probe FM1-43, destaining was reduced by latrunculin treatment, suggesting that transmitter release was partially blocked.
- 3Latrunculin treatment did not influence the amplitude or time course of spontaneous miniature endplate potentials (MEPPs). Similarly, endplate potentials (EPPs) evoked at low frequency were comparable in control and latrunculin-treated curarized preparations.
- 4Brief tetanic stimulation of the muscle nerve (25 Hz, 90 s) depressed EPP amplitudes in both control and latrunculin-treated preparations. After tetanus, EPPs elicited at 0.2 Hz in control preparations recovered rapidly (0–5 min) and completely (usually potentiating to above pre-tetanus levels; 130 ± 11%, mean ±s.e.m.). In contrast, EPPs evoked in latrunculin-treated preparations recovered slowly (8–10 min) and incompletely (84 ± 8%).
- 5The influence of latrunculin on post-tetanic EPPs depended on its concentration in the bath (KD= 3.1 μm) and on time of incubation.
- 6These observations argue that actin filaments facilitate transmitter release rather than impede it. Specifically, actin may facilitate mobilization of vesicles towards the releasable pools.