Chlorpromazine and diltiazem effects in muscle: blockage of acetylcholine-evoked contractures, membrane currents and tracer calcium uptake.

Contractures evoked by 0.1 mmol/l acetylcholine (ACh) in bundles from mouse soleus muscles denervated for 3-7 days were partly inhibited for more than 1 h following 2- to 10-min exposure to 10-100 mumol/l chlorpromazine (CP). The effect was stronger in sucrose than in Na+ solutions.

Comparison of the effects of Ca2+ and those of Mg2+ and La3+ on endplate currents in mouse interosseus muscles.

Acetylcholine-induced currents were measured in dissociated muscle fibres from the mouse interosseus. Fast and slow desensitization could be distinguished, the latter ending in a steady-state current. The time constants of the two phases of current decrease and the steady-state current were decreased when the superfusing solution contained di- or trivalent cations in addition to the 0.

Acetylcholine contractures of skeletal muscles: inhibition by chlorpromazine and diltiazem.

The maximum contractures evoked by 100 microM ACh of mouse soleus muscles denervated for 3-7 days are completely inhibited by a 10 min exposure to 100 microM chlorpromazine (CP). Recovery on washout of CP takes more than 1 hr to complete. ACh evoked contractures are also inhibited by diltiazem (D); washout of D is immediately followed by recovery.

Acetylcholine-evoked currents in juvenile mouse muscles.

Single fibres were obtained from juvenile (8-12 days old) mice by enzymatic dissociation. Whole-cell voltage-clamped soleus and interosseus fibres were jet-superfused by Cl-free solutions. Current responses to ACh (0.

Acetylcholine-induced currents in denervated mouse soleus muscle: effects of antagonists.

Acetylcholine-induced currents were measured in partially depolarized mouse soleus muscles, denervated for 3-6 days by using a point voltage clamp. When 0.25 microM d-tubocurarine (d-Tc) was used, the weak currents provoked by 0.