The Effects of Curare in the Cockroach

For many years insects were believed to be insensitive to curare (Harlow, 1958; Hopf, 1952; Krupp, Lendle & Stapenhorst, 1952; Roeder, 1948, 1953; Roeder & Weiant, 1950; Usherwood, 1963). However, Larsen, Miller & Yamamoto (1966) have demonstrated that intra-abdominal injection of d-tubocurarine chloride (dTC) into insects causes paralysis. The nature of this paralysis is of interest because the principles of both vertebrate and invertebrate physiology predict that curare should be without effect in insects. Since the work of Claude Bernard (1856), it has been generally maintained that curare acts specifically at the vertebrate, acetylcholine-mediated, neuromuscular junction to cause flaccid paralysis (Cutting, 1964). The neuromuscular junction of arthropods, in contrast, has been shown to be responsive to glutamic acid (Kerkut et al. 1965 a; Kerkut, Shapira & Walker, 19656), and, consequently, glutamic acid is reputed to be the transmitter at excitatory neuromuscular junctions in insects. As Cottrell & Laverack (1968) have stated in a recent review, the ability of curare to produce paralysis in insects means, ' that either ACh is the transmitter at the (neuromuscular) junctions, or that curare can block non-cholinergic synapses'. Since the initial observation of curare-induced paralysis in insects by Larsen et al. (1966) two other reports have appeared concerned with the site and mechanism of curare action in insects. One of these reports (McCann, 1966) concludes that dTC acts at the neuromuscular junction of insects, while the other (Flattum, Friedman & Larsen, 1967) concludes that curare does not act at the neuromuscular junction but, rather, on some 'unidentified co-ordination centres'. The current investigation was therefore undertaken to determine the site of curare-induced paralysis in the cockroach, Periplaneta americana.