Abstract

The LD 50 of 1-(4-ethynylphenyl)-4- n-propyl-2,6,7-trioxabicyclo[2.2.2]octane (EPTBO) is 1–3 μg/g on topical application to adult males of the cockroaches Periplaneta americana and Blabera craniifer. Intoxication in P. americana is closely associated with bursting activity in the central nervous system (CNS) as monitored in situ for the abdominal nerve cord with associated connectives. this EPTBO-induced bursting activity appears before poisoning signs are evident and increases in intensity with dose and as the severity of poisoning progresses with time. EPTBO acts in vitro directly on the isolated P. americana abdominal nerve cord to give bursting of similar type but lesser intensity than that observed in situ in poisoned insects. This action of EPTBO in vitro is also evident in nerve cords treated with urea to reduce the background activity. There are several lines of evidence that the EPTBO-induced bursting behavior in P. americana originates primarily in the sixth abdominal ganglion; i.e., in isolated nerve cords the activity is known to come mainly from the sixth abdominal ganglion, in sucrose gap studies it is induced with direct application on the sixth ganglion, and in in situ experiments bursting in the nerve cord is only slightly reduced when the cord is cut anterior but is abolished when cut posterior to the recording electrodes. Additionally, in B. craniifer, the bursting activity recorded in the nerve cord does not originate from the cercal nerves since, when these nerves are cut centrally (i.e., between the recording electrodes and the sixth ganglion), the bursting behavior is no longer recorded in the cercal nerves whereas it remains in the nerve cord. In a P. americana nerve cord with one cercal nerve (X or XI) intact, EPTBO action does not increase the excitatory postsynaptic potentials and is independent of normal cercal nerve to giant axon transmission. These actions of EPTBO on the cockroach CNS are consistent with but do not in themselves establish the expected block in GABA-mediated chloride channels.

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