Nervous System of Periplaneta americana Cockroach as a Model in Toxinological Studies: A Short Historical and Actual View

Nervous system of Periplaneta americana cockroach is used in a wide range of pharmacological studies, including electrophysiological techniques. This paper presents its role as a preparation in the development of toxinological studies in the following electrophysiological methods: double-oil-gap technique on isolated giant axon, patch-clamp on DUM (dorsal unpaired median) neurons, microelectrode technique in situ conditions on axon in connective and DUM neurons in ganglion, and single-fiber oil-gap technique on last abdominal ganglion synapse. At the end the application of cockroach synaptosomal preparation is mentioned.

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Adult neurones were obtained by dissociation of the dorsal area of the sixth abdominal (A6) ganglion of the cockroach, and electrical properties were studied with the patch-clamp technique. The neurones showed spontaneous fast action potentials, similar to those recorded with microelectrodes in neurones in situ along the dorsal median line of the A6 ganglion. Synthetic saxitoxin (sSTX) at concentrations of 10 × 10−8 to 1.0×10−7mol l−1 suppressed the action potential (AP) and induced a dose-dependent hyperpolarization of the resting potential, suggesting that two types of sSTX-sensitive Na+ channels are present. The resting potential was dependent on the external concentration of both Na+ and K+, with a similar sensitivity to each, yielding a slope of about 43 mV per 10-fold change in concentration. The delayed outward rectification present under control conditions was reduced by tetraethylammonium chloride (TEA-Cl, 1.0×10−2mol l−1). TEA-Cl or Ca2+-free saline abolished the afterhype.

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1. Ionophoresis of acetylcholine (ACh) onto the cell body membrane of an identified giant interneurone (GI2) in the central nervous system of the cockroach Periplaneta americana induced a depolarizing response at resting potential which was attributed to a population of extrasynaptic ACh receptors. 2. The sensitivity of the cell body membrane of GI 2 to ionophoresis of ACh was determined. 3. Perfusion of 1.0 × 10−6M neostigmine, an inhibitor of acetylcholinesterase, potentiated the ACh sensitivity of the cell body membrane of GI2. This indicated that a high acetylcholinesterase activity was present in the periphery of the sixth abdominal ganglion (A6). 4. The nicotinic antagonist, α-bungarotoxin (at a concentration of 1.0 × 10−7M) was found to block the ACh response of the cell body membrane of GI2. By contrast, the muscarinic antagonist, quinuclidinyl benzilate, (at concentrations up to 1.0 × 10−5 M) had no detectable effect on the ACh response. 5. It is suggested that an extrasyna.

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