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G R Athey

Publications and source records attributed to G R Athey.

3 recordsLinked to original sources

Synaptic activation of erratic burst-type myenteric neurons in cat small intestine.

To study further the ongoing spike discharge of burst-type myenteric neurons, extracellular recordings were made with either Teflon-insulated Pt wire electrodes (tip diam, 20 micrometers) or 3 M NaCl-filled glass micropipettes (tip diam, 1-2 micrometers). Presynaptic fibers to the erratic bursters were activated by electrical shocks delivered through Teflon-insulated Pt wire electrodes. Single electrical shocks applied to either the surface of the ganglion or an interganglionic connective elicited bursts of spikes that had parameters (interspike intervals and spikes per burst) that closely resembled the spontaneously occurring bursts in the same neuron. The latencies of the responses to electrical stimulation ranged from 5 to 30 ms. The responses were reversibly abolished when the concentration of Mg2+ in the bathing solution was elevated to 12 mM. The responses to electrical stimulation were unaffected by atropine, hexamethonium, d-tubocurarine, epinephrine, norepinephrine, methysergide, morphine, naloxone, and substance P. The ongoing burst-type discharge of cat myenteric neurons appeared to reflect a synaptic event that could be mimicked by electrical stimulation of presynaptic fibers. The identity of the neurotransmitter that elicits the burst-type discharge is unknown. The transmitter is probably not acetylcholine, serotonin, norepinephrine, an opiatelike peptide, nor substance P.

Action Potentials↗

Analysis of frog neuromuscular function at hyperbaric pressures.

Nerve and muscle compound action potentials were measured in the frog sciatic nerve-gastrocnemius muscle preparation in a hyperbaric helium-air environment. Helium pressure to 69 ATA induced a reversible depression in muscle compound action potential amplitude without significantly affecting other parameters. Blockade other parameters. Blockade induced by tetraethylammonium while at pressure could be partially reversed by decompression. A desensitization-type of neuromuscular block produced at pressure after neostigmine infusion could also be partially reversed by decompression. These results suggest a possible involvement of the acetylcholine receptor complex in pressure-induced depression of synaptic transmission.

Acetylcholine↗