A study of the interaction between motoneurones in the frog spinal cord.
1. A short-latency interaction between motoneurones has been studied with intracellular and root potential recordings from the isolated spinal cord of the frog. Antidromic stimulation of one ventral root causes brief depolarization (VR-EPSP) of the motoneurones of adjacent, non-excited motoneurones. The summed activity of many such VR-EPSPs can be seen as a brief depolarization (VR-VRP) passing out an adjacent ventral root.2. Both intracellular and root-recorded signs of this interaction are graded in amplitude.3. It was found that this interaction decreased with increasing temperature. This is in contrast to the behaviour of the ventral root potential resulting from dorsal root stimulation (DR-VRP) or the dorsal root potentials resulting from either dorsal root (DR-DRP) or ventral root (VR-DRP) stimulation, all of which increased in amplitude from below 10 to about 17 degrees C.4. Pharmacological evidence suggests that the interaction between motoneurones is not chemically mediated. The VR-VRP was not affected by a large variety of transmitter blocking agents, including curare, dihydro-beta-erythroidine, atropine, succinylcholine, hexamethonium and DOPA, while the VR-DRP, which probably originates with the release of ACh from an axon collateral, was consistently blocked.5. Mg(2+) suppressed the VR-VRP more slowly than the other potentials, and this suppression was increased by adding Ca(2+), rather than reversed, as in the case of the other root potentials, which are presumably mediated by chemical transmission.6. The interaction between motoneurones is strongly facilitated by orthodromic depolarization of the motoneurones being antidromically stimulated. Extracellular recordings within the cord support the conclusion that this facilitation is a result of the enhancement of antidromic invasion, perhaps especially of the dendrites, by slight depolarization.7. One VR-VRP (or VR-EPSP) first suppresses response to another (for about 10 msec), then facilitates response to the second, with maximum effect around 20-40 msec. This is the case whether both stimuli go to the same or to different ventral roots, although occlusion is less and facilitation greater in the latter case. Occlusion of the VR-EPSP also results from full excitation of the cell in which recording is being done.8. The mechanism of this interaction remains uncertain, but it would seem likely that overlapping dendrites of adjacent motoneurones interact with each other electrically through close apposition or specialized contacts. Occlusion would result from the refractoriness of strongly depolarized dendrites, facilitation from the enhancement of invasion of antidromically stimulated motoneurones by the weaker (or residual) depolarization occurring after earlier activity of motoneurones or their dendrites.
D000818:Animals; D001001:Anura; D002118:Calcium / Q000494:pharmacology; D004558:Electric Stimulation; D004594:Electrophysiology; D006584:Hexamethonium Compounds / Q000494:pharmacology; D008274:Magnesium / Q000494:pharmacology; D009046:Motor Neurons / Q000502:physiology*; D010276:Parasympatholytics / Q000494:pharmacology; D010424:Pentobarbital / Q000494:pharmacology; D010852:Picrotoxin / Q000494:pharmacology; D013116:Spinal Cord / Q000502:physiology*; D014403:Tubocurarine / Q000494:pharmacology
D002118:Calcium; D006584:Hexamethonium Compounds; D008274:Magnesium; D010276:Parasympatholytics; D010424:Pentobarbital; D010852:Picrotoxin; D014403:Tubocurarine