The Journal of Neurophysiology Vol. 81 No. 6 June 1999, pp. 2977-2987
Copyright ©1999 by the American Physiological Society

Reciprocal Interactions in the Turtle Hindlimb Enlargement Contribute to Scratch Rhythmogenesis

Department of Neuroscience, University of California, Riverside, California 92521

Currie, Scott N. and Gregory G. Gonsalves. Reciprocal Interactions in the Turtle Hindlimb Enlargement Contribute to Scratch Rhythmogenesis. J. Neurophysiol. 81: 2977-2987, 1999.Reciprocal interactions in the turtle hindlimb enlargement contribute to scratch rhythmogenesis. We examined interactions between the spinal networks that generate right and left rostral scratch motor patterns in turtle hindlimb motoneurons before and after transecting the spinal cord within the anterior hindlimb enlargement. Our results provide evidence that reciprocal inhibition between hip circuit modules can generate hip rhythmicity during the rostral scratch reflex. "Module" refers here to the group of coactive motoneurons and interneurons that controls either flexion or extension of the hip on one side and coordinates that activity with synergist and antagonist motor pools in the same limb and in the contralateral limb. The "bilateral shared core" hypothesis states that hip flexor and extensor (HF and HE) circuit modules interact via crossed and uncrossed spinal pathways: HF modules make reciprocal inhibitory connections with contralateral HF and ipsilateral HE modules and mutual excitatory connections with contralateral HE modules. It is currently unclear how much reciprocal inhibition between modules contributes to scratch rhythmogenesis. To address this issue, fictive scratch motor patterns were recorded bilaterally as electroneurograms from HF, HE, knee extensor (KE), and respiratory (d.D8) muscle nerves in immobilized animals. D₃-end (low-spinal) preparations had intact spinal cords posterior to a complete D₂-D₃ transection. Unilateral stimulation of rostral scratch in D₃-end turtles elicited rhythmic alternation between ipsilateral HF and HE bursts in most cycles; consecutive HF bursts were separated by complete silent (HF-OFF ) periods. D₃-D₉ and D₃-D₈ preparations received a second spinal transection at the caudal end of segment D₉ or D₈, respectively, within the anterior hindlimb enlargement. This second transection disconnected most HE circuitry (located mainly in segments D₁₀-S₂ of the posterior enlargement) from the rostral scratch network and thereby reduced the HE-associated inhibition of HF circuitry. Unilateral stimulation of rostral scratch in most D₃-D₉ and D₃-D₈ preparations evoked rhythmic or weakly modulated ipsilateral HF discharge without HF-OFF periods between bursts and without ipsilateral HE activity in the majority of cycles. In contrast, bilateral stimulation in D₃-D₉ and D₃-D₈ preparations reconstructed the HF-OFF periods, increased HF rhythmicity (assessed by fast Fourier transform power spectra and autocorrelation analyses), and reestablished weak HE-phase motoneuron activity. We suggest that bilateral stimulation produced these effects by simultaneously activating reciprocally inhibitory hip modules on opposite sides (right and left HF) and the same side (HF and residual ipsilateral HE circuitry). Our data support the hypothesis that reciprocal inhibition can contribute to spinal rhythmogenesis during the scratch reflex.