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. 2017 Apr 24;10:114. doi: 10.3389/fnmol.2017.00114

Figure 3.

Figure 3

Normal monosynaptic but abnormal polysynaptic stretch-reflex circuits. (A) Spinal reflex at E18.5. Electric stimuli to L4DR normally activate Ia afferents and elicit an action potential in motor neurons. Monosynaptic reflex circuits appeared normal, but the polysynaptic reflex circuits were disrupted in the Δαβγ mutant. No differences were detected in the latency of the response onset (B), the peak response amplitude (C), or the latency of the peak response (D). Error bars represent SEM; data were compared by Student's t-test. (E) ChAT staining of the E18.5 Δαβγ spinal cord. The number of neurons and the size and distribution of motor neurons were indistinguishable between genotypes. (F) Whole-mounted E18.5 diaphragm muscles were stained with FITC-conjugated α-bungarotoxin, which binds specifically to acetylcholine receptors (AChRs). As in the control (+/+:TGtaf7) mice, AChR clusters were aligned normally in the central region of the muscles of the mutant mice. Bars: 100μm.