Afferent and efferent connections of the rat tail flick reflex (a model used to analyze pain control mechanisms)

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Abstract
Although the rat tail flick reflex (TFR) is widely used to study neural mechanisms of analgesia, its underlying anatomy has not been systematically studied. In the present study axonal transport of horseradish peroxidase (HRP) was used to trace the efferent and afferent connections of the TFR. The extensor caudae medialis (ECM), extensor caudae lateralis (ECL), and abductor caudae dorsalis (ACD) were identified as tail flick muscles and injected with HRP. Labeled motor neurons were found in lumbar segments L4–L6, sacral segments S1–S4, and coccygeal segments Co1–Co2; ECL injections also labeled cells in Co3. Motor neurons were concentrated at levels L5‐S2 for ECM, at levels S2‐Co2 for ECL, and at levels L5‐Co1 for ACD.To label the terminals of tail flick afferents, the dorsolateral tail nerve (DLTN) and the ventrolateral tail nerve (VLTN) which innervate the skin of the tail were cut and exposed to HRP. Application of HRP to either DLTN or VLTN labeled afferent terminals in S4, Co1, Co2, and Co3. For DLTN, the greatest density of afferent label was observed in the lateral half of laminae I and II of the dorsal horn. In contrast, labeled afferents from VLTN were concentrated in the medial half of laminae I–II. With longer survival times afferent terminals were also labeled in S3, and in the ventral horn of segments L6‐S2. Bilateral dorsal rhizotomies at levels S3‐Co3 were necessary and sufficient to abolish the tail flick. This corroborated the results from the anatomical studies.Although tail flick motor neurons were present in ten spinal segments, L4‐Co3, tail flick afferents were concentrated caudally in segments S3‐Co3. Thus, in addition to segmental connections, the TFR requires an ascending propriospinal connection from coccygeal and caudal sacral dorsal horn to S1, S2, and to the lumbar enlargement. The intense labeling from tail afferents found in the substantia gelatinosa (SG) is consistent with pharmacological, anatomical, and physiological studies implicating the SG as an important site for inhibition of the tail flick reflex by opiates and by brainstem stimulation.