Role of Midbrain Central Gray in Pain-Induced Defensive Boxing of Rats
Results Page 5

Title/Summary Page

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Figures 1-7
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Analysis of Lesions

Lesions which bilaterally destroyed the lateral central gray beneath the superior colliculus, plus small portions of the adjacent tegmentum, produced deficits in boxing, escape and open field behavior. The lesion damage common to all animals for each deficit is represented in Fig, 5. It can be seen that the damage common in all rats with boxing deficits included the total anterior-posterior extent of the lateral central gray beneath the superior colliculus. Part or all of the same region was also destroyed in all rats with escape and open field deficits.

Conversely, lesions which spared at least a 1 mm segment of this region at anyone anterior-posterior level did not produce a boxing deficit, though they produced the other deficits. As may be seen in Fig. 6, the lateral central gray was intact at level +2.0 in Rat A7, at level + 1.0 in Rat H8, and at level 0.0 in Rat A11, all of which animals had normal or increased boxing percentages despite destruction of the remainder of central gray at the level of the superior colliculus. These same rats were unable to learn escape and had high open field scores.

An analysis of lesions extending in different directions from the lateral central gray at superior collicular levels has a bearing on which connections to this region are necessary for boxing behavior. Boxing was not disrupted by lesions which extended in anterior, posterior, or ventral directions from the critical region (Fig. 6). The anterior central gray was totally destroyed in Rat A11, the posterior central gray was destroyed in Rat A9, and both the anterior central gray and the tegmentum immediately ventral to the central gray were totally destroyed in Rat H4, yet all 3 rats showed boxing behavior one week postoperatively.

Threshold for Boxing

Restricted damage to the central gray in the 10 animals without boxing deficits led to hyper-reactivity in the shock box, as measured by lowered thresholds for boxing (mean change from preoperative performance: -36.2%). Control animals, if anything, usually became slightly less reactive on their second test (mean change in threshold: +13.0%).

Recovery of Function

If animals were kept alive for a number of weeks, there was usually some recovery of boxing behavior, the amount of recovery being roughly correlated with the amount of damage to the reticular formation lateral to the midbrain central gray (Fig. 7). Rat H3, which showed almost full recovery after 3 weeks, had little damage outside the central gray (for histology, see Fig. 5a). Three rats with some recovery showed intermediate levels of damage beyond the central gray. Rat B41 , which showed no recovery after 3 weeks, had a particularly large lesion which included extensive damage to the reticular formation lateral to the central gray (Fig. 5a).

Other behaviors differed in terms of recovery. No animal with an escape deficit ever showed recovery, but feeding deficits were usually recovered by the second or third post-operative week. Open field scores showed a decrease towards normal scores on retest 2 weeks after surgery, but they were still higher than those of controls tested for a second time. No correlation was observed between recovery of different behaviors, suggesting that they had overlapping, but not identical neural organizations.

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