Effects of damage to the monoamine axonal constituents of the medical forebrain bundle on reactivity to foot shock and ingestive behavior in the rat.

Rats suffering damage to the medial forebrain bundle evidenced significant decreases in forebrain norepinephrine and 5-hydroxytryptamine as compared to controls; the threshold amount of shock required to elicit a jump response decreased significantly in rats with lesions in the medial forebrain bundle. Rats with lesions in which norepinephrine, but not 5-hydroxytryptamine, was reduced (norepinephrine group) showed a comparable significant decrease in jump threshold. The jump threshold of rats in which 5-hydroxytryptamine, but not norepinephrine, was reduced by midbrain raphe lesions did not change significantly. These results support the conclusion that damage to the ascending norepinephrine axon system is responsible for medial forebrain bundle lesion induced increases in pain sensitivity, as assessed by reactivity to noxious levels of foot shock. Rats in which forebrain dopamine was reduced showed a loss of body weight which was significantly different from the weight gains shown by the control animals. Four of the animals with lesions in the medial forebrain bundle and four of the norepinephrine group animals showed increases in body weight that were well above the weight gains observed in any control animals. Forebrain dopamine level of the norepinephrine group increased significantly over the control level; a number of reasons for this increase, and its possible functional implications, are discussed.