Footshock treatment activates catecholamine synthesis in slices of mouse brain regions

Abstract

Synthesis of catecholamines was measured in slices of frontal cortex, hypothalamus, striatum, hippocampus and brainstem by the accumulation of [ 3H]norepinephrine (NE) and [ 3H]dopamine (DA) following incubation with [ 3H]tyrosine. Following acute footshock (60 shocks, 0.3 mA 30 min), consistent increases in [ 3H]DA accumulation were seen in frontal cortex slices, but no significant effect was seen in striatal slices. The accumulation of [ 3H]NE was not altered consistently in frontal cortex, hypothalamus, hippocampus or brainstem. Brain slices from mice adrenalectomized 24–48 h before footshock showed similar results. However, in hypophysectomized mice, footshock did not increase the [ 3H]DA accumulation in slices of frontal cortex. Administration of dexamethasone before footshock prevented the footshock-induced increase in frontal cortex [ 3H]DA accumulation, but footshock then significantly increased [ 3H]NE accumulation in the hypothalamus and brainstem. Chronic footshock (5 days) had little effect on frontal cortex [ 3H]catecholamine accumulation but produced a consistent elevation of [ 3H]NE accumulation in slices from the hypothalamus. In confirmation that the slices data reflected in vivo metabolism, both dihydroxyphenylacetic acid and homovanillic acid were significantly elevated in the frontal cortex but not the striatum of mice receiving acute footshock. Since previous studies have shown that ACTH administered intracerebroventricularly also accelerated [ 3H]DA accumulation in frontal cortex slices, these results are consistent with the involvement of ACTH in the effects of footshock on frontal cortex DA. The effects of chronic footshock are consistent with the activation of hypothalamic tyrosine hydroxylase by corticosterone.