Chronic effects of transient forebrain ischemia on monoamines in the spontaneously hypertensive rat brain

Using the 3-hr common carotid occlusion model in spontaneously hypertensive rats (SHRs), we investigated the changes in monoamines and their metabolites up to the chronic phase, 6 months alter the transient forebrain ischemia, in various brain regions. In the striatum, the levels of dopamine (DA) at the 3rd week and serotonin (5-HT) at the 2nd week were 1.6-fold and 2.4-fold higher than the levels in the respective sham-operated controls coinciding with increases in their metabolites, homovanillic acid and 5-hydroxyindoleacetic acid. However, these marked increases in both transmitter; were transient aid their levels recovered to the sham-operated levels. This transient increase in DA release in the striatum may be caused by ischemia-induced disruption of nerve endings, and may aggravate tissue damage in the striatum at the chronic phase after ischemia. Transient or lasting changes in noradrenaline, DA, 5-HT and their metabolites were also observed in other brain regions, the thalamus+midbrain and the hippocampus of SHRs after transient ischemia. These ischemia-induced alterations in monoamines at the chronic phase may be partly involved in die late-onset sequelae seen in the cerebrovascular disorders.