We tested the hypothesis that capsaicin-sensitive mechanisms play a role in the cortical spreading depression (CSD)-related changes in cortical blood flow (CBF). CBF was measured with laser Doppler flowmetry in anesthetized rats. The animals were treated with capsaicin before (48 h-2 weeks) or during the experiments. This agent is thought to stimulate small-diameter sensory nerve fibers selectively and to deplete stored peptides. In the vehicle-treated group (n = 8), the peak value of the CSD-associated hyperperfusion was 257 ± 12% above the baseline (mean ± SEM, P < 0.05). In the groups treated with 20 and 40 μg/kg or 20 mg/kg capsaicin, there were only small decreases in CBF. In the groups treated with 100 mg/kg capsaicin, the CSD-associated hyperemia was reduced at 48 h (158 ± 7%, P < 0.05). However, at 96 h a transient hyperresponsiveness (390 ± 38%, P < 0.05) was observed, which had disappeared by 2 weeks. These results indicate that the manipulation of sensory neuropeptide stores results in a biphasic effect on CSD-induced CBF responses. (C) 2000 Elsevier Science Ireland Ltd.
- Cortical spreading depression
- Laser Doppler
- Trigeminal nerve
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