Yoshimoto Kanji, Hori Masafumi, Shinmen Natsuko, Kakiuchi Kazuo, Kato Hideaki, Sakabe Masaaki, Ikegaya Hiroshi
Department of Forensic Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Leg Med (Tokyo). 2009 Apr;11 Suppl 1:S279-81. doi: 10.1016/j.legalmed.2009.02.041. Epub 2009 Apr 1.
In this study, we used in vivo brain microdialysis to examine the effects of stimulations of ischemia and/or potassium on the release of dopamine (DA) and serotonin (5-HT) in the nucleus accumbens (ACC) of anesthetized rats. Ischemia (Four-vessels occlusion: 4VO) for 10 min increased DA and 5-HT release in the ACC 200-fold and 15-fold in the first experiment, respectively. In the second experiment, releases of DA and 5-HT in the ACC increased 350-400% and 150-180% by first and second K(+) stimulation, respectively, in the K(+)-K(+) groups. The 4VO treatment induced significant and massive increases of DA and 5-HT releases in the ACC, following K(+) stimulation increased 5-HT release in the Ischemia-K(+) group compared with the K(+)-K(+) group. Also the 4VO treatment in the rotenone (an inhibitor of mitochondorial electric chain)-treated rats showed lower magnitudes of DA and 5-HT massive increases compared with the non-treated control rats in 4VO groups in the third experiment. Different brain vulnerability was shown in the dopaminergic and serotonergic neurons in the same area of the ACC. These findings suggested that the ACC neurons showed a resistance to dysfunction of 10 min-ischemia and maintained neural function, monoamine synthesis and neurotransmitter releases within the transient neural damage, not chronic neural degenerations.
