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. 2013;8(3):e60037.
doi: 10.1371/journal.pone.0060037. Epub 2013 Mar 20.

A new non-human primate model of photochemically induced cerebral infarction

Satoshi Ikeda  1 , Katsuhiro Harada, Akihiko Ohwatashi, Yurie Kamikawa, Akira Yoshida, Kazumi Kawahira
Affiliations

A new non-human primate model of photochemically induced cerebral infarction

Satoshi Ikeda et al. PLoS One. 2013.

Abstract

Background and purpose: Rat models of photochemically induced cerebral infarction have been readily studied, but to date there are no reports of transcranial photochemically induced infarctions in the marmoset. In this report, we used this non-human primate as a model of cerebral thrombosis and observed the recovery process.

Methods: Five common marmosets were used. Cerebral ischemia was produced via intravascular thrombosis induced by an intravenous injection of Rose Bengal and irradiation with green light. After inducing cerebral infarction, we observed the behavior of marmosets via a continuous video recording. We evaluated maximum speed, mean speed, and distance traveled in 1 min. In addition, we evaluated scores for feeding behavior, upper limb grip, and lower limb grip. We confirmed the infarct area after cerebral infarction using 2,3,5-triphenyltetrazolium chloride staining in a separate marmoset.

Results: We found functional decreases 2 days after creating the cerebral infarction in all measurements. Total distance traveled, average speed, upper limb score, and feeding behavior score did not recover to pre-infarction levels within 28 days. Maximum speed in 1 min and lower limb score recovered 28 days after infarction as compared to pre-infarction levels. We confirmed the infarct area of 11.4 mm × 6.8 mm as stained with 2,3,5-triphenyltetrazolium chloride.

Conclusion: We were able to create a primate photothrombosis-induced cerebral infarction model using marmosets and observe functional recovery. We suggest that this is a useful model for basic research of cerebral infarction.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. TTC (2,3,5-Triphenyltetrazolium chloride) staining.
Normal region of mitochondrial activity was stained, while the ischemic area was not.
Figure 2
Figure 2. Behavioral analysis including feeding motion.
a) Distance traveled per minute. We show the mean value and standard error of total distance traveled, including feeding behavior, for a 1-min period 28 days after surgery. b) Mean speed/min. The mean and standard error of the moving speed during 1 min 28 days after operation. c) Maximum speed/min. The mean and standard error of the maximum speed, including feeding behavior, for 1 min 28 days after operation. * P<0.05 in comparison with preoperative values indicating presence of deficit. † P<0.05 in comparison with the lowest value (2 days after operation) indicating recovery.
Figure 3
Figure 3. Behavior score.
a) Hind limb score. The mean and standard error of lower limb scores pre-surgery to postoperative day 28. b) Feeding behavior score. The mean and standard error of feeding behavior scores pre-surgery to postoperative day 28. c) Total behavior score. The mean and standard error of the total score of feeding behavior, upper limb grip, and lower limb. * P<0.05 in comparison with preoperative values indicating presence of deficit. † P<0.05 in comparison with the lowest value (2 days after operation) indicating recovery.
Figure 4
Figure 4. Photomicrograph of cerebral cortex 28 days after photochemical infarction with Nissl staining.
a) Low power field; b) border area of infarction; c) intact cortex; and d) infarcted area with high power field.
See this image and copyright information in PMC

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