Spatial Cognitive Performance after Chronic Focal Cerebral Ischemia in Rats

Abstract

The authors investigated the impairment of spatial cognitive performance in rats with chronic focal cerebral ischemia using the Morris maze, and examined the correlation between this deficit and other behavioral changes, such as step-through latency in passive avoidance task and neurologic score, or pathologic changes. The authors focused on the relationship between the damaged brain region and the affected spatial learning behavior. In the Morris maze task at 8 weeks after the middle cerebral artery (MCA) occlusion, escape latency, swimming path length, and percent time spent in goal quadrant of MCA-occluded rats were impaired, which correlated with shrinkage of the cortex involving parietal cortex, but not caudate-putamen (CP). Middle cerebral artery-occluded rats were also impaired in the percent time spent in the outermost annulus and in turning ratio, which significantly correlated with shrinkage of CP, but not cortex. Middle cerebral artery-occluded rats showed two typical search patterns; one was almost the same as that of sham-operated and intact rats, and the other was round shaped and had less turning behavior. Both subgroups of MCA-occluded rats divided by turning ratio had significantly impaired spatial cognitive performance, which indicates that the changes of search pattern did not affect cognitive performance in the Morris maze. The neurologic deficits recovered gradually after MCA occlusion, which correlated with shrinkage of cortex and CP. The step-through latency in passive avoidance task of the MCA-occluded rats was impaired, but did not correlate with shrinkage of cortex or CP. These results suggest that the long-term spatial cognitive deficit of MCA-occluded rats is in part associated with damage to the cortex involving parietal cortex, and that the change of search strategies is associated with damage to CP. These findings support the idea that different brain regions contribute differently to cognitive performance, search strategies, avoidance task, and neurologic performance, and may be useful for estimating the related region of functional disorder in the clinical situation.

Watermaze Performance after Middle Cerebral Artery Occlusion in the Rat: The Role of Sensorimotor versus Memory Impairments

“…However, a neurologic test battery revealed sensorimotor impairments such as abnormal posture and hemiparesis at the time of watermaze testing. During watermaze acquisition after MCAO, an increased latency to reach the platform (Pavlichenko et al, 2008;Sadamoto et al, 1998;Shinoda et al, 1996) or an increased latency plus an increased path length (Smith et al, 1997;Markgraf et al, 1992;Yonemori et al, 1999) have been observed as evidence of memory deficits. Smith et al (1997) and Yonemori et al (1999) showed extensive thigmotactic swimming in the MCAO group compared with the sham group.…”

“…During watermaze acquisition after MCAO, an increased latency to reach the platform (Pavlichenko et al, 2008;Sadamoto et al, 1998;Shinoda et al, 1996) or an increased latency plus an increased path length (Smith et al, 1997;Markgraf et al, 1992;Yonemori et al, 1999) have been observed as evidence of memory deficits. Smith et al (1997) and Yonemori et al (1999) showed extensive thigmotactic swimming in the MCAO group compared with the sham group. In other studies (Yonemori et al, 1996;Markgraf et al, 1992;Shinoda et al, 1996;Sadamoto et al, 1998;Pavlichenko et al, 2008), thigmotaxis was not measured.…”

Endovascular middle cerebral artery occlusion in rats as a model for studying vascular dementia

“…In addition to sensorimotor dysfunction, deficits in cognitive function have repeatedly been reported in this model (Yonemori et al 1996(Yonemori et al , 1999Modo et al 2000;Puurunen et al 2001;Jolkkonen et al 2003). For example, impairments of performance in the Morris water maze, considered to be a robust test of hippocampal-dependent spatial learning and memory functions, were found in rats following MCA occlusion (Markgraf et al 1992(Markgraf et al , 1994(Markgraf et al , 1997Yonemori et al 1996Yonemori et al , 1999Smith et al 1997;Stroemer et al 1998).…”

“…Sensorimotor performance has been quantified by assessing postural abnormalities, coordinated movements, balance, forelimb strength, locomotor activity, or sensory capabilities (DeVries et al 2001). Spontaneous partial or complete recovery of sensorimotor function has been frequently reported over time after ischemic stroke in this model (Markgraf et al 1994(Markgraf et al , 1997Yonemori et al 1999;DeVries et al 2001;Roof et al 2001;Karhunen et al 2003). Indeed, the validity of MCA occlusion as a model for human ischemic stroke has been criticized because of the transitory nature of the sensorimotor deficits (Cheng et al 2004).…”

“…For example, impairments of performance in the Morris water maze, considered to be a robust test of hippocampal-dependent spatial learning and memory functions, were found in rats following MCA occlusion (Markgraf et al 1992(Markgraf et al , 1994(Markgraf et al , 1997Yonemori et al 1996Yonemori et al , 1999Smith et al 1997;Stroemer et al 1998). With the administration of repeated tests, performance differences between MCA occlusion rats and controls tended to persist following the lesion, although the magnitude of the difference was sometimes diminished.…”