Optically imposed defocus can alter the shape and pattern of peripheral refraction in infant primates. Like those of form deprivation, the effects of optical defocus in primates are dominated by mechanisms that integrate visual signals in a spatially restricted manner and exert their influence in a regionally selective manner.

Perinatal hypoxia is a major cause of neurodevelopmental deficits. Neuronal migration patterns are particularly sensitive to perinatal hypoxia/ischemia and are associated with the clinical deficits. The rat model of hypoxia/ischemia at P7 mimics that of perinatal injury in humans. Before assessing the effects of postnatal injury on brain development, it is essential to determine the normal developmental trajectories of various brain structures in individual animals. In vivo longitudinal diffusion tensor imaging (DTI) was performed from postnatal day 0 (P0) to P56 on Wistar rats. The DTI metrics, mean diffusivity (MD), fractional anisotropy (FA), axial (lambdal) and radial (lambdat) diffusivities, were determined for four gray matter and eight white matter structures. The FA of the cortical plate and the body of corpus callosum decreased significantly during the first 3 weeks after birth. The decrease in the cortical plate's FA value was associated mainly with an increase in lambdat. The initial decrease in FA of corpus callosum was associated with a significant decrease in lambdal. The FA of corpus callosum increased during the rest of the observational period, which was mainly associated with a decrease in lambdat. The FA of gray matter structures, hippocampus, caudate putamen, and cortical mantle did not show significant changes between P0 and P56. In contrast, the majority of white matter structures showed significant changes between P0 and P56. These temporal changes in the DTI metrics were related to the neuronal and axonal pruning and myelination that are known to occur in the developing brain.

PURPOSE To determine whether refractive development in primates is mediated by local retinal mechanisms, we examined the effects of hemi-retinal form deprivation on ocular growth and the pattern of peripheral refractions in rhesus monkeys. METHODS Beginning at about 3 weeks of age, 9 infant monkeys were reared wearing monocular diffuser lenses that eliminated form vision in the nasal field (nasal field diffusers, NFD). Control data were obtained from the non-treated fellow eyes, 24 normal monkeys, and 19 monkeys treated with full-field diffusers (FFD). Refractive development was assessed by retinoscopy performed along the pupillary axis and at eccentricities of 15, 30 and 45 deg. Central axial dimensions and eye shape were assessed by A-scan ultrasonography and magnetic resonance imaging (MRI), respectively. RESULTS Hemi-retinal form deprivation altered refractive development in a regionally selective manner, typically producing myopia in the treated hemi-fields. In particular, 6 of the NFD monkeys exhibited substantial amounts (−1.81 to −9.00 D) of relative myopia in the nasal field that were most obvious at the 15 and 30 deg nasal field eccentricities. The other 3 NFD monkeys exhibited small amounts of relative hyperopia in the treated field. The alterations in peripheral refraction were associated with local, region-specific alterations in vitreous chamber depth in the treated hemi-retina. CONCLUSIONS The effects of form deprivation on refractive development and eye growth in primates are mediated by mechanisms, presumably retinal, that integrate visual signals in a spatially restricted manner and exert their influence locally.

Time‐lapse diffusion‐weighted magnetic resonance imaging (DWI) was used to detect and characterize complex waves of cortical spreading depression (CSD) evoked with KCl placed upon the suprasylvian gyrus of anaesthetized cats. The time‐lapse representations successfully demonstrated primary CSD waves that propagated with elliptical wavefronts selectively over the ipsilateral cerebral hemispheres with a velocity of 3.8 ± 0.70 mm min−1 (mean ± s.e.m. of 5 experiments). In contrast, the succeeding secondary waves often remained within the originating gyrus, were slower (velocity 2.0 ± 0.18 mm min−1), more fragmented and varied in number. Computed traces of the apparent diffusion coefficients (ADCs) showed negative deflections followed by monotonic decays (amplitudes: primary wave, ‐19.9 ± 2.8 %; subsequent waves, ‐13.6 ± 1.9 %; duration at half‐maximal decay, 150‐200 s) when determined from regions of interest (ROIs) through which both primary and succeeding CSD waves propagated. The passage of both the primary and the succeeding waves often correlated with transient DC potential deflections recorded from the suprasylvian gyrus. The detailed waveforms of the ADC and the T2*‐weighted (blood oxygenation level‐dependent: BOLD) traces showed a clear reciprocal correlation. These imaging features that reflect disturbances in cellular water balance agree closely with BOLD measurements that followed the propagation velocities of the first and subsequent CSD events. They also provide a close physiological correlate for clinical observations of cortical blood flow disturbances associated with human migraine.

The majority of people who sustain a traumatic brain injury (TBI) have an injury that can be classified as mild (often referred to as concussion). Although head CT scans for most subjects who have sustained a mild TBI (mTBI) are negative, these persons may still suffer from neurocognitive and neurobehavioral deficits. In order to expedite pre-clinical research and develop therapies, there is a need for well-characterized animal models of mTBI that reflect the neurological, neurocognitive, and pathological changes seen in human patients. In the present study, we examined the motor, cognitive, and histopathological changes resulting from 1.0 and 1.5 atmosphere (atm) overpressure fluid percussion injury (FPI). Both 1.0 and 1.5 atm FPI injury caused transient suppression of acute neurological functions, but did not result in visible brain contusion. Animals injured with 1.0 atm FPI did not show significant motor, vestibulomotor, or learning and memory deficits. In contrast, 1.5 atm injury caused transient motor disturbances, and resulted in a significant impairment of spatial learning and short-term memory. In addition, 1.5 atm FPI caused a marked reduction in cerebral perfusion at the site of injury that lasted for several hours. Consistent with previous studies, 1.5 atm FPI did not cause visible neuronal loss in the hippocampus or in the neocortex. However, a robust inflammatory response (as indicated by enhanced GFAP and Iba1 immunoreactivity) in the corpus callosum and the thalamus was observed. Examination of fractional anisotropy color maps after diffusion tensor imaging (DTI) revealed a significant decrease of FA values in the cingulum, an area found to have increased silver impregnation, suggesting axonal injury. Increased silver impregnation was also observed in the corpus callosum, and internal and external capsules. These findings are consistent with the deficits and pathologies associated with mild TBI in humans, and support the use of mild FPI as a model to evaluate putative therapeutic options.