Date of Completion
Children born prematurely (< 37 weeks gestational age) or at very low birth weight (VLBW; < 1500 grams at birth) are at increased risk for hypoxic ischemic injury. Infants born full term can be diagnosed with HIE resulting from birth complications. In both populations, blood and/or oxygen delivery to the brain is compromised, resulting in long-term brain damage. In preterm children, damage is often localized in white matter and fiber tracts, while full-term brain damage is more frequently seen in gray matter areas. Both populations show subsequent cognitive deficits, including in language development. Moreover, some literature suggests that these language delays may be associated with underlying deficits in rapid auditory processing (RAP; i.e., the ability to process acoustic differences such as between phonemes in speech). Data demonstrating a relationship between RAP and language impairments in infants/children has also led to studies of RAP in dyslexic populations. From this convergent research a magnocellular theory has been put forward suggesting that damage to large or “magno” cells of the medial geniculate nucleus (MGN; which are hypothesized to be responsible for encoding temporal aspects of acoustic information), may underlie or contribute to RAP deficits - - with cascading effects on both language and reading development. In animal models of HIE, persistent deficits in RAP are seen in postnatal (P) 7 hypoxic-ischemic (HI) injured rodents (comparable to human term birth injury), but not in P1 HI injured animals (comparable to human pre-term injury). Given this cumulative evidence, the current study sought to investigate the average cell size, and proportion of large to small cells, in the MGN of P1 and P7 HI injured males rats that had previously demonstrated rapid auditory processing deficits (McClure et al., 2006; Hill et al., in review). Results showed that average MGN cell size was in fact significantly decreased in P7 HI injured male rats as compared to P1 HI injured and sham treated male rats. Results also showed an abnormal distribution of small to large cells in the right MGN of P7 HI injured rats as compared to P1 HI injured and sham animals with more small cells. These results are consistent with behavioral data from the same subjects, specifically showing persistent deficits in RAP in P7 but not in P1 HI injured male rodents. Together, these results suggest that P1 HI injured rodents may be more resilient to the effects of HI injury, whereas P7 HI injured rodents may suffer more robust and persistent deficits possibly tied to long term changes in MGN physiology. When applied to human clinical populations, these results suggest an anatomic marker that may index potential for long-term language disability, and this index could prove useful in the study of outcomes for term-injured and with HIE.
Alexander, Michelle, "Cell Size Distribution in the MGN and Associated Auditory Temporal Processing Deficits in P1 and P7 HI Injured Rodents" (2011). Master's Theses. Paper 98.