Sherman G F, Stone L V, Denenerg V H, Beier D R
Dyslexia Research Laboratory, Beth Israel Hospital, Boston, MA 02215.
Neuroreport. 1994 Feb 24;5(6):721-4. doi: 10.1097/00001756-199402000-00016.
Two experiments investigated the heritability of neocortical ectopias seen in 30-40% of New Zealand Black (NZB/BINJ) autoimmune mice. The first study examined the brains of mice from the NZB x SM/J recombinant inbred (RI) strains. Fifteen RI inbred strains were examined and over half had ectopias suggesting that a major gene was involved in ectopia production. A follow-up experiment comparing the incidence of ectopias among crosses between NZB and control DBA/2 strains showed that the predisposition to develop ectopias in NZB is a recessively inherited trait with incomplete penetrance.
两项实验研究了在30%-40%的新西兰黑（NZB/BINJ）自身免疫小鼠中出现的新皮质异位的遗传性。第一项研究检查了NZB×SM/J重组近交（RI）品系小鼠的大脑。检查了15个RI近交品系，超过一半的品系有异位，这表明一个主要基因参与了异位的产生。一项后续实验比较了NZB与对照DBA/2品系杂交后代中异位的发生率，结果表明，NZB发生异位的易感性是一种隐性遗传性状，且外显率不完全。
