Table 1.

Granule cells in the cerebellar molecular layer of normal and tPA-knockout mice

Age	Genotype	Cells/mm2 molecular layer
		Midline	lateral	lateral
P7	tPA+/+	1,008  ± 38	924  ± 39	683  ± 33
	tPA−/−	1,747  ± 55	1,842  ± 73	1,600  ± 67
P10	tPA+/+	746  ± 27	1,036  ± 44	724  ± 27
	tPA−/−	1,523  ± 36	1,381  ± 34	1,342  ± 37
	C57BL tPA+/+	885  ± 40	652  ± 30	1,031  ± 60
	C57BL tPA−/−	1,272  ± 75	1,738  ± 92	1,389  ± 91
	uPA−/−	836  ± 32	ND	852  ± 32
P13	tPA+/+	328  ± 13	349  ± 13	435  ± 14
	tPA−/−	657  ± 26	561  ± 19	207  ± 17
P16	tPA+/+	124  ± 10	167  ± 12	273  ± 24
	tPA−/−	149  ± 17	94  ±  9	94  ±  6

Elongated migrating granule neurons in the cerebellar molecular layer were counted in sagittal 10-μm sections of whole mouse brain stained with hematoxylin/eosin. Significantly more (P < 0.001) granule neurons were seen in the molecular layer of tPA^−/− mice at all times between P7 and P13 than in their tPA^+/+ counterparts. Only at the end of the granule cell migratory period (P16) did the two genotypes show similar numbers of granule cells in the molecular layer. tPA-knockout mice maintained on a more pure (>98%) C57BL/6 genetic background and their normal counterparts were also compared at P10, and showed results similar to those of the transgenic hybrids. An additional control was the P10 uPA^−/− knockout mouse, which mimicked the normal control mice, thus confirming the tPA gene specificity of this effect.