Biomedical subjects

D Wahlsten

Publications and source records attributed to D Wahlsten.

58 records · Page 4Linked to original sources

PubMedDate not supplied

Effects of d-amphetamine and scopolamine on activity before and after shock in three mouse strains.

In three experiments the following results were obtained: (a) Activity was greater both prior to and following exposure to shock among C57BL/6J mice than in DBA/2J mice, which in turn was greater than that of A/J mice. (b) Scopolamine hydrobromide increased general activity in DBA/2 and A mice, but had either no effect or decreased activity in the C57BL/6 strain. Following exposure to shock, however, the disinhibitory effects of scopolamine were apparent in all three strains. (c) d-amphetamine increased activity in all three strains. Moreover, following the single shock d-amphetamine had excitatory effects among both A and DBA/2 mice such that activity exceeded the level observed with d-amphetamine alone. Following several shock presentations a small but significant excitation was observed in C57BL/6 mice as well. Data were interpreted in terms of disinhibitory and excitatory effects of scopolamine and d-amphetamine, respectively, as well as possible interactions between the catecholaminergic and cholinergic systems. In addition, implications for sources of strain differences in avoidance behavior are discussed.

Animals↗

PubMedDate not supplied

Mode of inheritance of deficient corpus callosum in mice.

Many mice of the inbred strain BALB/cCF have deficient corpus callosum, and a few of them have total absence of this large forebrain commissure. Reciprocal F1 hybrid crosses with the inbred strains A/J, C57BL/6J, and DBA/2J revealed that inheritance of the defect is completely recessive. Reciprocal backcrosses to BALB/cCf revealed that inheritance is not attributable to a single Mendelian locus with the same degree of penetrance as in the parent strain. The ac locus has not been rediscovered. Instead, there is good reason to withdraw ac from current listings of Mendelian loci in the mouse.

Age Factors↗

PubMedDate not supplied

Inheritance of retarded forebrain commissure development in fetal mice: results from classical crosses and recombinant inbred strains.

Deficiency of the adult corpus callosum in BALB/c mice shows incomplete penetrance and is clearly polygenic, whereas the defect in fetuses shows complete penetrance and a much less complex mode of inheritance. Retardation of the growth of the corpus callosum and the hippocampal commissure in the fetal mouse forebrain was expressed by a standard score (z) derived from body weight, such that a fetus with a score less than -2.0 was held to have commissures abnormally small for the body size. By this index, almost all C57BL/6 fetuses were normal, whereas BALB/c fetuses in the body weight range 0.5 to 1.0 g were often 5 standard deviations below the expected value of 0.0. In classical crosses between C57BL/6J and BALB/cWah, inheritance of the index of abnormality (z) was recessive, and about half of the fetuses in backcrosses to BALB/c were below -2.0. However, the distribution of scores was not bimodal. The results were consistent with a two-locus but not a single-locus difference between parent strains. Among the seven recombinant inbred strains derived from the By strains of C57BL/6 and BALB/c, there were three or possibly four distinct clusters of strains, which also suggested two-locus inheritance and excluded a single-locus difference. Although substantial retardation of commissure growth was evident in fetuses, deficiency or absence of the corpus callosum in weanling and adult By recombinant inbred mice was extremely rare in all strains except BALB/cByJ. These data confirm anatomical results showing that, in all but the most extremely retarded cases, the corpus callosum recovers from an obvious prenatal defect.

Agenesis of Corpus Callosum↗

PubMedDate not supplied

Tests of genetic allelism between four inbred mouse strains with absent corpus callosum.

Inbred mouse strains that lack the corpus callosum connecting the cerebral hemispheres in the adult differ from the C57BL/6J strain at several relevant but unknown loci. To identify at least one major locus that influences axon guidance, different strains showing phenotypically similar defects were crossed to test for allelism. If the F1 hybrid between two strains with the same brain defect is phenotypically normal, it is much more likely that the two strains will differ at fewer loci than will an acallosal strain and C57BL/6J. This approach proved to be very informative. Five reasonable models of inheritance involving two or three loci were assessed, and the data justified rejection of all but one hypothesis. A total of 479 mice were obtained from four inbred strains prone to absence of the corpus callosum (BALB/cWah1, BALB/cWah2, I/LnJ, and 129/ReJ), one normal strain (C57BL/6J), and 11 F1 hybrids among them. Because the size of forebrain axon bundles is generally greater in mice with larger brains, and because whole brain size is certainly polygenic, the phenotypically normal groups were used to derive a standard index of the degree of corpus callosum deficiency relative to brain size. Results demonstrated clearly that the hybrid between BALB/cWah1 and 129/ReJ is normal, whereas the crosses among the BALB/c substrains and I/LnJ yielded many mice with deficient corpus callosum. I/LnJ crossed with 129/ReJ also produced some animals with callosal defects. The data were consistent with a model in which the difference between BALB/c and 129/ReJ involves two loci, whereas the defect in I/LnJ involves homozygosity at three loci, which impairs development more severely.(ABSTRACT TRUNCATED AT 250 WORDS)

Alleles↗