Effects of sex and MK-801 on auditory-processing deficits associated with developmental microgyric lesions in rats.

Fitch, R. Holly; Brown, Christine P.; Tallal, Paula; Rosen, Glenn D.

doi:10.1037/0735-7044.111.2.404

Cited by 43 publications

(49 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Another interesting aspect uncovered in these studies is that only male rats and mice with microgyri or ectopias were initially found to have impaired auditory function [26,27]. Female rats showed normal auditory performance and did not show a similar anatomical disruption of the MGN, even though they presented with microgyri as severe as those in males [22].…”

Section: More Insights From Animal Modelsmentioning

confidence: 91%

Neurobiology of dyslexia: a reinterpretation of the data

Ramus¹

2004

Trends in Neurosciences

292

196

View full text Add to dashboard Cite

Section: More Insights From Animal Modelsmentioning

confidence: 91%

Neurobiology of dyslexia: a reinterpretation of the data

Ramus¹

2004

Trends in Neurosciences

292

196

View full text Add to dashboard Cite

“…Male rats with induced cortical malformation, which develop secondary changes in the thalamus, show deficits in auditory processing (Fitch, Brown, Tallal, & Rosen, 1997;Herman, Galaburda, Fitch, Carter, & Rosen, 1997). Animals showing neuronal changes in the thalamus (males) cannot process rapidly changing sound stimuli, while control males and females with malformations perform normally.…”

Section: Neuronal Migration Anomalies and Behavior: Animal Studiesmentioning

confidence: 99%

Dyslexia—A molecular disorder of neuronal migration

Galaburda

2005

Ann. of Dyslexia

View full text Add to dashboard Cite

For 25 years now, there has been a serious attempt to get at the fundamental cause(s) of dyslexia in our laboratory. A great deal of research has been carried out on the psychological and brain underpinnings of the linguistic dysfunctions seen in dyslexia, but attempts to get at its cause have been limited. Initially, observations were made on the brains of persons with dyslexia who had died and their brains donated for research. These observations were modeled in animal models in order to better understand the full extent of anatomical and developmental brain characteristics. More recently, models have begun to employ genetic manipulations in order to close the gap between genes, brain, and behavior. In this article based on a lecture given in memory of Dr. Norman Geschwind to the International Dyslexia Association assembly in Philadelphia in 2004, I outline the history of the research leading up to the most recent findings. These findings consist of experiments using methods that interfere with the function of DNA, using as constructs genes that have been implicated in dyslexia, which cause developmental problems of neuronal migration in rats, secondary brain changes in response to the migration problems, and abnormal processing of sounds.

show abstract

“…In the current experiment we have extended these results to include the VB nucleus. We have previously reported that male rats with induced microgyria have defects in rapid auditory processing (Fitch et al, 1994(Fitch et al, , 1997aClark et al, 2000a,b;Peiffer et al, 2001Peiffer et al, , 2003Peiffer et al, , 2004, suggesting that these changes in the thalamus have functional consequences. In the current experiment, we report that there are significantly more FJB-positive profiles in VB at 24 h in males when compared with females.…”

Section: Sexually Dimorphic Effects Of Early Injurymentioning

confidence: 99%

“…Thus, focal collections of neurons in the molecular layer can be induced by puncture wounds at or around birth (Rosen et al, 1992b), and freezing injury to the developing cortical plate induces malformations that resemble human four-layered microgyria (Dvorák and Feit, 1977;Dvorák et al, 1978;Humphreys et al, 1991;Rosen et al, 1992a;Ferrer et al, 1993;Marret et al, 1995). These induced malformations have been used to model a variety of disorders, including epilepsy (Luhmann et al, 1998;Chevassus-au-Louis et al, 1999;Jacobs et al, 1999a;Jacobs and Prince, 2005) and developmental dyslexia (Humphreys et al, 1991;Fitch et al, 1994Fitch et al, , 1997aHerman et al, 1997;Rosen et al, 1999;Peiffer et al, 2004).…”

mentioning

confidence: 99%

Histometric changes and cell death in the thalamus after neonatal neocortical injury in the rat

et al. 2006

View full text Add to dashboard Cite

Freezing injury to the developing cortical plate results in a neocortical malformation resembling four-layered microgyria. Previous work has demonstrated that following freezing injury to the somatosensory cortex, males (but not females) have more small and fewer large cells in the medial geniculate nucleus. In the first experiment, we examined the effects of induced microgyria to the somatosensory cortex on neuronal numbers, neuronal size, and nuclear volume of three sensory nuclei: ventrobasal complex, dorsal lateral geniculate nucleus, and medial geniculate nucleus. We found that there was a decrease in neuronal number and nuclear volume in ventrobasal complex of microgyric rats when compared with shams, whereas there were no differences in these variables in the dorsal lateral geniculate nucleus or medial geniculate nucleus. We also found that there were more small and fewer large neurons in both ventrobasal complex and medial geniculate nucleus. In experiment 2, we attempted to determine the role of cell death in the thalamus on these histometric measures. We found that cell death peaked within 24 h of the freezing injury and was concentrated mostly in ventrobasal complex. In addition, there was evidence of greater cell death in males at this age. Taken together, these results support the notion that males are more severely affected by early injury to the cerebral cortex than females.Keywords cell death; dorsal lateral geniculate nucleus; medial geniculate nucleus; microgyria; stereology; ventrobasal thalamus Neuronal migration disorders of the cerebral cortex, such as heterotopias, microgyria, porencephaly, and lissencephaly, have been associated with a wide variety of disorders including intractable epilepsy (Meencke and Janz, 1984; Palmini et al., 1991a, b;Crino, 2004), dyslexia (Galaburda and Kemper, 1979;Galaburda et al., 1985), and developmental delay (Barkovich et al., 1988;Barkovich and Raybaud, 2004 NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript developed for many of these neuronal migration disorders. Some of these are the result of spontaneous genetic mutations, such as the reeler or scrambler mouse (Caviness et al., 1972;Goffinet, 1984;Sweet et al., 1996;D'Arcangelo et al., 1997;Rice et al., 1998) or the Tish rat (Lee et al., 1997;Chen et al., 2000), whereas others are induced in otherwise normal rodents such as by prenatal injection with methylazoxymethanol (Ferrer et al., 1982;Chevassus-au-Louis et al., 1999) or neurotrophin-4 (Brunstrom et al., 1997.Malformations have also been induced by mechanical disturbances of the cortical plate. Thus, focal collections of neurons in the molecular layer can be induced by puncture wounds at or around birth (Rosen et al., 1992b), and freezing injury to the developing cortical plate induces malformations that resemble human four-layered microgyria (Dvorák and Feit, 1977;Dvorák et al., 1978;Humphreys et al., 1991;Rosen et al., 1992a;Ferrer et al., 1993;Marret et al., 1995). These induced malformations have been used to mod...

show abstract

Effects of sex and MK-801 on auditory-processing deficits associated with developmental microgyric lesions in rats.

Cited by 43 publications

References 57 publications

Neurobiology of dyslexia: a reinterpretation of the data

Neurobiology of dyslexia: a reinterpretation of the data

Dyslexia—A molecular disorder of neuronal migration

Histometric changes and cell death in the thalamus after neonatal neocortical injury in the rat

Contact Info

Product

Resources

About