Biomedical subjects

Anna Mattsson

Publications and source records attributed to Anna Mattsson.

3 recordsLinked to original sources

PubMed2006

Sex-dependent gene expression in early brain development of chicken embryos.

BACKGROUND: Differentiation of the brain during development leads to sexually dimorphic adult reproductive behavior and other neural sex dimorphisms. Genetic mechanisms independent of steroid hormones produced by the gonads have recently been suggested to partly explain these dimorphisms. RESULTS: Using cDNA microarrays and real-time PCR we found gene expression differences between the male and female embryonic brain (or whole head) that may be independent of morphological differentiation of the gonads. Genes located on the sex chromosomes (ZZ in males and ZW in females) were common among the differentially expressed genes, several of which (WPKCI-8, HINT, MHM non-coding RNA) have previously been implicated in avian sex determination. A majority of the identified genes were more highly expressed in males. Three of these genes (CDK7, CCNH and BTF2-P44) encode subunits of the transcription factor IIH complex, indicating a role for this complex in neuronal differentiation. CONCLUSION: In conclusion, this study provides novel insights into sexually dimorphic gene expression in the embryonic chicken brain and its possible involvement in sex differentiation of the nervous system in birds.

Age Factors↗

PubMed2005

Increased phencyclidine-induced hyperactivity following cortical cholinergic denervation.

Altered cholinergic function is considered as a potential contributing factor in the pathogenesis of schizophrenia. We hypothesize that cortical cholinergic denervation may result in changes in glutamatergic activity. Therefore, we lesioned the cholinergic corticopetal projections by local infusion of 192 IgG-saporin into the nucleus basalis magnocellularis of rats. Possible effects of this lesion on glutamatergic systems were examined by phencyclidine-induced locomotor activity, and also by N-methyl-D-aspartate receptor binding. We find that cholinergic lesioning of neocortex leads to enhanced sensitivity to phencyclidine in the form of a dramatic increase in horizontal activity. Further, N-methyl-D-aspartate receptor binding is unaffected in denervated rats. These results suggest that aberrations in cholinergic function might lead to glutamatergic dysfunctions, which might be of relevance for the pathophysiology for schizophrenia.

Acetylcholine↗

PubMed2002

Facilitation of dopamine-mediated locomotor activity in adult rats following cholinergic denervation.

The dopamine hypothesis of schizophrenia postulates hyperactivity of dopaminergic neurotransmission in the mesolimbic system. However, the possible underlying causes for this dopaminergic overfunction are not well understood. Therefore, the main aim of this study was to examine the effect of central cholinergic denervation on dopamine-mediated functions. We also examined the effect of neonatal cholinergic denervation upon adult brain function. The immunotoxin 192 IgG-saporin causes severe lesions of the basal forebrain cholinergic system when infused into the lateral ventricles by targeting neurons expressing the p75 neurotrophin receptor. The toxin may also damage p75-expressing Purkinje neurons in the cerebellum. We have compared the behavioral effects of intracerebroventricular injections of 192 IgG-saporin to adult rats with that of injections to neonate rats. As expected, adult treated rats displayed an almost complete cholinergic denervation of forebrain corticohippocampal areas concomitant with a marked impairment in the Morris water maze. When tested as adults, neonatally treated animals had a less complete cholinergic denervation and showed lesser impairments in water maze behaviors. Interestingly, adult treated rats showed increased spontaneous horizontal activity and a remarkable increase in locomotor response to d-amphetamine as evidenced by increased horizontal and vertical activity. There were no marked changes of spontaneous or drug-induced locomotor activity in adult rats treated with 192 IgG-saporin as neonates. These results suggest that cholinergic denervation of the forebrain causes a marked enhancement of behavioral responses related to dopaminergic activity, probably mainly mediated presynaptically. However, it cannot be fully excluded that damage to noncholinergic systems, e.g., Purkinje cells, might contribute to the effects. The striking overreaction to dopaminergic stimuli, presumably caused by the cholinergic deficit, is discussed in relation to the suggested role of cholinergic malfunctioning in schizophrenia.

Aging↗