Neuroscience
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Glial cell line-derived neurotrophic factor (GDNF) signals through multisubunit receptor complex consisting of RET tyrosine kinase and a glycosylphosphatidylinositol-anchored coreceptor called GDNF family receptor alpha1 (GFRalpha1). In the current study, we cloned a human SEP1 gene as a GDNF-inducible gene using human neuroblastoma cells that express RET and GFRalpha1. The induction of the SEP1 gene showed two peaks at 0.5-2 h and 24-48 h after GDNF stimulation by Northern blotting and quantitative real-time reverse transcriptase polymerase chain reaction. ⋯ In addition, we found a high level of SEP1 expression in neurons of the dorsal root and superior cervical ganglia and motor neurons of the spinal cord of mice in which RET is also expressed. SEP1 was co-immunoprecipitated with alpha- and beta-tubulins from the lysate of mouse brain. These results thus suggested that SEP1 is a GDNF-inducible and microtubule-associated protein that may play a role in the nervous system.
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Comparative Study
Impaired dendritic spine maturation in GABAA receptor alpha1 subunit knock out mice.
In this study we investigated the functional implications of GABAA receptor alpha1 subunit deletion on dendritic arborization and spine maturation in the visual cortex. This subunit is normally strongly upregulated during early postnatal development. ⋯ In contrast, dendritic arborization was not altered in these mice. We propose that an increased efficacy of the inhibitory synaptic transmission in the alpha1 knock out mice may lead to an enhancement of the outgrowth of filopodia around eye opening, but to a failure in spine maturation at later stages.
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Comparative Study
Molecular and behavioral analysis of the R6/1 Huntington's disease transgenic mouse.
Transgenic mice expressing exon 1 of the human Huntington's disease (HD) gene carrying a 115 CAG repeat (line R6/1) are characterized by a neurologic phenotype involving molecular, behavioral and motor disturbances. We have characterized the R6/1 to establish a set of biomarkers, which could be semi-quantitatively compared. We have measured motor fore- and hindlimb coordination, fore- and hindpaw footprinting, general activity and anxiety, feetclasping, developmental instability. ⋯ Mice tested at 23 and 24 weeks of age showed significant impairments in open field and plus-maze analysis respectively. We observed no significant abnormalities in stride length of the R6/1 mouse model. As the analyzed parameters are easily detected and measured, the R6/1 mouse appears to be a good model for evaluating new drugs or types of therapy for HD.
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Comparative Study
Calbindin expression in the hamster suprachiasmatic nucleus depends on day-length.
The mammalian circadian clock located in the suprachiasmatic nucleus (SCN) of the hypothalamus controls many physiological and behavioral rhythms. The SCN is compartmentalized in two functionally distinct subregions: a dorsomedial subregion that rhythmically expresses clock genes, and a ventrolateral subregion which, in contrast, mainly expresses clock genes at a constant level. In the golden hamster, this ventrolateral part of the SCN contains a subpopulation of neurons expressing calbindin D28k. ⋯ We show that calbindin expression is negatively correlated to the day-length. The number of calbindin immunopositive neurons and calbindin mRNA levels were markedly increased in hamsters exposed to short photoperiods (light/dark cycle [LD] 6:18 and LD10:14) when compared with hamster exposed to long photoperiods (LD18:6 and LD14:10). This suggests that calbindin neurons are involved in the encoding of seasonal information by the SCN.
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The neurochemistry of aggression and rage has largely focused on the roles played by neurotransmitters and their receptor mechanisms. In contrast, little attention has been given to the possible functions of other substances. Interleukin-1beta is an immune and brain-derived cytokine that is present in the hypothalamus. ⋯ In the third experiment, pretreatment with a selective 5-HT2 receptor antagonist, LY-53857, blocked the facilitating effects of interleukin-1beta upon defensive rage. These findings reveal for the first time that brain cytokines can dramatically alter aggressive behavior. In particular, interleukin-1beta in the medial hypothalamus potentiates defensive rage behavior elicited from the periaqueductal gray in the cat, and the potentiating effects of interleukin-1beta on this form of emotional behavior are mediated via a 5-HT2 receptor mechanism.