Neurochemical and morphological consequences of axon terminal degeneration in cerebellar deep nuclei of mice with inherited purkinje cell degeneration

@article{RofflerTarlov1979NeurochemicalAM,
  title={Neurochemical and morphological consequences of axon terminal degeneration in cerebellar deep nuclei of mice with inherited purkinje cell degeneration},
  author={Suzanne Roffler-Tarlov and Philip Mark Beart and Stephen O’Gorman and Richard L. Sidman},
  journal={Brain Research},
  year={1979},
  volume={168},
  pages={75-95}
}
The concentrations of free amino acids and the activities of transmitter-related enzymes, glutamic acid decarboxylase (GAD), choline acetylase (ChAC) and GABA-transaminase (GABA-t) were measured in cerebellar cortex and deep cerebellar nuclei from the mouse mutant Purkinje cell degeneration (pcd) at various times before and after Purkinje cell loss. Axosomatic synapses on target cells in pcd deep nuclei were quantified by electron microscopy during and after degeneration. The concentration of… 
Effects of Purkinje cell degeneration on the noradrenergic projection to mouse cerebellar cortex
TLDR
The effects of a genetically programmed target cell death on the noradrenergic afferent projection to mouse cerebellar cortex are examined and changes appear to be permanent as they are still present in 6 month-old mutant animals, the oldest studied.
Cerebellar benzodiazepine receptors: cellular localization and consequences of neurological mutations in mice
TLDR
The authors' autoradiographic data suggest that a proportion of cerebellar cortical benzodiazepine receptors are associated with Purkinje cells; it is proposed that the remainder of the receptors are localized on Golgi cells, while granule cells are devoid of receptors.
GABAA receptor messenger RNA expression in the deep cerebellar nuclei of Purkinje cell degeneration mutants is maintained following the loss of innervating Purkinje neurons
TLDR
Quantitative analysis of the hybridization signals over individual neurons revealed that Purkinje cell loss differentially affected the expression of GABAA receptor subunit messenger RNAs.
Non-Purkinje cell GABAergic innervation of the deep cerebellar nuclei: A quantitative immunocytochemical study in C57BL and in Purkinje cell degeneration mutant mice
TLDR
This important residual innervation of the deep nuclei might arise from local GABAergic neurons, which were identified in the normal and mutant cerebella by immunostaining with an anti-GABA antibody.
The content of amino acids in the developing cerebellar cortex and deep cerebellar nuclei of granule cell deficient mutant mice
TLDR
An early and transient deficit in taurine in weaver cerebellar cortex during the period of granule cell migration is found and it is found that aspartic and glutamic acid deficits result from failure to increase concentrations at the normal rate after birth rather than from a fall from normal levels.
Diverse effects of Purkinje cell loss on deep cerebellar and vestibular nuclei neurons in Purkinje cell degeneration mutant mice: A possible compensatory mechanism
TLDR
Extracellular recordings of PCD mutant and corresponding wild‐type VN neurons under sinusoidal vestibular stimulation are performed and show an increased and thus electrophysiologically detectable activity of the respective neurons.
Degeneration of thalamic neurons in “Purkinje cell degeneration” mutant mice. II. Cytology of neuron loss
  • S. O’Gorman
  • Biology, Medicine
    The Journal of comparative neurology
  • 1985
TLDR
Cytopathological alterations in the neuropil of P50 and older mutants were dominated by degenerating dendritic profiles; there was no evidence that the loss of thalamic neurons in pcd mutants was associated with synaptic agenesis or dysgenesis or the prior or concurrent degeneration of afferent synaptic terminals.
Differential number of glycine‐ and GABA‐immunopositive neurons and terminals in the deep cerebellar nuclei of normal and Purkinje cell degeneration mutant mice
The total number of glycine‐immunopositive (Gly+) neurons in the deep cerebellar nuclei (DCN) was quantified under normal conditions in wild‐types (B6C3Fe) and compared with the Purkinje
Altered histofluorescent pattern of noradrenergic innervation of the cerebellum of the mutant mouse Purkinje cell degeneration
TLDR
Findings indicate that the relative number of noradrenergic afferents to the molecular layer of the cerebellum is not reduced following spontaneous degeneration of Purkinje cells, andPurkinje target cells do not appear to be essential for maintenance of afferent inputs in mature cerebellar cortex.
Degeneration of thalamic neurons in “Purkinje cell degeneration” mutant mice. I. Distribution of neuron loss
TLDR
It is found that discrete populations of thalamic neurons degenerate rapidly between P50 and P60 and in restricted portions of the lateral ventrobasal, dorsal lateral geniculate, and lateral posterior nuclei, but even at P180 these nuclei are not markedly atrophic.
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