scholarly journals CEREBELLAR ALTERATIONS IN THE WEAVER MOUSE

1973 ◽  
Vol 56 (2) ◽  
pp. 478-486 ◽  
Author(s):  
Asao Hirano ◽  
Herbert M. Dembitzer
Keyword(s):  
Fine Structure ◽  
Purkinje Cell ◽  
Purkinje Cells ◽  
Dendritic Spines ◽  
Granule Cells ◽  
Parallel Fibers ◽  
Mechanisms Of Development ◽  
Weaver Mouse

The fine structure of the cerebellum of weaver mouse was examined and the paucity of granule cells and their axons, the parallel fibers, was confirmed. Unexpectedly, however, the dendritic spines of the Purkinje cells which, in normal animals, are the postsynaptic mates of the parallel fibers, were present. Furthermore, their essential morphology and their staining reactions were indistinguishable from those of the Purkinje cell dendritic spines in normal animals. Possible mechanisms of development are discussed.

scholarly journals Acid-sensitive channel inhibition prevents fetal alcohol spectrum disorders cerebellar Purkinje cell loss

2008 ◽  
Vol 295 (2) ◽  
pp. R596-R603 ◽  
Author(s):  
Jayanth Ramadoss ◽  
Emilie R. Lunde ◽  
Nengtai Ouyang ◽  
Wei-Jung A. Chen ◽  
Timothy A. Cudd
Keyword(s):  
Purkinje Cell ◽  
Purkinje Cells ◽  
Granule Cells ◽  
Cell Number ◽  
Ethanol Exposure ◽  
Ph Sensitive ◽  
Mitigation Strategies ◽  
Cerebellar Purkinje Cell ◽  
Prenatal Ethanol Exposure ◽  
Channel Inhibition

Ethanol is now considered the most common human teratogen. Educational campaigns have not reduced the incidence of ethanol-mediated teratogenesis, leading to a growing interest in the development of therapeutic prevention or mitigation strategies. On the basis of the observation that maternal ethanol consumption reduces maternal and fetal pH, we hypothesized that a pH-sensitive pathway involving the TWIK-related acid-sensitive potassium channels (TASKs) is implicated in ethanol-induced injury to the fetal cerebellum, one of the most sensitive targets of prenatal ethanol exposure. Pregnant ewes were intravenously infused with ethanol (258 ± 10 mg/dl peak blood ethanol concentration) or saline in a “3 days/wk binge” pattern throughout the third trimester. Quantitative stereological analysis demonstrated that ethanol resulted in a 45% reduction in the total number of fetal cerebellar Purkinje cells, the cell type most sensitive to developmental ethanol exposure. Extracellular pH manipulation to create the same degree and pattern of pH fall caused by ethanol (manipulations large enough to inhibit TASK 1 channels), resulted in a 24% decrease in Purkinje cell number. We determined immunohistochemically that TASK 1 channels are expressed in Purkinje cells and that the TASK 3 isoform is expressed in granule cells of the ovine fetal cerebellum. Pharmacological blockade of both TASK 1 and TASK 3 channels simultaneous with ethanol effectively prevented any reduction in fetal cerebellar Purkinje cell number. These results demonstrate for the first time functional significance of fetal cerebellar two-pore domain pH-sensitive channels and establishes them as a potential therapeutic target for prevention of ethanol teratogenesis.

scholarly journals Cerebellar nuclei excitatory neurons regulate developmental scaling of presynaptic Purkinje cell number and organ growth

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Ryan T Willett ◽  
N Sumru Bayin ◽  
Andrew S Lee ◽  
Anjana Krishnamurthy ◽  
Alexandre Wojcinski ◽  
...  
Keyword(s):  
Purkinje Cell ◽  
Purkinje Cells ◽  
Cerebellar Cortex ◽  
Granule Cells ◽  
Postnatal Growth ◽  
Cerebellar Nuclei ◽  
Cell Number ◽  
Conditional Knockout ◽  
Neural Systems ◽  
Scaling Down

For neural systems to function effectively, the numbers of each cell type must be proportioned properly during development. We found that conditional knockout of the mouse homeobox genes En1 and En2 in the excitatory cerebellar nuclei neurons (eCN) leads to reduced postnatal growth of the cerebellar cortex. A subset of medial and intermediate eCN are lost in the mutants, with an associated cell non-autonomous loss of their presynaptic partner Purkinje cells by birth leading to proportional scaling down of neuron production in the postnatal cerebellar cortex. Genetic killing of embryonic eCN throughout the cerebellum also leads to loss of Purkinje cells and reduced postnatal growth but throughout the cerebellar cortex. Thus, the eCN play a key role in scaling the size of the cerebellum by influencing the survival of their Purkinje cell partners, which in turn regulate production of granule cells and interneurons via the amount of sonic hedgehog secreted.

scholarly journals The cerebellum and timing: Lessons from mormyrids

1997 ◽  
Vol 20 (2) ◽  
pp. 258-258 ◽  
Author(s):  
J. Meek
Keyword(s):  
Purkinje Cells ◽  
Granule Cells ◽  
Parallel Fiber ◽  
Parallel Fibers ◽  
Tidal Waves ◽  
Cerebellar Function

Mormyrid teleosts have Purkinje cells with palisade dendrites, which probably represent coincidence detectors of parallel fiber activity. Their existence strongly supports the ideas of Braitenberg et al. on cerebellar function. However, the organization of mormyrid granule cells and parallel fibers suggests that a key to cerebellar function is not in interactions within one wave, but between two opposite tidal waves.

Cerebellar cortex

2020 ◽  
pp. 497-504
Author(s):  
Edmund T. Rolls
Keyword(s):  
Purkinje Cell ◽  
Purkinje Cells ◽  
Cerebellar Cortex ◽  
Network Architecture ◽  
Granule Cells ◽  
Feedforward Control ◽  
Synaptic Depression ◽  
Climbing Fibre ◽  
Regular Sampling

The cerebellar cortex appears to be involved in predictive feedforward control to generate smooth movements. There is a beautiful network architecture which suggests that the granule cells perform expansion recoding of the inputs; that these connect to the Purkinje cells via an architecture that ensures regular sampling; and that each Purkinje cell has a single teacher, the climbing fibre, which produces associative long-term synaptic depression as part of perceptron-like learning.

Development of the rodent cerebellum and synaptic re-formation of donor climbing terminals on spines of the host Purkinje dendrites after chemical deafferentation

1990 ◽  
Vol 153 (1) ◽  
pp. 289-303
Author(s):  
K. Kawamura ◽  
S. Murase ◽  
S. Yuasa
Keyword(s):  
Purkinje Cells ◽  
Dendritic Spines ◽  
Ultrastructural Level ◽  
Climbing Fibers ◽  
Normal Brain ◽  
Parallel Fibers ◽  
Synaptic Contacts ◽  
Axonal Sprouts ◽  
Inferior Olivary ◽  
The Brain

Reinnervation of host Purkinje cells by donor climbing fibers was observed in the following experiments. Medullary primordial tissue (from E14-E16) containing the inferior olive was grafted into a host rat cerebellum, in which the inferior olivary complex and climbing fibers had been destroyed by intraperitoneal injection of 3-acetylpyridine (3-AP). After 3 weeks, immature as well as mature types of climbing fiber terminals bearing packed round vesicles were found that had established synaptic contacts on dendritic spines of the host Purkinje cells. Quantitative analysis at the ultrastructural level has been carried out. The main results are as follows. (1) The number of preterminals that formed synaptic contacts with spines of the host Purkinje dendrites in the transplanted material increased by 3.4-fold compared to the control (3-AP-treated non-grafted material). (2) The number of mature climbing-type preterminals increased from 0.3-0.9% to 5% after grafting (cf. 22% in normal brain tissue), and the number of immature climbing-type preterminals also increased from 2–10% (control) to 20% after grafting. These changes were statistically significant (P less than 0.01). (3) The number of parallel-type preterminals increased from 13% (control) to 27% after grafting, which was also statistically significant (P less than 0.01). Thus, it appears that the donor climbing fibers grow and develop to find unoccupied spines on the host Purkinje dendrites and establish synaptic contacts, and also that the host parallel fibers may generate axonal sprouts to search their new targets and ultimately to form synaptic contacts with unoccupied spines. In the process of re-modeling the brain, competition for targets is likely to occur between the two kinds of axonal processes, i.e. the donor climbing fibers and the host parallel fibers.

Ammonium ions abolish excitatory synaptic transmission between cerebellar neurons in primary dissociated tissue culture

1992 ◽  
Vol 68 (1) ◽  
pp. 93-99 ◽  
Author(s):  
W. Raabe
Keyword(s):  
Tissue Culture ◽  
Synaptic Transmission ◽  
Purkinje Cell ◽  
Purkinje Cells ◽  
Granule Cells ◽  
Conduction Block ◽  
Excitatory Synaptic Transmission ◽  
Extracellular Solution ◽  
Cell Soma ◽  
Cerebellar Neurons

1. Transmitter glutamate is thought to be derived from glutamine via cleavage by glutaminase. NH+4 inhibits glutaminase. Therefore the decrease of glutamatergic excitatory synaptic transmission by NH+4 was thought to be due to the inability of glutamine to serve as precursor for glutamate. However, in cat spinal cord, NH+4 abolished excitatory synaptic transmission by a conduction block for action potentials in presynaptic terminals. The conduction block prevented inferences as to the effects of NH+4 on the availability of glutamate for synaptic transmission. This study reexamines the effects of NH+4 on glutamatergic excitatory synaptic transmission in cerebellar neurons in tissue culture. 2. Whole-cell patch voltage-clamp recordings were obtained from presumed Purkinje cells. Extracellular stimulation of presumed granule cells produced mono- and polysynaptic excitatory postsynaptic currents (EPSCs). In addition, presumed Purkinje cells showed spontaneous EPSCs that occurred independently of the addition of tetrodotoxin (TTX) or Cd2+ to the extracellular solution. 3. NH+4 (5–10 mM) abolished evoked mono- and polysynaptic EPSCs without abolishing spontaneous EPSCs and without significant effects on action currents in the Purkinje cell soma. 4. Increase of K+ in the extracellular solution to 10-12 from 5 mM abolished evoked EPSCs without abolishing spontaneous EPSCs and without significant effects on action currents in the Purkinje cell soma. 5. Mixtures of NH+4 and K+, with each ion in a concentration insufficient to affect evoked EPSCs when given alone, abolished evoked EPSCs when the sum of NH+4 and K+ exceeded 10–12 mM. 6. Increase of intracellular pH by trimethylamine had no effect on evoked and spontaneous EPSCs.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Membrane specializations of dentritic spines and glia in the weaver mouse cerebellum: a freeze-fracture study.

1976 ◽  
Vol 68 (3) ◽  
pp. 403-410 ◽  
Author(s):  
R B Hanna ◽  
A Hirano ◽  
G D Pappas
Keyword(s):  
Electron Microscopy ◽  
Dendritic Spines ◽  
Synaptic Input ◽  
Freeze Fracture ◽  
Fracture Face ◽  
Entire Region ◽  
Parallel Fibers ◽  
Fracture Study ◽  
Weaver Mouse ◽  
Center Distance

Electron microscopy of thin-sectioned and freeze-fractured preparations of the cerebellum of the weaver mouse indicates that the dendritic spines are morphologically identical to those of their normal littermates. The weaver dendritic spines have been characterized as "unattached" since the synaptic input from the parallel fibers is absent (8-10). The entire region around the dendritic spines is taken up by astrocytic processes in the weaver. The outer fracture face of a normal dendritic spine contains aggregations of 10-nm wide particles in the immediate postsynaptic region. Similar particle aggregations occur in the unattached spines of the weaver. Freeze-fracture preparations reveal rectilinear arrays of particles, having a 7-nm center-to-center distance in the glial membranes. Rectilinear arrays are apparently distributed throughout the astrocyte membrane.

scholarly journals On-beam synchrony in the cerebellum as the mechanism for the timing and coordination of movement

2007 ◽  
Vol 104 (18) ◽  
pp. 7658-7663 ◽  
Author(s):  
D. H. Heck ◽  
W. T. Thach ◽  
J. G. Keating
Keyword(s):  
Purkinje Cell ◽  
Purkinje Cells ◽  
Parallel Fibers ◽  
Simple Spike ◽  
Spike Firing

In trained reaching rats, we recorded simple spikes of pairs of Purkinje cells that, with respect to each other, were either aligned on a beam of shared parallel fibers or instead were located off beam. Rates of simple spike firing in both on-beam and off-beam Purkinje cell pairs commonly showed great variety in depth of modulation during reaching behavior. But with respect to timing, on-beam Purkinje cell pairs had simple spikes that were tightly time-locked to each other (either delayed or simultaneous) and to movement, despite the variability in rate. By contrast, off-beam Purkinje cell pairs had simple spikes that were not time-locked to each other, neither delayed nor simultaneous. We discuss the implications of these observations for the cerebellar role in timing and coordinating movement.

scholarly journals Purkinje cell degeneration associated with erythroid ankyrin deficiency in nb/nb mice.

1991 ◽  
Vol 114 (6) ◽  
pp. 1233-1241 ◽  
Author(s):  
L L Peters ◽  
C S Birkenmeier ◽  
R T Bronson ◽  
R A White ◽  
S E Lux ◽  
...  
Keyword(s):  
Purkinje Cell ◽  
Purkinje Cells ◽  
Granule Cells ◽  
Cell Loss ◽  
Chromosome 8 ◽  
Cell Degeneration ◽  
Purkinje Cell Loss ◽  
Cell Stability ◽  
Cerebellar Purkinje Cells

Mice homozygous for the nb mutation (Chromosome 8) have a severe hemolytic anemia and develop a psychomotor disorder at 6 mo of age. The nb/nb mice are deficient in erythroid ankyrin (Ank-1) but, until the present study, the role of Ank-1 and of Ank-2 (brain ankyrin) in disease genesis was unknown. In normal erythroid tissues, we show that two major transcripts are expressed from Ank-1, and one of these is also present at high levels in the cerebellum. By in situ hybridization and immunocytochemistry, Ank-1 localizes to the cerebellar Purkinje cells and, to a lesser extent, the granule cells. In nb/nb mice, Ank-1 transcripts are markedly reduced in both erythroid and neural tissue, and nb/nb Purkinje cells and granule cells are nearly devoid of Ank-1. The neurological syndrome appears concurrently with a dramatic loss of Purkinje cells. Ank-2 maps to Chromosome 3 and its expression is unaffected by the nb mutation. We conclude that Ank-1 is specifically required for Purkinje cell stability and, in its absence, Purkinje cell loss and neurological symptoms appear.

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