Calbindin in Cerebellar Purkinje Cells Is a Critical Determinant of the Precision of Motor Coordination

Barski, Jarosław Jerzy; Hartmann, Jana; Rose, Christine R.; Hoebeek, Freek E.; Mörl, Karin; Noll‐Hussong, Michael; Zeeuw, C. I. De; Konnerth, Arthur; Meyer, Michaël

doi:10.1523/jneurosci.23-08-03469.2003

Cited by 169 publications

(167 citation statements)

References 49 publications

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“…Additionally the fastest speed is strongly reduced (Table 2C). This is in line with the previously reported impairment in motor coordination seen in CB−/− mice [12,30]. …”

Section: Repeated Analysis Of Locomotor Activity and Locomotor Activisupporting

confidence: 93%

“…It seems that this parameter is strongly correlated with the motor coordination deficits observed in CB-deficient and also in double knockout mice ( [12] and this study). The impaired motor coordination in CB−/− mice can be selectively attributed to the elimination of CB from Purkinje cells, since Purkinje cell-specific CB knockout mice display marked permanent deficits of motor coordination [30] in the runway assay similar to mice where CB expression is globally deleted. Also our results of the rotarod assay point in the direction that the absence of CB is the main factor for the motor impairment, while the effect of PV-deficiency is rather subtle and beyond detection in most assays.…”

Section: Discussionmentioning

confidence: 99%

“…Each mouse was tested in five consecutive trials per day for 5 days on a rod (100 cm × 2 cm × 2 cm) with small obstacles [29], as used before for the CB−/− mice [12,30]. Slips of the forelimb and hindlimb were counted on the side visible for the experimenter.…”

Section: Runway Assaymentioning

confidence: 99%

“…CB−/− mice manifest impairment in motor coordination including deficits in the runway assay [12] that can be attributed to the absence of CB in Purkinje cells [30]. Since PV is also abundantly expressed in Purkinje cells and molecular layer interneurons, PV−/− and mice deficient for both CB and PV were tested in the same runway assay under the same experimental conditions.…”

Section: Testing Of Motor Coordination In the Runway Assaymentioning

confidence: 99%

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Differences in locomotor behavior revealed in mice deficient for the calcium-binding proteins parvalbumin, calbindin D-28k or both

FARRECASTANY

Schwaller

Gregory

et al. 2007

Behavioural Brain Research

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We investigated the role of the two calcium-binding proteins parvalbumin (PV) and calbindin D-28k (CB) in the locomotor activity and motor coordination using null-mutant mice for PV (PV−/−), CB (CB−/−) or both proteins (PV−/−CB−/−). These proteins are expressed in distinct, mainly non-overlapping populations of neurons of the central and peripheral nervous system and PV additionally in fast-twitch muscles. In a test measuring repeated locomotor activity during 18-20 days, the analysis revealed a slightly increased activity in mice lacking either protein, while the lack of both decreased the number of beams crossed during active periods. An increase in the characteristic speed during the first 8 days could be attributed to PVdeficiency, while the elimination of CB in CB−/− and double-KO mice decreased the percentage of fast movements at all time points. In the latter, additionally a reduction of the fastest speed was observed. The alterations in locomotor activity (fast movements, fastest speed) strongly correlate with the impairment in locomotor coordination in mice deficient for CB evidenced in the runway assay and the rotarod assay. The graded locomotor phenotype (CB > PV) is qualitatively correlated with alterations in Purkinje cell firing reported previously in these mice. The presence or absence of either protein did not affect the spontaneous locomotor activity when animals were placed in a novel environment and tested only once for 30 min. In summary, the lack of these calcium-binding proteins yields characteristic, yet distinct phenotypes with respect to locomotor activity and coordination.

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“…Additionally the fastest speed is strongly reduced (Table 2C). This is in line with the previously reported impairment in motor coordination seen in CB−/− mice [12,30]. …”

Section: Repeated Analysis Of Locomotor Activity and Locomotor Activisupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Runway Assaymentioning

confidence: 99%

Section: Testing Of Motor Coordination In the Runway Assaymentioning

confidence: 99%

See 2 more Smart Citations

Differences in locomotor behavior revealed in mice deficient for the calcium-binding proteins parvalbumin, calbindin D-28k or both

FARRECASTANY

Schwaller

Gregory

et al. 2007

Behavioural Brain Research

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show abstract

“…CB-D28k 2/2 mice show a mildhowever more severe than PV 2/2 mice-impairment in motor coordination/motor learning (Airaksinen et al 1997;Farre-Castany et al 2007), likely resulting from the 160-Hz oscillations in the cerebellum (Cheron et al 2004;Servais et al 2005). The motor coordination phenotype is due to CB-D28k's absence in Purkinje cells, since this phenotype and alterations in Purkinje cell physiology also occur in mice with Purkinje cell-specific Calb1 ablation (Barski et al 2003). At the cellular level, shortterm plasticity between cortical multipolar bursting cells and pyramidal cells, or at the mossy fiber-CA3 pyramidal cell synapse in the hippocampus, is affected by CB-D28k (Blatow et al 2003).…”

Section: Functional Aspects Of Cb-d28kmentioning

confidence: 99%

Cytosolic Ca2+ Buffers

Schwaller¹

2010

Cold Spring Harbor Perspectives in Biology

348

305

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Calbindin‐D28K Immunoreactivity in the Human Cerebellar Cortex

Flace¹,

Lorusso²,

Laiso³

et al. 2014

The Anatomical Record

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Calbindin-D28k (CB) is a calcium-binding protein largely distributed in the cerebellum of various species of vertebrates. As regards the human cerebellar cortex, precise data on the distribution of CB have not yet been reported. Aim of the present work was to analyze the distribution of CB in postmortem samples of human cerebellar cortex using light microscopy immunohistochemical techniques. Immunoreactivity to CB was detected within neuronal bodies and processes distributed in all cortex layers. In the molecular layer, the immunoreactivity was observed in subpopulations of stellate and basket neurons. In the Purkinje neuron layer, the immunoreactivity was observed in practically all the Purkinje neurons. In the granular layer, the immunoreactivity was observed in subpopulations of granules, of Golgi neurons, and also of other types of large neurons (candelabrum, Lugaro neurons, etc.). Immunoreactivity to CB was also observed in axon terminals distributed throughout the cortex according to layerspecific patterns of distribution. The qualitative and quantitative patterns of distribution of CB showed no difference among the different lobes of the cerebellar cortex. This study reports that CB is expressed by different neuron types, both inhibitory (GABAergic) and excitatory (glutamatergic), involved in both intrinsic and extrinsic circuits of the human cerebellar cortex. The study provides further insights on the functional role of CB and on the neuronal types of the cerebellar cortex in which it is expressed. Anat Rec, 297:1306Rec, 297: -1315Rec, 297: , 2014. V C 2014 Wiley Periodicals, Inc.Key words: Calbindin-D28k; cerebellum; immunohistochemistry; purkinje neurons; non-traditional neurons Calcium ions (Ca 21 ) act in neurons as major secondary messengers which control many neuronal activities, including gene expression, developmental processes of proliferation, differentiation and morphogenesis, membrane excitability and conductivity, axonal transport, synthesis and release of neuroactive substances, phenomena of synaptic plasticity. The effects of Ca 21 basically depend on the presence of a number of structurally related proteins, generally indicated as calcium-binding proteins, which are expressed by neurons with a certain degree of specificity

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Calbindin in Cerebellar Purkinje Cells Is a Critical Determinant of the Precision of Motor Coordination

Abstract: Long-term depression (LTD) of

Cited by 169 publications

References 49 publications

Differences in locomotor behavior revealed in mice deficient for the calcium-binding proteins parvalbumin, calbindin D-28k or both

Differences in locomotor behavior revealed in mice deficient for the calcium-binding proteins parvalbumin, calbindin D-28k or both

Cytosolic Ca2+ Buffers

Calbindin‐D28K Immunoreactivity in the Human Cerebellar Cortex

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