Evidence map›Paper›PMID 25673739›Full record

ArticleJournal of neurophysiology2015

Calcium-dependent inactivation of calcium channels in the medial striatum increases at eye opening.

R C Evans, G A Herin, S L Hawes, K T Blackwell

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 38% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 5 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

R C EvansGeorge Mason University, The Krasnow Institute for Advanced Studies, Fairfax, Virginia; and.
G A HerinEastern Mennonite University, Harrisonburg, Virginia.
S L HawesGeorge Mason University, The Krasnow Institute for Advanced Studies, Fairfax, Virginia; and.
K T BlackwellGeorge Mason University, The Krasnow Institute for Advanced Studies, Fairfax, Virginia; and kblackw1@gmu.edu.
George Mason University · USEastern Mennonite University · US

Funding

CRCNS: Spatio-temporal Dynamics of Dopamine Activated 2nd Messenger PathwaysR01AA016022 · NIAAA · GEORGE MASON UNIVERSITY · PI BLACKWELL, KIM L, LOVINGER, DAVID · 2005 to 2017
$2.6M
CRCNS: US-French Collaboration: Dopamine modulation of calcium in STDPR01DA038890 · NIDA · GEORGE MASON UNIVERSITY · PI BLACKWELL, KIM L · 2014 to 2017
$637k
The Role of PKA Activity and AKAP anchoring in Striatal Synaptic PlasticityF31NS066645 · NINDS · GEORGE MASON UNIVERSITY · PI EVANS, REBEKAH COLEMAN · 2011 to 2012
$40k
NIAAA NIH HHS R01 AA016022NIDA NIH HHS R01 DA038890NIDA NIH HHS R01-DA-038890NINDS NIH HHS 1F31-NS-066645NINDS NIH HHS F31 NS066645
6 · The paper itself

Abstract

Influx of calcium through voltage-gated calcium channels (VGCCs) is essential for striatal function and plasticity. VGCCs expressed in striatal neurons have varying kinetics, voltage dependences, and densities resulting in heterogeneous subcellular calcium dynamics. One factor that determines the calcium dynamics in striatal medium spiny neurons is inactivation of VGCCs. Aside from voltage-dependent inactivation, VGCCs undergo calcium-dependent inactivation (CDI): inactivating in response to an influx of calcium. CDI is a negative feedback control mechanism; however, its contribution to striatal neuron function is unknown. Furthermore, although the density of VGCC expression changes with development, it is unclear whether CDI changes with development. Because calcium influx through L-type calcium channels is required for striatal synaptic depression, a change in CDI could contribute to age-dependent changes in striatal synaptic plasticity. Here we use whole cell voltage clamp to characterize CDI over developmental stages and across striatal regions. We find that CDI increases at the age of eye opening in the medial striatum but not the lateral striatum. The developmental increase in CDI mostly involves L-type channels, although calcium influx through non-L-type channels contributes to the CDI in both age groups. Agents that enhance protein kinase A (PKA) phosphorylation of calcium channels reduce the magnitude of CDI after eye opening, suggesting that the developmental increase in CDI may be related to a reduction in the phosphorylation state of the L-type calcium channel. These results are the first to show that modifications in striatal neuron properties correlate with changes to sensory input.

Indexed as

AgingAnimalsCalciumCalcium Channels, L-TypeCalcium SignalingCorpus StriatumEye MovementsFemaleIon Channel GatingMaleMiceMice, Inbred C57BLNeuronal PlasticityWakefulnessCalciumCalcium Channels, L-Typecalcium-dependent inactivationeye openingmedium spiny neuronstriatumvoltage-gated calcium channel

Identifiers

PMID25673739
PMCPMC4416611
OpenAlexW2094206269

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.