Evidence map›Paper›PMID 24554785›Full record

ArticleJournal of neurophysiology2014

In vivo and in vitro analyses of amygdalar function reveal a role for copper.

E D Gaier, R M Rodriguiz, J Zhou, M Ralle, W C Wetsel, B A Eipper, R E Mains

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Identifying roles for peptidergic signaling in mice.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  7. Article
  8. Article
  9. Article
  10. Copper signaling in the brain and beyond.The Journal of biological chemistry · 2018
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Copper: from neurotransmission to neuroproteostasis.Frontiers in aging neuroscience · 2014
    Review
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

7 authors at 4 institutions in 1 country.

E D GaierNeuroscience Department, University of Connecticut Health Center, Farmington, Connecticut;
R M RodriguizDepartment of Psychiatry and Behavioral Sciences, Mouse Behavioral and Neuroendocrine Analysis Core Facility, Duke University Medical Center, Durham, North Carolina;
J ZhouDepartment of Psychiatry and Behavioral Sciences, Mouse Behavioral and Neuroendocrine Analysis Core Facility, Duke University Medical Center, Durham, North Carolina;
M RalleDepartment of Biochemistry and Molecular Biology, Oregon Health & Science University, Portland, Oregon;
W C WetselDepartment of Psychiatry and Behavioral Sciences, Mouse Behavioral and Neuroendocrine Analysis Core Facility, Duke University Medical Center, Durham, North Carolina; Department of Neurobiology, Duke University Medical Center, Durham, North Carolina; and Department of Cell Biology, Duke University Medical Center, Durham, North Carolina.
B A EipperNeuroscience Department, University of Connecticut Health Center, Farmington, Connecticut;
R E MainsNeuroscience Department, University of Connecticut Health Center, Farmington, Connecticut; mains@uchc.edu.
UConn Health · USDuke Medical Center · USDuke University Hospital · USOregon Health & Science University · US

Funding

Recruitment and Assessment Core Patient RecruitmentP50MH060451 · NIMH · DUKE UNIVERSITY · PI MCCARTHY, GREGORY E · 2001 to 2010
$22.3M
BIOCHEMISTRY AND PHYSIOLOGY OF PEPTIDE AMIDATIONR01DK032949 · NIDDK · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI EIPPER, ELIZABETH ANNE, KING, STEPHEN M · 1986 to 2017
$6.4M
BIOCHEMISTRY AND PHYSIOLOGY OF PEPTIDE AMIDATIONR37DK032949 · NIDDK · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI EIPPER, ELIZABETH A · 1989 to 2004
$2.8M
The Role of Hepatic Copper Accumulation in Wilson DiseaseR01GM090016 · NIGMS · OREGON HEALTH & SCIENCE UNIVERSITY · PI RALLE, MARTINA · 2010 to 2014
$1.4M
Neuroscience Training at University of Connecticut Health CenterT32NS041224 · NINDS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI EIPPER, ELIZABETH ANNE · 2001 to 2010
$1.3M
ICP-MS to Measure Elemental ConcentrationsS10RR025512 · NCRR · OREGON HEALTH & SCIENCE UNIVERSITY · PI RALLE, MARTINA · 2009 to 2009
$168k
BIOCHEMISTRY AND PHYSIOLOGY OF PEPTIDE AMIDATIONR56DK032949 · NIDDK · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI EIPPER, ELIZABETH A · 2005 to 2005
$104k
NCRR NIH HHS S10 RR025512NIDDK NIH HHS DK-32949NIDDK NIH HHS R01 DK032949NIGMS NIH HHS R01 GM090016NIMH NIH HHS MH-60451NINDS NIH HHS NS-41224
6 · The paper itself

Abstract

Mice with a single copy of the peptide amidating monooxygenase (Pam) gene (PAM(+/-)) are impaired in contextual and cued fear conditioning. These abnormalities coincide with deficient long-term potentiation (LTP) at excitatory thalamic afferent synapses onto pyramidal neurons in the lateral amygdala. Slice recordings from PAM(+/-) mice identified an increase in GABAergic tone (Gaier ED, Rodriguiz RM, Ma XM, Sivaramakrishnan S, Bousquet-Moore D, Wetsel WC, Eipper BA, Mains RE. J Neurosci 30: 13656-13669, 2010). Biochemical data indicate a tissue-specific deficit in Cu content in the amygdala; amygdalar expression of Atox-1 and Atp7a, essential for transport of Cu into the secretory pathway, is reduced in PAM(+/-) mice. When PAM(+/-) mice were fed a diet supplemented with Cu, the impairments in fear conditioning were reversed, and LTP was normalized in amygdala slice recordings. A role for endogenous Cu in amygdalar LTP was established by the inhibitory effect of a brief incubation of wild-type slices with bathocuproine disulfonate, a highly selective, cell-impermeant Cu chelator. Interestingly, bath-applied CuSO₄ had no effect on excitatory currents but reversibly potentiated the disynaptic inhibitory current. Bath-applied CuSO₄ was sufficient to potentiate wild-type amygdala afferent synapses. The ability of dietary Cu to affect signaling in pathways that govern fear-based behaviors supports an essential physiological role for Cu in amygdalar function at both the synaptic and behavioral levels. This work is relevant to neurological and psychiatric disorders in which disturbed Cu homeostasis could contribute to altered synaptic transmission, including Wilson's, Menkes, Alzheimer's, and prion-related diseases.

Indexed as

AmygdalaAnimalsConditioning, PsychologicalCopperDietFearFemaleHippocampusLong-Term PotentiationMaleMice, Inbred C57BLMice, TransgenicMixed Function OxygenasesMultienzyme ComplexesNeural InhibitionNeuronal PlasticityCopperMixed Function OxygenasesMultienzyme Complexespeptidylglycine monooxygenasefearGABAlearning and memorypeptidylglycine alpha-amidating monooxygenasesynaptic plasticity

Identifiers

PMID24554785
PMCPMC4044343
OpenAlexW2015726495

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.