Evidence map›Paper›PMID 26365505›Full record

ArticleBrain structure & function2016

Structure and function of the amygdaloid NPY system: NPY Y2 receptors regulate excitatory and inhibitory synaptic transmission in the centromedial amygdala.

J Wood, D Verma, G Lach, P Bonaventure, H Herzog, G Sperk, R O Tasan

Open access · hybridAbstract read
In one paragraph

Article in Brain structure & function, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

32 citing papers in PubMed, 59 citations in OpenAlex.

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  20. The role of BDNF methylation and ValHuman brain mapping · 2020
    Article
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 5 institutions in 5 countries.

J WoodDepartment of Pharmacology, Medical University Innsbruck, Peter-Mayr-Strasse 1a, 6020, Innsbruck, Austria.
D VermaDepartment of Pharmacology, Medical University Innsbruck, Peter-Mayr-Strasse 1a, 6020, Innsbruck, Austria.
G LachDepartment of Pharmacology, Medical University Innsbruck, Peter-Mayr-Strasse 1a, 6020, Innsbruck, Austria.
P BonaventureJanssen Research & Development, LLC, San Diego, CA, USA.
H HerzogNeuroscience Division, Garvan Institute of Medical Research, Darlinghurst, Sydney, NSW, 2010, Australia.
G SperkDepartment of Pharmacology, Medical University Innsbruck, Peter-Mayr-Strasse 1a, 6020, Innsbruck, Austria.
R O TasanDepartment of Pharmacology, Medical University Innsbruck, Peter-Mayr-Strasse 1a, 6020, Innsbruck, Austria. ramon.tasan@i-med.ac.at.
Innsbruck Medical University · ATGarvan Institute of Medical Research · AUJanssen (United States) · USMinistry of Education · BRUniversity of Münster · DE

Funding

Austrian Science Fund FWF M 1783Austrian Science Fund FWF P 22830
6 · The paper itself

Abstract

The amygdala is essential for generating emotional-affective behaviors. It consists of several nuclei with highly selective, elaborate functions. In particular, the central extended amygdala, consisting of the central amygdala (CEA) and the bed nucleus of the stria terminalis (BNST) is an essential component actively controlling efferent connections to downstream effectors like hypothalamus and brain stem. Both, CEA and BNST contain high amounts of different neuropeptides that significantly contribute to synaptic transmission. Among these, neuropeptide Y (NPY) has emerged as an important anxiolytic and fear-reducing neuromodulator. Here, we characterized the expression, connectivity and electrophysiological function of NPY and Y2 receptors within the CEA. We identified several NPY-expressing neuronal populations, including somatostatin- and calretinin-expressing neurons. Furthermore, in the main intercalated nucleus, NPY is expressed primarily in dopamine D1 receptor-expressing neurons but also in interspersed somatostatin-expressing neurons. Interestingly, NPY neurons did not co-localize with the Y2 receptor. Retrograde tract tracing experiments revealed that NPY neurons reciprocally connect the CEA and BNST. Functionally, the Y2 receptor agonist PYY3-36, reduced both, inhibitory as well as excitatory synaptic transmission in the centromedial amygdala (CEm). However, we also provide evidence that lack of NPY or Y2 receptors results in increased GABA release specifically at inhibitory synapses in the CEm. Taken together, our findings suggest that NPY expressed by distinct populations of neurons can modulate afferent and efferent projections of the CEA via presynaptic Y2 receptors located at inhibitory and excitatory synapses.

Indexed as

Excitatory Postsynaptic PotentialsInhibitory Postsynaptic PotentialsAmygdalaAnimalsCalbindin 2Central Amygdaloid NucleusMaleMiceMice, Inbred C57BLNeuronsNeuropeptide YReceptors, Dopamine D1Receptors, Neuropeptide YSeptal NucleiSomatostatinCalb2 protein, mouseCalbindin 2Neuropeptide Yneuropeptide Y2 receptorReceptors, Dopamine D1Receptors, Neuropeptide YSomatostatinCentral amygdalaDopamine D1 receptorIntercalated neuronsNeuropeptide YNPYY2 receptor

Identifiers

PMID26365505
PMCPMC4696156
OpenAlexW1903951249

What OpenQuestion holds

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LicenceCC BY
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.