Evidence map›Paper›PMID 29217283›Full record

ReviewNeuropharmacology2018

Insulin-mediated synaptic plasticity in the CNS: Anatomical, functional and temporal contexts.

Carrie R Ferrario, Lawrence P Reagan

Open access · hybridAbstract readReview
In one paragraph

Review in Neuropharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 4% 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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 150 citations in OpenAlex.

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  18. GLP-1 selectively enhances tonic GABAFrontiers in cellular neuroscience · 2025
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20 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Carrie R FerrarioDepartment of Pharmacology, University of Michigan Medical School, Ann Arbor, MI 48109, USA. Electronic address: Ferrario@umich.edu.
Lawrence P ReaganDepartment of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine, Columbia, SC 29208, USA; W.J.B. Dorn VA Medical Center, Columbia, SC 29208, USA.
University of Michigan · USWm. Jennings Bryan Dorn VA Medical Center · US

Funding

Alterations in Motivated Behavior in Rodent Models of ObesityR01DK106188 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FERRARIO, CARRIE · 2015 to 2019
$1.9M
Effects of insulin on NAc excitatory transmission and motivation for foodR01DK115526 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FERRARIO, CARRIE · 2018 to 2020
$1.3M
Decreased CNS leptin activity in co-morbid depression and obesityI01BX001804 · VA · VETERANS HEALTH ADMINISTRATION · PI REAGAN, LAWRENCE P · 2013 to 2021
–
Immune basis for hippocampal cholinerginc deficits in pyridostigmine-treated ratsI01BX002664 · VA · VETERANS HEALTH ADMINISTRATION · PI LAWRENCE P REAGAN · 2015 to 2026
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BLRD VA I01 BX001804BLRD VA I01 BX002664NIDDK NIH HHS R01 DK106188NIDDK NIH HHS R01 DK115526
6 · The paper itself

Abstract

For decades the brain was erroneously considered an insulin insensitive organ. Although gaps in our knowledge base remain, conceptual frameworks are starting to emerge to provide insight into the mechanisms through which insulin facilitates critical brain functions like metabolism, cognition, and motivated behaviors. These diverse physiological and behavioral activities highlight the region-specific activities of insulin in the CNS; that is, there is an anatomical context to the activities of insulin in the CNS. Similarly, there is also a temporal context to the activities of insulin in the CNS. Indeed, brain insulin receptor activity can be conceptualized as a continuum in which insulin promotes neuroplasticity from development into adulthood where it is an integral part of healthy brain function. Unfortunately, brain insulin resistance likely contributes to neuroplasticity deficits in obesity and type 2 diabetes mellitus (T2DM). This neuroplasticity continuum can be conceptualized by the mechanisms through which insulin promotes cognitive function through its actions in brain regions like the hippocampus, as well as the ability of insulin to modulate motivated behaviors through actions in brain regions like the nucleus accumbens and the ventral tegmental area. Thus, the goals of this review are to highlight these anatomical, temporal, and functional contexts of insulin activity in these brain regions, and to identify potentially critical time points along this continuum where the transition from enhancement of neuroplasticity to impairment may take place. This article is part of the Special Issue entitled 'Metabolic Impairment as Risk Factors for Neurodegenerative Disorders.'

Indexed as

AnimalsCentral Nervous SystemHumansInsulinNeuronal PlasticityInsulinCognitionGlutamateHippocampusMotivationNucleus accumbensVentral tegmental area

Identifiers

PMID29217283
PMCPMC5988909
OpenAlexW2773526606

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.