Evidence map›Paper›PMID 28087816›Full record

ArticlePhysiological reports2017

Acetazolamide potentiates the afferent drive to prefrontal cortex in vivo.

Lezio S Bueno-Junior, Rafael N Ruggiero, Matheus T Rossignoli, Elaine A Del Bel, Joao P Leite, Osvaldo D Uchitel

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2017. 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
0.5field-weighted citation impact, top 44% 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, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. The role of carbonic anhydrases in extinction of contextual fear memory.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  4. Review
  5. 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

6 authors at 4 institutions in 3 countries.

Lezio S Bueno-JuniorDepartment of Neuroscience and Behavioral Sciences, Ribeirao Preto Medical School University of Sao Paulo, Ribeirao Preto, Brazil.
Rafael N RuggieroDepartment of Neuroscience and Behavioral Sciences, Ribeirao Preto Medical School University of Sao Paulo, Ribeirao Preto, Brazil.
Matheus T RossignoliDepartment of Neuroscience and Behavioral Sciences, Ribeirao Preto Medical School University of Sao Paulo, Ribeirao Preto, Brazil.
Elaine A Del BelDepartment of Morphology, Physiology and Stomatology, Dentistry School of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, Brazil.
Joao P LeiteDepartment of Neuroscience and Behavioral Sciences, Ribeirao Preto Medical School University of Sao Paulo, Ribeirao Preto, Brazil jpleite@fmrp.usp.br.
Osvaldo D UchitelDepartment of Physiology, Molecular and Cell Biology, Institute of Physiology Molecular Biology and Neuroscience University of Buenos Aires, Buenos Aires, Argentina.
Clinics Hospital of Ribeirão Preto · BRUniversidade de Ribeirão Preto · BRUniversidade de São Paulo · BRUniversity of Buenos Aires · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The knowledge on real-time neurophysiological effects of acetazolamide is still far behind the wide clinical use of this drug. Acetazolamide - a carbonic anhydrase inhibitor - has been shown to affect the neuromuscular transmission, implying a pH-mediated influence on the central synaptic transmission. To start filling such a gap, we chose a central substrate: hippocampal-prefrontal cortical projections; and a synaptic phenomenon: paired-pulse facilitation (a form of synaptic plasticity) to probe this drug's effects on interareal brain communication in chronically implanted rats. We observed that systemic acetazolamide potentiates the hippocampal-prefrontal paired-pulse facilitation. In addition to this field electrophysiology data, we found that acetazolamide exerts a net inhibitory effect on prefrontal cortical single-unit firing. We propose that systemic acetazolamide reduces the basal neuronal activity of the prefrontal cortex, whereas increasing the afferent drive it receives from the hippocampus. In addition to being relevant to the clinical and side effects of acetazolamide, these results suggest that exogenous pH regulation can have diverse impacts on afferent signaling across the neocortex.

Indexed as

AcetazolamideAnimalsCarbonic Anhydrase InhibitorsCarbonic AnhydrasesElectric StimulationHippocampusMaleNeuronal PlasticityNeurons, AfferentPrefrontal CortexRatsRats, WistarSynaptic TransmissionAcetazolamideCarbonic Anhydrase InhibitorsCarbonic AnhydrasesCarbonic anhydrasehippocampusprefrontal cortexsingle‐unit activitysynaptic plasticity

Identifiers

PMID28087816
PMCPMC5256155
OpenAlexW2577173091

What OpenQuestion holds

Textmetadata
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.