The anti‐epileptic actions of neuropeptide Y in the hippocampus are mediated by Y₂ and not Y₅ receptors

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none

Consensus categories

none

Domain

Candidate signal: noneConsensus signal: none

Study design

Candidate signal: Bench or experimentalConsensus signal: Bench or experimental

Genre

Candidate signal: EmpiricalConsensus signal: Empirical

Teacher disagreement score

0.138

Threshold uncertainty score

0.856

Validation status

machine_predicted_unvalidated · codex-gemma-dda1882f352a

Codex and Gemma teacher scores by category

Machine scores (provisional)

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Teacher spread

0.216 · how far apart the two teachers sit on this one work

Validation status

score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Abstract

Neuropeptide Y (NPY) potently inhibits glutamate release and seizure activity in rodent hippocampus in vitro and in vivo, but the nature of the receptor(s) mediating this action is controversial. In hippocampal slices from rats and several wild-type mice, a Y2-preferring agonist mimicked, and the Y2-specific antagonist BIIE0246 blocked, the NPY-mediated inhibition both of glutamatergic transmission and of epileptiform discharges in two different slice models of temporal lobe epilepsy, stimulus train-induced bursting (STIB) and 0-Mg2+ bursting. Whereas Y5 receptor-preferring agonists had small but significant effects in vitro, they were blocked by BIIE0246, and a Y5 receptor-specific antagonist did not affect responses to any agonist tested in any preparation. In slices from mice, NPY was without effect on evoked potentials or in either of the two slice seizure models. In vivo, intrahippocampal injections of Y2- or Y5-preferring agonists inhibited seizures caused by intrahippocampal kainate, but again the Y5 agonist effects were insensitive to a Y5 antagonist. Neither Y2- nor Y5-preferring agonists affected kainate seizures in mice. A Y5-specific antagonist did not displace the binding of two different NPY ligands in WT or mice, whereas all NPY binding was eliminated in the mouse. Thus, we show that Y2 receptors alone mediate all the anti-excitatory actions of NPY seen in the hippocampus, whereas our findings do not support a role for Y5 receptors either in vitro or in vivo. The results suggest that agonists targeting the Y2 receptor may be useful anticonvulsants.

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The record

Venue

European Journal of Neuroscience

Topic

Neuropeptides and Animal Physiology

Field

Neuroscience

Canadian institutions

Université du Québec à MontréalUniversité de MontréalUniversity of Alberta

Funders

not available

Keywords

Kainate receptorNeuropeptide Y receptorAgonistHippocampal formationAntagonistReceptorChemistryKainic acidGlutamate receptorGlutamatergicExcitatory postsynaptic potentialNeuropeptideInternal medicineEndocrinologyNeuroscienceBiologyAMPA receptorMedicineBiochemistry

Has abstract in OpenAlex

yes

API

/api/v1/works/W1933062462