Nowa wersja platformy, zawierająca wyłącznie zasoby pełnotekstowe, jest już dostępna.
Przejdź na https://bibliotekanauki.pl

PL EN


Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników
2019 | 79 | Suppl.1 |
Tytuł artykułu

Mice with a deletion of the mammal-specific microRNA 379‑410 cluster display altered ultrasonic communication

Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
INTRODUCTION: microRNAs (miRNAs) represent a group of small, noncoding RNA molecules that play a major role in the posttranscriptional regulation of gene expression. Members of a large placental mammal‑specific miRNA cluster, miR379‑410 have been implicated in a variety of neurodevelopmental disorders. Recently, we have shown that deletion of this cluster in mice leads to hypersocial behavior and increased emission of ultrasonic vocalizations (USV), which is accompanied by altered excitatory synaptic transmission and exaggerated expression of ionotropic glutamate receptor complexes in the hippocampus. To further investigate the contribution of the miR379‑410 cluster to communication deficits present in neurodevelopmental disorders, here we performed a detailed analysis of acoustic features of isolation-induced pup USV and juvenile USV. AIM(S): We aimed to investigate mania-like elevated drive by studying effects of the psychostimulant d-amphetamine (AMPH) on locomotor activity. METHOD(S): To measure isolation-induced pup USV, mice were isolated from the mother and littermates for 10min on postnatal day (PND) 3, 6, 9, and 12. Juvenile reciprocal social interaction was tested on PND 23. Mania-like elevated drive was investigated by treating mice with 2.5mg/kg AMPH. RESULTS: In addition to increased call rate, mouse pups lacking the miR379‑410 cluster displayed increased peak amplitude and frequency modulation. Juvenile knockout pairs spent significantly more time interacting with each other and emitted more pro-social USV as compared to wildtype pairs. Mutant as well as wildtype mice reacted to AMPH treatment by a significant increase in locomotor activity, and no genotype differences were evident, indicating lack of mania-like behavior in miR379‑410 mutants. CONCLUSIONS: Taken together, the present study confirms and extends previous findings, showing that deletion of the miR379‑410 cluster leads to altered communication without affecting psychostimulant-induced hyperactivity.
Słowa kluczowe
Wydawca
-
Rocznik
Tom
79
Numer
Opis fizyczny
p.LXIX-LXX
Twórcy
autor
  • Department of Behavioral Neuroscience, Experimental and Biological Psychology, Philipps University Marburg, Marburg, Germany
  • Center for Mind, Brain and Behavior (CMBB), Philipps University Marburg, Marburg, Germany
autor
  • Institute of Physiological Chemistry, Philipps University Marburg, Marburg, Germany
autor
  • Department of Behavioral Neuroscience, Experimental and Biological Psychology, Philipps University Marburg, Marburg, Germany
autor
  • Department of Behavioral Neuroscience, Experimental and Biological Psychology, Philipps University Marburg, Marburg, Germany
  • Institute of Physiological Chemistry, Philipps University Marburg, Marburg, Germany
  • Department of Behavioral Neuroscience, Experimental and Biological Psychology, Philipps University Marburg, Marburg, Germany
  • Center for Mind, Brain and Behavior (CMBB), Philipps University Marburg, Marburg, Germany
autor
  • Institute of Physiological Chemistry, Philipps University Marburg, Marburg, Germany
  • Laboratory of Systems Neuroscience, Department of Health Science and Technology, Institute for Neuroscience, Swiss Federal Institute of Technology, Zurich, Switzerland
autor
  • Department of Behavioral Neuroscience, Experimental and Biological Psychology, Philipps University Marburg, Marburg, Germany
  • Center for Mind, Brain and Behavior (CMBB), Philipps University Marburg, Marburg, Germany
Bibliografia
Typ dokumentu
Bibliografia
Identyfikatory
Identyfikator YADDA
bwmeta1.element.agro-dfa7bea9-ff83-42b8-86af-78464f3e59e1
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.