Preferencje help
Polish version English version Język
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 4

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
1

Autism as a synaptopathy: behavioral studies in genetic mouse models

100%
Wohr M.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
Autism is a neurodevelopmental disorder characterized by abnormal reciprocal social interactions, communication deficits, and repetitive, stereotyped patterns of behaviors. While the causes of autism remain unknown, the high concordance between monozygotic twins supports a strong genetic component. Genome-wide and pathway-based association studies led to the identification of several susceptibility genes for autism, many of which code for proteins involved in synapse formation and function, including the NLGN and SHANK genes families. NLGN genes code for postsynaptic cell adhesion molecules, Neuroligins, that bridge the synaptic cleft by forming heterophilic complexes with their presynaptic binding partners, Neurexins. SHANK genes code for scaffolding proteins located in the postsynaptic density of excitatory synapses. To test the hypothesis that mutations in NLGN and SHANK gene family members contribute to the symptoms of autism, we evaluated various mutant models for behavioral phenotypes with relevance to autism, focusing on social communication, namely ultrasonic vocalizations and the deposition of scent marks, which appear to be two major modes of mouse communication. Results indicate that mice lacking Neuroligin or Shank family members display an autism-like behavioral phenotype, including social communication deficits. Often, these deficits are paralleled by cognitive dysfunctions, such as impaired object recognition. Our studies support the notion that autism is a synaptopathy.
2

Ultrasonic communication in rodents: genes, brain and behavior

100%
Wohr M.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Mice and rats emit distinct types of ultrasonic vocalizations (USVs), which serve as situation-dependent affective signals. Recently, it was demonstrated that aversive 22-kHz-USVs and appetitive 50-kHz-USVs induce call-specific behavioral responses in the receiver. While 22-kHz-USVs induce freezing behavior, indicating an alarm function, 50-kHz-USVs induce social approach behavior, supporting the notion that they serve as social contact calls. The opposite behavioral responses are paralleled by distinct patterns of brain activation. While 22-kHz-USVs induce activation in amygdala and periaqueductal gray, 50-kHz-USVs are followed by activation in the nucleus accumbens. Social approach behavior in response to 50-kHz-USVs is regulated by the endogenous opioid system. Enhanced social approach behavior was found in morphine treated rats, whereas naloxone treatment caused its reduction. Social approach in response to 50-kHz USVs further depends on social interactions during adolescence as no preference towards 50-kHz-USVs was found in rats exposed to long-term post-weaning social isolation, highlighting the importance of social experience during adolescence for affiliative behavior. Measuring USV production and behavioral responses to USVs provides therefore a unique tool to study rodent communication. This is particularly relevant for rodent models of autism as delayed language and poor communication skills are fundamental to the diagnosis of autism. Candidate genes for autism include the SHANK family of synaptic scaffolding proteins. When tested for isolation-induced USVs as pups, Shank1 null mutants emitted fewer USVs as compared to wildtype littermates; and as adults in response to female urine, the USV production by Shank1 null mutant males was characterized by an unusual time pattern and unresponsiveness to social experience. These data support the relevance of USVs for rodent models of neuropsychiatric disorders characterized by social and communication deficits.
3

Ultrasonic communication in rodents

100%
Wohr M.
Acta Neurobiologiae Experimentalis
|
2014
|
tom 74
|
nr 3
Rats emit distinct types of ultrasonic vocalizations (USV), which serve as situation-dependent affective signals with important communicative functions. Low-frequency 22-kHz USV typically occur in aversive situations, such as social defeat or predator exposure, whereas high-frequency 50-kHz USV can be observed in appetitive situations, like social play in juveniles or mating in adults. Importantly, the two main USV types serve distinct communicative functions and induce call-specific behavioral responses in the receiver. While 22-kHz USV probably serve as alarm calls and induce freezing behavior in the receiver, 50-kHz USV lead to social approach behavior, indicating a pro-social, affiliative communicative function. The opposite behavioral responses are paralleled by distinct patterns of brain activation. Freezing elicited by 22-kHz USV is accompanied by increased neuronal activity in brain areas regulating fear and anxiety, such as the amygdala. In contrast, social approach behavior evoked by 50-kHz USV is paralleled by reduced activity levels in the amygdala, but enhanced activity and dopamine release in the nucleus accumbens, a brain area implicated in reward processing. Together, this indicates that affective USV might be an important tool for studying the neurobiology underlying socio-affective communication, which is particularly relevant for rodent models of neuropsychiatric disorders characterized by social and communication deficits, such as autism and schizophrenia.
4

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

39%
Sungur A. O., Lackinger M., Stemmler L., Grosse R., Schwarting R., Schratt G., Wohr M.
Acta Neurobiologiae Experimentalis
|
2019
|
tom 79
|
nr Suppl.1
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.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.