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David Bannerman

Name	David Bannerman
Ort	Oxford (Wirkungsort) Großbritannien
Akademischer Grad bzw. Titel	B.Sc.(Hons), Ph.D.
Variante	David M. Bannerman
Beziehung	The University of Edinburgh (Promotion) (1995) University of Oxford (1995-)
Datensatztyp	Person
GND-Nummer	1205824685
Datensatz-ID	1205824685
Beteiligt an alle anzeigen Rebound activation of 5-HT neurons following SSRI discontinuation Lasting dynamic effects of the psychedelic 2,5-dimethoxy-4-iodoamphetamine ((±)-DOI) on cognitive flexibility Voltage-independent GluN2A-type NMDA receptor Ca2+ signaling promotes audiogenic seizures, attentional and cognitive deficits in mice Oligodendrocyte dynamics dictate cognitive performance outcomes of working memory training in mice GRIN2A (NR2A): a gene contributing to glutamatergic involvement in schizophrenia Adult-born dentate granule cells promote hippocampal population sparsity Voltage-independent GluN2A-type NMDA receptor Ca2+ signaling promotes audiogenic seizures, attentional and cognitive deficits in mice Somatic accumulation of GluA1-AMPA receptors leads to selective cognitive impairments in mice Persistent microglial activation and synaptic loss with behavioral abnormalities in mouse offspring exposed to CASPR2-antibodies in utero

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David Bannerman

Rebound activation of 5-HT neurons following SSRI discontinuation

Lasting dynamic effects of the psychedelic 2,5-dimethoxy-4-iodoamphetamine ((±)-DOI) on cognitive flexibility

Voltage-independent GluN2A-type NMDA receptor Ca2+ signaling promotes audiogenic seizures, attentional and cognitive deficits in mice

Oligodendrocyte dynamics dictate cognitive performance outcomes of working memory training in mice

GRIN2A (NR2A): a gene contributing to glutamatergic involvement in schizophrenia

Adult-born dentate granule cells promote hippocampal population sparsity

Voltage-independent GluN2A-type NMDA receptor Ca2+ signaling promotes audiogenic seizures, attentional and cognitive deficits in mice

Somatic accumulation of GluA1-AMPA receptors leads to selective cognitive impairments in mice

Persistent microglial activation and synaptic loss with behavioral abnormalities in mouse offspring exposed to CASPR2-antibodies in utero