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The nob2 mouse, a null mutation in Cacna1f: Anatomical and functional abnormalities in the outer ret...

The nob2 mouse, a null mutation in Cacna1f: Anatomical and functional abnormalities in the outer ret...

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2831086

The nob2 mouse, a null mutation in Cacna1f: Anatomical and functional abnormalities in the outer retina and their consequences on ganglion cell visual responses

About this item

Full title

The nob2 mouse, a null mutation in Cacna1f: Anatomical and functional abnormalities in the outer retina and their consequences on ganglion cell visual responses

Publisher

New York, USA: Cambridge University Press

Journal title

Visual neuroscience, 2006-01, Vol.23 (1), p.11-24

Language

English

Formats

Publication information

Publisher

New York, USA: Cambridge University Press

More information

Scope and Contents

Contents

Glutamate release from photoreceptor terminals is controlled by
voltage-dependent calcium channels (VDCCs). In humans, mutations in the
Cacna1f gene, encoding the α1F subunit of VDCCs,
underlie the incomplete form of X-linked congenital stationary night
blindness (CSNB2). These mutations impair synaptic transmission from rod
and cone...

Alternative Titles

Full title

The nob2 mouse, a null mutation in Cacna1f: Anatomical and functional abnormalities in the outer retina and their consequences on ganglion cell visual responses

Identifiers

Primary Identifiers

Record Identifier

TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2831086

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2831086

Other Identifiers

ISSN

0952-5238

E-ISSN

1469-8714

DOI

10.1017/S095252380623102X

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