Synaptogenesis in the photoreceptor terminal of the mouse retina

Blanks, Janet C.; Adinolfi, Anthony M.; Lolley, Richard N.

doi:10.1002/cne.901560107

Cited by 199 publications

(150 citation statements)

References 22 publications

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“…In contrast, HBCs make flat synapses with cone terminals outside of the invaginations (Haverkamp et al, 2003). In the mouse retina, the development of the invaginating synapses is established by P14 (Blanks et al, 1974). The early stages of synapse development appear to be genetically determined, although full maturation is thought to depend upon activity-dependent processes that occur after eye opening (Mumm et al, 2005).…”

Section: Role Of the α 1f Subunit Of The Vdcc In Synaptic Developmentmentioning

confidence: 99%

Thenob2mouse, a null mutation inCacna1f: Anatomical and functional abnormalities in the outer retina and their consequences on ganglion cell visual responses

et al. 2006

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Glutamate release from photoreceptor terminals is controlled by voltage-dependent calcium channels (VDCCs). In humans, mutations in the Cacna1f gene, encoding the α 1F subunit of VDCCs, underlie the incomplete form of X-linked congenital stationary night blindness (CSNB2). These mutations impair synaptic transmission from rod and cone photoreceptors to bipolar cells. Here, we report anatomical and functional characterizations of the retina in the nob2 (no b-wave 2) mouse, a naturally occurring mutant caused by a null mutation in Cacna1f. Not surprisingly, the b-waves of both the light-and dark-adapted electroretinogram are abnormal in nob2 mice. The outer plexiform layer (OPL) is disorganized, with extension of ectopic neurites through the outer nuclear layer that originate from rod bipolar and horizontal cells, but not from hyperpolarizing bipolar cells. These ectopic neurites continue to express mGluR6, which is frequently associated with profiles that label with the

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Section: Role Of the α 1f Subunit Of The Vdcc In Synaptic Developmentmentioning

confidence: 99%

Thenob2mouse, a null mutation inCacna1f: Anatomical and functional abnormalities in the outer retina and their consequences on ganglion cell visual responses

et al. 2006

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“…6C). When the HC's processes invaginate into cones at age P7 (Blanks et al, 1974;Rich et al, 1997;Sherry et al, 2003), a band of weak staining appeared in the OPL (Fig. 6D).…”

Section: Localization Of Nkcc1 In Developing Mouse Retinasmentioning

confidence: 99%

Spatial and temporal distribution patterns of Na-K-2Cl cotransporter in adult and developing mouse retinas

McKERNAN

Shen

2008

Vis Neurosci

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The Na-K-2Cl cotransporter (NKCC) is a Cl − uptake transporter that is responsible for maintaining a Cl − equilibrium potential positive to the resting potential in neurons. If NKCC is active, GABA and glycine can depolarize neurons. In view of the abundance of GABAergic and glycinergic synapses in retina, we undertook a series of studies using immunocytochemical techniques to determine the distribution of NKCC in retinas of both developing and adult mice. We found NKCC antibody (T4) labeling present in retinas from wild-type mice, but not in NKCC1-deficient mice, suggesting that the NKCC1 subtype is a major Cl − uptake transporter in mouse retina. Strong labeling of NKCC1 was present in horizontal cells and rod-bipolar dendrites in adult mice. Interestingly, we also found that a diffuse labeling pattern was present in photoreceptor terminals. However, NKCC1 was barely detectable in the inner retina of adult mice. Using an antibody against K-Cl cotransporter 2 (KCC2), we found that KCC2, a transporter that extrudes Cl − , was primarily expressed in the inner retina. The expression of NKCC1 in developing mouse retinas was studied from postnatal day (P) 1 to P21, NKCC1 labeling first appeared in the dendrites of horizontal and rod-bipolar cells as early as P7, followed by photoreceptor terminals between P10-P14; with expression gradually increasing concomitantly with the growth of synaptic terminals and dendrites throughout retinal development. In the inner retina, NKCC1 labeling was initially observed in the inner plexiform layer at P1, but labeling diminished after P5. The developmental increase in NKCC expression only occurred in the outer retina. Our results suggest that the distal synapses and synaptogenesis in mouse retinas undergo a unique process with a high intracellular Cl − presence due to NKCC1 expression.

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“…Such a mechanism, dependent on relative distance, ensures that a constant anatomical coverage at the pedicle will be maintained across variation in density. The change occurs after synaptic triads have formed (Olney, 1968;Blanks et al, 1974) and after photoreceptors become functional (Furukawa et al, 1999;Rohrer et al, 1999), suggesting that visual activity may drive this interaction.…”

Section: Colonization Of a Pedicle Is Dependent On The Relative Proximentioning

confidence: 99%

“…The OPL is not present when horizontal cells begin this transformation, forming at about the time that the horizontal processes coalesce within a distinct stratum. Because synaptogenesis between the pedicles and horizontal cells may be initiated slightly before this (Blanks et al, 1974;Rich et al, 1997), it remains possible that contact with the cones, even before their pedicles become stratified, triggers this morphological change, but their subsequent stratification at this depth would still require explanation. Some other signal may already presage the positioning of the OPL, because the horizontal cells settle at this depth within the neuroblast layer as early as the day of birth.…”

Section: Afferents Selectively Regulate the Dendritic Morphology Of Hmentioning

confidence: 99%

Afferents and Homotypic Neighbors Regulate Horizontal Cell Morphology, Connectivity, and Retinal Coverage

Reese¹,

Raven²,

Stagg³

2005

J. Neurosci.

101

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Horizontal cells are inhibitory interneurons with laterally oriented dendrites that overlap one another, contacting the pedicles of cone photoreceptors. Because of their regular spacing, the network of horizontal cells provides a uniform coverage of the retinal surface. The developmental processes establishing these network properties are undefined, but cell-intrinsic instructions and interactions with other cells have each been suggested to play a role. Here, we show that the intercellular spacing of horizontal cells is essentially independent of genetic background and is predicted by local density, suggesting that horizontal cell positioning is modulated by proximity to other horizontal cells. Dendritic field area compensates for this variation in intercellular spacing, maintaining constant dendritic coverage between strains. Functional dendritic overlap is achieved anatomically at the level of the pedicles, where horizontal cells interact with one another to establish their connectivity: the number of dendritic terminals contacting a pedicle changes, reciprocally, between neighboring horizontal cells during development based on their relative proximity to each pedicle. Cellular morphology is also shown to be regulated by the afferents themselves: afferent elimination before innervation does not alter dendritic field size nor stratification but compromises dendritic branching and prevents terminal formation. Afferent and homotypic interactions therefore generate the morphology, spacing, and connectivity of horizontal cells underlying their functional coverage of the retina.

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Synaptogenesis in the photoreceptor terminal of the mouse retina

Cited by 199 publications

References 22 publications

Thenob2mouse, a null mutation inCacna1f: Anatomical and functional abnormalities in the outer retina and their consequences on ganglion cell visual responses

Thenob2mouse, a null mutation inCacna1f: Anatomical and functional abnormalities in the outer retina and their consequences on ganglion cell visual responses

Spatial and temporal distribution patterns of Na-K-2Cl cotransporter in adult and developing mouse retinas

Afferents and Homotypic Neighbors Regulate Horizontal Cell Morphology, Connectivity, and Retinal Coverage

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