Mirror-symmetrical populations of wide-field amacrine cells of the macaque monkey retina

2008 ◽  
Vol 508 (1) ◽  
pp. 13-27 ◽  
Author(s):  
Sriparna Majumdar ◽  
Heinz Wässle ◽  
Patricia R. Jusuf ◽  
Silke Haverkamp
Keyword(s):  
Amacrine Cells ◽  
Macaque Monkey ◽  
Wide Field

scholarly journals Neural sensitization improves encoding fidelity in the primate retina

2018 ◽  
Author(s):  
Todd R. Appleby ◽  
Michael B. Manookin
Keyword(s):  
Visual Processing ◽  
Visual Information ◽  
Amacrine Cells ◽  
Macaque Monkey ◽  
Bipolar Cells ◽  
Wide Field ◽  
Plasticity Mechanism ◽  
The Face ◽  
Neural Sensitization ◽  
Sensory Encoding

ABSTRACTAn animal’s motion through the environment can induce large and frequent fluctuations in light intensity on the retina. These fluctuations pose a major challenge to neural circuits tasked with encoding visual information, as they can cause cells to adapt and lose sensitivity. Here, we report that sensitization, a short-term plasticity mechanism, solves this difficult computational problem by maintaining neuronal sensitivity in the face of these fluctuations. The numerically dominant output pathway in the macaque monkey retina, the midget (parvocellular-projecting) pathway, undergoes sensitization under specific conditions, including simulated eye movements. Sensitization is present in the excitatory synaptic inputs from midget bipolar cells and is mediated by presynaptic disinhibition from wide-field amacrine cells. Direct physiological recordings and a computational model indicate that sensitization in the midget pathway supports accurate sensory encoding and prevents a loss of responsiveness during dynamic visual processing.

Amacrine-to-amacrine cell inhibition: Spatiotemporal properties of GABA and glycine pathways

2011 ◽  
Vol 28 (3) ◽  
pp. 193-204 ◽  
Author(s):  
XIN CHEN ◽  
HAIN ANN HSUEH ◽  
FRANK S. WERBLIN
Keyword(s):  
Amacrine Cell ◽  
Ganglion Cells ◽  
Amacrine Cells ◽  
Peak Level ◽  
Wide Field ◽  
Gabaergic Inhibition ◽  
Onset Latency ◽  
Temporal Properties ◽  
Glycinergic Inhibition ◽  
Cell Inhibition

AbstractWe measured the spatial and temporal properties of GABAergic and glycinergic inhibition to amacrine cells in the whole-mount rabbit retina. The amacrine cells were parsed into two morphological classes: narrow-field cells with processes spreading less than 200 μm and wide-field cells with processes extending more than 300 μm. The inhibition was also parsed into two types: sustained glycine and transient GABA. Narrow-field amacrine cells receive 1) very transient GABAergic inhibition with a fast onset latency of 140 ± 16 ms decaying to 30% of the peak level within 208 ± 27 ms elicited broadly over a lateral distance of up to 1500 μm and 2) sustained glycinergic inhibition with a medium onset latency of 286 ± 23 ms that was elicited over a spatial area often broader than the processes of the narrow-field amacrine cells. Wide-field amacrine cells received sustained glycinergic inhibition but no broad transient GABAergic inhibition. Surprisingly, neither of these amacrine cell classes received sustained local GABAergic inhibition, commonly found in an earlier study of ganglion cells.

Neurofibrillar long-range amacrine cells in mammalian retinae

1988 ◽  
Vol 235 (1280) ◽  
pp. 203-219 ◽  
Keyword(s):  
Ganglion Cell ◽  
Long Range ◽  
Plexiform Layer ◽  
Amacrine Cells ◽  
Wide Field ◽  
Inner Plexiform Layer ◽  
Distinct Population ◽  
Effective Coverage ◽  
Dendritic Field ◽  
Cell Layers

A distinct population of wide-field, unistratified amacrine cells are shown to be selectively stained by using neurofibrillar methods in rabbit and cat retinae. Their cell bodies may be located in the inner nuclear, inner plexiform or ganglion cell layers and they branch predominantly in stratum 2 of the inner plexiform layer. Characteristically, each cell has two or more long-range distal processes which extend for 2-3 mm beyond a more symmetrical, proximal dendritic field of 0.6-0.8 mm diameter. Although the neurofibrillar long-range amacrines account for less than 1 amacrine in 500, they achieve effective coverage of the retina by both the proximal and distal dendrites.

scholarly journals Wide-field diffuse amacrine cells in the monkey retina contain immunoreactive Cocaine- and Amphetamine-Regulated Transcript (CART)

Peptides ◽  
2016 ◽  
Vol 84 ◽  
pp. 22-35 ◽  
Author(s):  
Ye Long ◽  
Andrea S. Bordt ◽  
Weiley S. Liu ◽  
Elizabeth P. Davis ◽  
Stephen J. Lee ◽  
...  
Keyword(s):  
Amacrine Cells ◽  
Wide Field

Physiology of the A1 amacrine: A spiking, axon-bearing interneuron of the macaque monkey retina

1997 ◽  
Vol 14 (3) ◽  
pp. 507-522 ◽  
Author(s):  
Donna K. Stafford ◽  
Dennis M. Dacey
Keyword(s):  
Receptive Field ◽  
Amacrine Cell ◽  
Dendritic Tree ◽  
Amacrine Cells ◽  
Cell Types ◽  
Macaque Monkey ◽  
Cell Type ◽  
Slow Potential ◽  
Spike Discharge

AbstractWe characterized the light response, morphology, and receptive-field structure of a distinctive amacrine cell type (Dacey, 1989), termed here the Al amacrine, by applying intracellular recording and staining methods to the macaque monkey retina in vitro. A1 cells show two morphologically distinct components: a highly branched and spiny dendritic tree, and a more sparsely branched axon-like tree that arises from one or more hillock-like structures near the soma and extends for several millimeters beyond the dendritic tree. Intracellular injection of Neurobiotin reveals an extensive and complex pattern of tracer coupling to neighboring A1 amacrine cells, to two other amacrine cell types, and to a single ganglion cell type. The A1 amacrine is an ON-OFF cell, showing a large (10–20 mV) transient depolarization at both onset and offset of a photopic, luminance modulated stimulus. A burst of fast, large-amplitude (Σ60 mV) action potentials is associated with the depolarizations at both the ON and OFF phase of the response. No evidence was found for an inhibitory receptive-field surround. The spatial extent of the ON-OFF response was mapped by measuring the strength of the spike discharge and/or the amplitude of the depolarizing slow potential as a function of the position of a bar or spot of light within the receptive field. Receptive fields derived from the slow potential and associated spike discharge corresponded in size and shape. Thus, the amplitude of the slow potential above spike threshold was well encoded as spike frequency. The diameter of the receptive field determined from the spike discharge was Σ10% larger than the spiny dendritic field. The correspondence in size between the spiking receptive field and the spiny dendritic tree suggests that light driven signals are conducted to the soma from the dendritic tree but not from the axon-like arbor. The function of the axon-like component is unknown but we speculate that it serves a classical output function, transmitting spikes distally from initiation sites near the soma.

scholarly journals Inputs Underlying the ON-OFF Light Responses of Type 2 Wide-Field Amacrine Cells in TH::GFP Mice

2011 ◽  
Vol 31 (13) ◽  
pp. 4780-4791 ◽  
Author(s):  
G. C. Knop ◽  
A. Feigenspan ◽  
R. Weiler ◽  
K. Dedek
Keyword(s):  
Amacrine Cells ◽  
Wide Field ◽  
Light Responses

scholarly journals Ldb1 and Rnf12-dependent regulation of Lhx2 controls the relative balance between neurogenesis and gliogenesis in retina

2017 ◽  
Author(s):  
Jimmy de Melo ◽  
Anand Venkataraman ◽  
Brian S. Clark ◽  
Cristina Zibetti ◽  
Seth Blackshaw
Keyword(s):  
Transcription Factor ◽  
Molecular Mechanisms ◽  
Critical Role ◽  
Amacrine Cells ◽  
Negative Regulator ◽  
Wide Field ◽  
Muller Glia ◽  
Müller Glia ◽  
Retinal Neurons ◽  
Bhlh Factors

AbstractPrecise control of the relative ratio of retinal neurons and glia generated during development is essential for visual function. We show that Lhx2, which encodes a LIM-homeodomain transcription factor essential for specification and differentiation of retinal Müller glia, also plays a critical role in the development of retinal neurons. Overexpression of Lhx2, and its transcriptional coactivator Ldb1, triggers cell cycle exit and inhibits both Notch signaling and retinal gliogenesis. Lhx2/Ldb1 overexpression also induced the formation of wide-field amacrine cells (wfACs). In contrast Rnf12, which encodes a negative regulator of LDB1, is necessary for the initiation of retinal gliogenesis. We also show that LHX2 protein binds upstream of multiple neurogenic bHLH factors including Ascl1 and Neurog2, which are necessary for suppression of gliogenesis and wfAC formation respectively, and activates their expression. Finally, we demonstrate that the relative level of the LHX2-LDB1 complex in the retina decreases in tandem with the onset of gliogenesis. These findings show that control of Lhx2 function by Ldb1 and Rnf12 acts as a molecular mechanism underpinning the coordinated differentiation of neurons and Müller glia in postnatal retina.Significance StatementThe molecular mechanisms that control the ratio neurons and glia that are generated by neuronal progenitors remain unclear. Here we show that Lhx2, a transcription factor essential for retinal gliogenesis, also controls development of retinal neurons. The Lhx2 coactivator Ldb1 promotes Lhx2-dependent neurogenesis, while the Lhx2 corepressor Rnf12 is necessary and sufficient for retinal gliogenesis. Furthermore, Lhx2 directly regulates expression of bHLH factors that promote neural development, which are necessary for Lhx2-dependent neurogenesis. Finally, we show that levels of the LHX2-LDB1 complex, which activates transcription, drop as gliogenesis begins. Dynamic regulation of Lhx2 activity by Ldb1 and Rnf12 thus controls the relative levels of retinal neurogenesis and gliogenesis, and may have similar functions elsewhere in the developing nervous system.

scholarly journals Analysis of local and wide-field movements in the superior temporal visual areas of the macaque monkey

1986 ◽  
Vol 6 (1) ◽  
pp. 134-144 ◽  
Author(s):  
K Tanaka ◽  
K Hikosaka ◽  
H Saito ◽  
M Yukie ◽  
Y Fukada ◽  
...  
Keyword(s):  
Macaque Monkey ◽  
Wide Field ◽  
Visual Areas

Colocalization of vasoactive intestinal polypeptide and GABA immunoreactivities in a population of wide-field amacrine cells in the rabbit retina

1992 ◽  
Vol 8 (4) ◽  
pp. 373-378 ◽  
Author(s):  
Giovanni Casini ◽  
Nicholas C. Brecha
Keyword(s):  
Cell Population ◽  
Vasoactive Intestinal Polypeptide ◽  
Plexiform Layer ◽  
Distinct Group ◽  
Amacrine Cells ◽  
Wide Field ◽  
Inner Plexiform Layer ◽  
Rabbit Retina ◽  
Double Label ◽  
Intestinal Polypeptide

AbstractVasoactive intestinal polypeptide (VIP) immunoreactive (IR) neurons in the rabbit retina constitute a population of wide-field amacrine cells. To better define this cell population, we examined the coexpression of VIP with other putative retinal transmitters or their biosynthetic enzymes, including γ-aminobutyric acid (GABA), tyrosine hydroxylase (TH), and somatostatin (SRIF). Colchicine-treated retinas were immersion fixed in 4% paraformaldehyde. The retinas were cut either perpendicular or parallel to the vitreal surface and processed by double-label immunofluorescence techniques using antibodies directed to VIP, GABA, TH, and SRIF. The immunoreactive staining patterns obtained with these antibodies were the same as those described in previous studies. GABA-IR neurons were localized to the proximal inner nuclear layer (INL) and ganglion cell layer (GCL) and processes were distributed throughout the inner plexiform layer (IPL). TH- and SR1F-IR neurons were sparsely distributed to the proximal INL and GCL, respectively. TH-IR processes ramified in laminae 1, 3, and 5, and SRIF-1R processes in laminae 1 and 5 of the IPL. Colocalization experiments showed that all VIP-IR neurons contain GABA immunoreactivity. In contrast, colocalization of VIP and TH or SRIF immunoreactivities was never observed. These results demonstrate that VIP-IR wide-field amacrines of the rabbit retina make up a neurochemically and morphologically distinct subpopulation of the GABA-IR amacrine cell population. Furthermore, VIP-IR amacrine cells constitute a distinct group with respect to the TH- and SRIF-IR amacrine cells.

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