Abstract

The long term goal of this research is to determine which visual cues are processed by amacrine cells to thereby provide a physiological/morphological classification scheme for these cells. The central theme of this proposal is to determine basic cellular properties and localized interactions of amacrine cells. The basic method used is intracellular recording from neurons in the superfused, isolated retina-eyecup preparation of the rabbit. Physiologically-characterized cells are subsequently labeled with intracellular stains, such as neurobiotin, to determine their soma-dendritic profiles.
The specific aims are to determine: (1) the response properties expressed by amacrine cells and to correlate these with their cellular morphologies; (2) the different sites (somatic vs. dendritic) at which spikes are generated within amacrine cells and how these spikes are propagated within their dendritic arbors; (3) what role active propagation of synaptic inputs plays in shaping the receptive fields of amacrine cells; (4) whether AII amacrine cells show visual responses in the light-adapted retina, thereby subserving cone vision; (5) the pharmacologic mechanisms underlying light- and dark- induced changes in coupling and receptive field size of horizontal and AII amacrine cells; and (6) whether the correlated spike activity of neighboring alpha ganglion cells is due to coupling between alpha ganglion cells, possibly mediated by coupling with amacrine cells.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Research Project (R01)
Project #
2R01EY007360-11
Application #
2615276
Study Section
Visual Sciences C Study Section (VISC)
Project Start
1988-03-01
Project End
2003-02-28
Budget Start
1998-03-01
Budget End
1999-02-28
Support Year
11
Fiscal Year
1998
Total Cost
Indirect Cost

  Institution

Name
New York University
Department
Ophthalmology
Type
Schools of Medicine
DUNS #
City
New York
State
NY
Country
United States
Zip Code
10016

  Publications

Slavi, Nefeli; Toychiev, Abduqodir H; Kosmidis, Stylianos et al. (2018) Suppression of connexin 43 phosphorylation promotes astrocyte survival and vascular regeneration in proliferative retinopathy. Proc Natl Acad Sci U S A 115:E5934-E5943
Roy, Kaushambi; Kumar, Sandeep; Bloomfield, Stewart A (2017) Gap junctional coupling between retinal amacrine and ganglion cells underlies coherent activity integral to global object perception. Proc Natl Acad Sci U S A 114:E10484-E10493
Akopian, Abram; Kumar, Sandeep; Ramakrishnan, Hariharasubramanian et al. (2017) Targeting neuronal gap junctions in mouse retina offers neuroprotection in glaucoma. J Clin Invest 127:2647-2661
Pan, Feng; Toychiev, Abduqodir; Zhang, Yi et al. (2016) Inhibitory masking controls the threshold sensitivity of retinal ganglion cells. J Physiol 594:6679-6699
Akopian, Abram; Atlasz, Tamas; Pan, Feng et al. (2014) Gap junction-mediated death of retinal neurons is connexin and insult specific: a potential target for neuroprotection. J Neurosci 34:10582-91
Völgyi, Béla; Pan, Feng; Paul, David L et al. (2013) Gap junctions are essential for generating the correlated spike activity of neighboring retinal ganglion cells. PLoS One 8:e69426
Farajian, Reza; Pan, Feng; Akopian, Abram et al. (2011) Masked excitatory crosstalk between the ON and OFF visual pathways in the mammalian retina. J Physiol 589:4473-89
Osterhout, Jessica A; Josten, Nicko; Yamada, Jena et al. (2011) Cadherin-6 mediates axon-target matching in a non-image-forming visual circuit. Neuron 71:632-9
Hu, Edward H; Pan, Feng; Völgyi, Béla et al. (2010) Light increases the gap junctional coupling of retinal ganglion cells. J Physiol 588:4145-63
Pan, Feng; Paul, David L; Bloomfield, Stewart A et al. (2010) Connexin36 is required for gap junctional coupling of most ganglion cell subtypes in the mouse retina. J Comp Neurol 518:911-27

Showing the most recent 10 out of 42 publications