Limits...
Response Properties of a Newly Identified Tristratified Narrow Field Amacrine Cell in the Mouse Retina.

Newkirk GS, Hoon M, Wong RO, Detwiler PB - PLoS ONE (2015)

Bottom Line: This suggests that the cell functions as a differentiator that generates an output signal (a transient reduction in inhibitory input to downstream retina neurons) that is proportional to the derivative of light input independent of its intensity.Canonical reagents that blocked excitatory (glutamatergic) and inhibitory (GABA and glycine) synaptic transmission had effects on responses to scotopic stimuli consistent with the rod driven component of the proposed circuit.However, responses evoked by photopic stimuli were paradoxical and could not be interpreted on the basis of conventional thinking about the neuropharmacology of synaptic interactions in the retina.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology & Biophysics and Program in Neurobiology & Behavior, University of Washington, Seattle, Washington, United States of America.

ABSTRACT
Amacrine cells were targeted for whole cell recording using two-photon fluorescence microscopy in a transgenic mouse line in which the promoter for dopamine receptor 2 drove expression of green fluorescent protein in a narrow field tristratified amacrine cell (TNAC) that had not been studied previously. Light evoked a multiphasic response that was the sum of hyperpolarizing and depolarization synaptic inputs consistent with distinct dendritic ramifications in the off and on sublamina of the inner plexiform layer. The amplitude and waveform of the response, which consisted of an initial brief hyperpolarization at light onset followed by recovery to a plateau potential close to dark resting potential and a hyperpolarizing response at the light offset varied little over an intensity range from 0.4 to ~10^6 Rh*/rod/s. This suggests that the cell functions as a differentiator that generates an output signal (a transient reduction in inhibitory input to downstream retina neurons) that is proportional to the derivative of light input independent of its intensity. The underlying circuitry appears to consist of rod and cone driven on and off bipolar cells that provide direct excitatory input to the cell as well as to GABAergic amacrine cells that are synaptically coupled to TNAC. Canonical reagents that blocked excitatory (glutamatergic) and inhibitory (GABA and glycine) synaptic transmission had effects on responses to scotopic stimuli consistent with the rod driven component of the proposed circuit. However, responses evoked by photopic stimuli were paradoxical and could not be interpreted on the basis of conventional thinking about the neuropharmacology of synaptic interactions in the retina.

No MeSH data available.


Related in: MedlinePlus

Response dependence on light intensity.Left column of traces show the collected average response (black), +/- standard deviation (red) and individual responses (gray) evoked by 2 s full field flashes (720 μm dia.) 440 nm light at indicated intensities (log10 Rh*/rod/s) recorded (current clamp) in different cells. The number of cells (n) that contributed to average response at each intensity (log10 R*/rod/s) were: n = 8 @ 0.39; n = 17 @ 0.49; n = 9 @ 0.77; n = 17, 1.25; n = 12 @ 2.15; n = 15 @ 3.34; n = 12 @ 4.24, n = 16 @ 5.30. Baseline voltage was set to the mean resting potential across all cells in the data set, i.e. -59.95 +/- 0.79 mV (+/- SEM, n = 21) range - 53 to -68 mV. The mean amplitude +/- SEM of the peak response within 400 ms of light onset, the response plateau (taken as mean voltage over 0.8 and 1.2 s of the 2 s step) and the peak hyperpolarizing response within 400 ms of light offset are plotted against light intensity in the three graphs to the right of the column of responses.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4564219&req=5

pone.0137702.g003: Response dependence on light intensity.Left column of traces show the collected average response (black), +/- standard deviation (red) and individual responses (gray) evoked by 2 s full field flashes (720 μm dia.) 440 nm light at indicated intensities (log10 Rh*/rod/s) recorded (current clamp) in different cells. The number of cells (n) that contributed to average response at each intensity (log10 R*/rod/s) were: n = 8 @ 0.39; n = 17 @ 0.49; n = 9 @ 0.77; n = 17, 1.25; n = 12 @ 2.15; n = 15 @ 3.34; n = 12 @ 4.24, n = 16 @ 5.30. Baseline voltage was set to the mean resting potential across all cells in the data set, i.e. -59.95 +/- 0.79 mV (+/- SEM, n = 21) range - 53 to -68 mV. The mean amplitude +/- SEM of the peak response within 400 ms of light onset, the response plateau (taken as mean voltage over 0.8 and 1.2 s of the 2 s step) and the peak hyperpolarizing response within 400 ms of light offset are plotted against light intensity in the three graphs to the right of the column of responses.

Mentions: The average response evoked by 2 s exposure to full field (720 μm diameter spot) 440 nm light at intensities ranging from 0.39 to 5.95 log10 Rh*/rod/s can be described as consisting of three components: (1) an initial hyperpolarization at light onset that (2) recovered to a shoulder that plateaued to a level close (~ 1–2 mVs) to the dark resting potential and (3) a hyperpolarizing response at light offset (Fig 3, black traces). Responses evoked by a particular intensity were not, however, identical from one cell to the next (Fig 3, gray traces). In some cells the plateau phase of the flash response was reduced to such an extent that the response appeared to consist of only a short lived hyperpolarizing potential change at both light on- and offset. In other cells light onset evoked a transient depolarization that either cut short the initial hyperpolarizing phase of the ON response or preceded it. Similar variations in the waveform of the OFF response were also seen in different cells. The cell-to-cell differences in the shape of the light response were not associated with differences in resting potential, cell morphology or cell body location relative to inner margin of the INL.


Response Properties of a Newly Identified Tristratified Narrow Field Amacrine Cell in the Mouse Retina.

Newkirk GS, Hoon M, Wong RO, Detwiler PB - PLoS ONE (2015)

Response dependence on light intensity.Left column of traces show the collected average response (black), +/- standard deviation (red) and individual responses (gray) evoked by 2 s full field flashes (720 μm dia.) 440 nm light at indicated intensities (log10 Rh*/rod/s) recorded (current clamp) in different cells. The number of cells (n) that contributed to average response at each intensity (log10 R*/rod/s) were: n = 8 @ 0.39; n = 17 @ 0.49; n = 9 @ 0.77; n = 17, 1.25; n = 12 @ 2.15; n = 15 @ 3.34; n = 12 @ 4.24, n = 16 @ 5.30. Baseline voltage was set to the mean resting potential across all cells in the data set, i.e. -59.95 +/- 0.79 mV (+/- SEM, n = 21) range - 53 to -68 mV. The mean amplitude +/- SEM of the peak response within 400 ms of light onset, the response plateau (taken as mean voltage over 0.8 and 1.2 s of the 2 s step) and the peak hyperpolarizing response within 400 ms of light offset are plotted against light intensity in the three graphs to the right of the column of responses.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4564219&req=5

pone.0137702.g003: Response dependence on light intensity.Left column of traces show the collected average response (black), +/- standard deviation (red) and individual responses (gray) evoked by 2 s full field flashes (720 μm dia.) 440 nm light at indicated intensities (log10 Rh*/rod/s) recorded (current clamp) in different cells. The number of cells (n) that contributed to average response at each intensity (log10 R*/rod/s) were: n = 8 @ 0.39; n = 17 @ 0.49; n = 9 @ 0.77; n = 17, 1.25; n = 12 @ 2.15; n = 15 @ 3.34; n = 12 @ 4.24, n = 16 @ 5.30. Baseline voltage was set to the mean resting potential across all cells in the data set, i.e. -59.95 +/- 0.79 mV (+/- SEM, n = 21) range - 53 to -68 mV. The mean amplitude +/- SEM of the peak response within 400 ms of light onset, the response plateau (taken as mean voltage over 0.8 and 1.2 s of the 2 s step) and the peak hyperpolarizing response within 400 ms of light offset are plotted against light intensity in the three graphs to the right of the column of responses.
Mentions: The average response evoked by 2 s exposure to full field (720 μm diameter spot) 440 nm light at intensities ranging from 0.39 to 5.95 log10 Rh*/rod/s can be described as consisting of three components: (1) an initial hyperpolarization at light onset that (2) recovered to a shoulder that plateaued to a level close (~ 1–2 mVs) to the dark resting potential and (3) a hyperpolarizing response at light offset (Fig 3, black traces). Responses evoked by a particular intensity were not, however, identical from one cell to the next (Fig 3, gray traces). In some cells the plateau phase of the flash response was reduced to such an extent that the response appeared to consist of only a short lived hyperpolarizing potential change at both light on- and offset. In other cells light onset evoked a transient depolarization that either cut short the initial hyperpolarizing phase of the ON response or preceded it. Similar variations in the waveform of the OFF response were also seen in different cells. The cell-to-cell differences in the shape of the light response were not associated with differences in resting potential, cell morphology or cell body location relative to inner margin of the INL.

Bottom Line: This suggests that the cell functions as a differentiator that generates an output signal (a transient reduction in inhibitory input to downstream retina neurons) that is proportional to the derivative of light input independent of its intensity.Canonical reagents that blocked excitatory (glutamatergic) and inhibitory (GABA and glycine) synaptic transmission had effects on responses to scotopic stimuli consistent with the rod driven component of the proposed circuit.However, responses evoked by photopic stimuli were paradoxical and could not be interpreted on the basis of conventional thinking about the neuropharmacology of synaptic interactions in the retina.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology & Biophysics and Program in Neurobiology & Behavior, University of Washington, Seattle, Washington, United States of America.

ABSTRACT
Amacrine cells were targeted for whole cell recording using two-photon fluorescence microscopy in a transgenic mouse line in which the promoter for dopamine receptor 2 drove expression of green fluorescent protein in a narrow field tristratified amacrine cell (TNAC) that had not been studied previously. Light evoked a multiphasic response that was the sum of hyperpolarizing and depolarization synaptic inputs consistent with distinct dendritic ramifications in the off and on sublamina of the inner plexiform layer. The amplitude and waveform of the response, which consisted of an initial brief hyperpolarization at light onset followed by recovery to a plateau potential close to dark resting potential and a hyperpolarizing response at the light offset varied little over an intensity range from 0.4 to ~10^6 Rh*/rod/s. This suggests that the cell functions as a differentiator that generates an output signal (a transient reduction in inhibitory input to downstream retina neurons) that is proportional to the derivative of light input independent of its intensity. The underlying circuitry appears to consist of rod and cone driven on and off bipolar cells that provide direct excitatory input to the cell as well as to GABAergic amacrine cells that are synaptically coupled to TNAC. Canonical reagents that blocked excitatory (glutamatergic) and inhibitory (GABA and glycine) synaptic transmission had effects on responses to scotopic stimuli consistent with the rod driven component of the proposed circuit. However, responses evoked by photopic stimuli were paradoxical and could not be interpreted on the basis of conventional thinking about the neuropharmacology of synaptic interactions in the retina.

No MeSH data available.


Related in: MedlinePlus