May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
Synaptic Plasticity Is Mediated by a Nonlinear Dynamic Interaction Between Excitation and Presynaptic Inhibition in the Inner Retina
Author Affiliations & Notes
  • B.T. Sagdullaev
    Ophthalmology, Washington Univ. Sch. of Medicine, St. Louis, MO
  • P.D. Lukasiewicz
    Ophthalmology, Washington Univ. Sch. of Medicine, St. Louis, MO
  • Footnotes
    Commercial Relationships  B.T. Sagdullaev, None; P.D. Lukasiewicz, None.
  • Footnotes
    Support  NIH Grants EY08922, EY02687, RPB.
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 1507. doi:
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      B.T. Sagdullaev, P.D. Lukasiewicz; Synaptic Plasticity Is Mediated by a Nonlinear Dynamic Interaction Between Excitation and Presynaptic Inhibition in the Inner Retina . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1507.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : The flow of visual information is modulated by presynaptic inhibition which limits excitatory synaptic transmission by reducing neurotransmitter (NT) release. We have explored how interactions between presynaptic inhibition, mediated by GABACRs, and excitation regulate the plasticity of the output at the synapse between bipolar and ganglion cells.

Methods: : Mouse bipolar cells were activated with paired electrical stimuli separated by varying interstimulus intervals (ISI). Bipolar cell output was measured by recording excitatory postsynaptic currents (EPSCs) from ganglion cells. We assessed synaptic plasticity by determining the paired–pulse response ratio (R2/R1) for different ISIs.

Results: : In the absence of presynaptic inhibition, when the probability of NT release is highest, we observed a prominent paired–pulse depression (PPD) that recovered with a time constant of 2–3 seconds. When we decreased release probability by reducing extracellular calcium, PPD was diminished, indicating that the depletion of a readily–releasable pool of vesicles in the bipolar cell terminal contributed to the development of PPD. When presynaptic GABACR–mediated inhibition reduced NT release, PPD was also decreased, however the alteration of PPD was different from that observed after lowering extracellular calcium. For ISIs > 0.3 s, PPD decreased linearly with increasingly longer ISI. For briefer ISIs, we observed an increase in the paired–pulse ratio characteristic of synaptic facilitation. The rebound of EPSCs for briefer ISIs could happen if the relative magnitudes of excitation and inhibition depended on the timing between EPSCs. We found that as the ISI shortened the inhibitory effect exerted on bipolar cell output progressively decreased for the second EPSC. Because presynaptic inhibition is frequency–dependent, synaptic depression was progressively reduced and often replaced by synaptic facilitation when the ISI was shortened.

Conclusions: : Taken together, our data indicate that synaptic plasticity of the retinal output is mediated by a nonlinear interaction between presynaptic inhibition and excitation in the inner retina. Plastic adjustment of the relative amounts of inhibition and excitation governs the magnitude of the paired–pulse ratio and might provide the means for dynamic control of synaptic efficacy during visual processing. This results in more reliable transmission, even during periods of relatively high activity.

Keywords: retina: proximal (bipolar, amacrine, and ganglion cells) • synapse • plasticity 
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