Presynaptic mechanism for slow contrast adaptation in mammalian retinal ganglion cells

Neuron. 2006 May 4;50(3):453-64. doi: 10.1016/j.neuron.2006.03.039.


Visual neurons, from retina to cortex, adapt slowly to stimulus contrast. Following a switch from high to low contrast, a neuron rapidly decreases its responsiveness and recovers over 5-20 s. Cortical adaptation arises from an intrinsic cellular mechanism: a sodium-dependent potassium conductance that causes prolonged hyperpolarization. Spiking can drive this mechanism, raising the possibility that the same mechanism exists in retinal ganglion cells. We found that adaptation in ganglion cells corresponds to a slowly recovering afterhyperpolarization (AHP), but, unlike in cortical cells, this AHP is not primarily driven by an intrinsic cellular property: spiking was not sufficient to generate adaptation. Adaptation was strongest following spatial stimuli tuned to presynaptic bipolar cells rather than the ganglion cell; it was driven by a reduced excitatory conductance, and it persisted while blocking GABA and glycine receptors, K((Ca)) channels, or mGluRs. Thus, slow adaptation arises from reduced glutamate release from presynaptic (nonspiking) bipolar cells.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Action Potentials / physiology
  • Adaptation, Physiological / physiology*
  • Animals
  • Calcium Channels / drug effects
  • Calcium Channels / metabolism
  • Contrast Sensitivity / drug effects
  • Contrast Sensitivity / physiology*
  • Glutamic Acid / metabolism*
  • Guinea Pigs
  • Organ Culture Techniques
  • Photic Stimulation
  • Presynaptic Terminals / drug effects
  • Presynaptic Terminals / metabolism*
  • Reaction Time / physiology*
  • Receptors, GABA / drug effects
  • Receptors, GABA / metabolism
  • Receptors, Glycine / antagonists & inhibitors
  • Receptors, Glycine / metabolism
  • Receptors, Metabotropic Glutamate / drug effects
  • Receptors, Metabotropic Glutamate / metabolism
  • Retinal Bipolar Cells / drug effects
  • Retinal Bipolar Cells / physiology
  • Retinal Ganglion Cells / drug effects
  • Retinal Ganglion Cells / metabolism*
  • Synaptic Transmission / drug effects
  • Synaptic Transmission / physiology*


  • Calcium Channels
  • Receptors, GABA
  • Receptors, Glycine
  • Receptors, Metabotropic Glutamate
  • Glutamic Acid