The ability to generate action potentials (spikes) in response to synaptic input determines whether a neuron participates in information processing. How a developing neuron becomes an active participant in a circuit or whether this process is activity dependent is not known, especially as spike-dependent plasticity mechanisms would not be available to non-spiking neurons. Here we use the optic tectum of awake Xenopus laevis tadpoles to determine how a neuron becomes able to generate sensory-driven spikes in vivo. At the onset of vision, many tectal neurons do not exhibit visual spiking behavior, despite being intrinsically excitable and receiving visuotopically organized synaptic inputs. However, a brief period of visual stimulation can drive these neurons to start generating stimulus-driven spikes. This conversion relies upon a selective increase in glutamatergic input and requires depolarizing GABAergic transmission and NMDA receptor activation. This permissive form of experience-dependent plasticity enables a neuron to start contributing to circuit function.
1050 - 1062
Action Potentials, Age Factors, Animals, Computer Simulation, Electric Stimulation, GABA Agents, Glutamic Acid, Larva, Models, Neurological, Movement, Neuronal Plasticity, Neurons, Patch-Clamp Techniques, Photic Stimulation, Superior Colliculi, Synapses, Vision, Ocular, Visual Pathways, Wakefulness, Xenopus laevis, gamma-Aminobutyric Acid