Hyperpolarization Induces a Long-Term Increase in the Spontaneous Firing Rate of Cerebellar Golgi Cells
| Autor: | Monica S. Thanawala, YunXiang Chu, Court Hull, Wade G. Regehr |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
Male
Cerebellum Patch-Clamp Techniques Time Factors Action Potentials In Vitro Techniques Biology Receptors Metabotropic Glutamate Inhibitory postsynaptic potential Article GABA Antagonists Propanolamines Rats Sprague-Dawley Potassium Channels Calcium-Activated Interneurons medicine Animals Patch clamp Enzyme Inhibitors General Neuroscience Membrane hyperpolarization Hyperpolarization (biology) Granule cell Phosphinic Acids Electric Stimulation Potassium channel Rats medicine.anatomical_structure Animals Newborn Inhibitory Postsynaptic Potentials Cerebellar cortex Female Calcium-Calmodulin-Dependent Protein Kinase Type 2 Excitatory Amino Acid Antagonists Neuroscience |
| Zdroj: | The Journal of Neuroscience. 33:5895-5902 |
| ISSN: | 1529-2401 0270-6474 |
| DOI: | 10.1523/jneurosci.4052-12.2013 |
| Popis: | Golgi cells (GoCs) are inhibitory interneurons that influence the cerebellar cortical response to sensory input by regulating the excitability of the granule cell layer. While GoC inhibition is essential for normal motor coordination, little is known about the circuit dynamics that govern the activity of these cells. In particular, although GoC spontaneous spiking influences the extent of inhibition and gain throughout the granule cell layer, it is not known whether this spontaneous activity can be modulated in a long-term manner. Here we describe a form of long-term plasticity that regulates the spontaneous firing rate of GoCs in the rat cerebellar cortex. We find that membrane hyperpolarization, either by mGluR2 activation of potassium channels, or by somatic current injection, induces a long-lasting increase in GoC spontaneous firing. This spike rate plasticity appears to result from a strong reduction in the spike after hyperpolarization. Pharmacological manipulations suggest the involvement of calcium-calmodulin-dependent kinase II and calcium-activated potassium channels in mediating these firing rate increases. As a consequence of this plasticity, GoC spontaneous spiking is selectively enhanced, but the gain of evoked spiking is unaffected. Hence, this plasticity is well suited for selectively regulating the tonic output of GoCs rather than their sensory-evoked responses. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|