Unbound MEDLINE

Dynamics of fast and slow inhibition from cerebellar golgi cells allow flexible control of synaptic integration. Neuron [Neuron] Journal article

 
TitleDynamics of fast and slow inhibition from cerebellar golgi cells allow flexible control of synaptic integration.
Author(s)Crowley JJ, Fioravante D, Regehr WG 
InstitutionDepartment of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.
SourceNeuron 2009 Sep 24; 63(6):843-53.
MeSHAction Potentials
Animals
Animals, Newborn
Biophysics
Cell Line, Transformed
Cerebellum
Electric Stimulation
Excitatory Amino Acid Antagonists
GABA Antagonists
Humans
Inhibitory Postsynaptic Potentials
Neural Inhibition
Neurons
Nonlinear Dynamics
Patch-Clamp Techniques
Phosphinic Acids
Photic Stimulation
Piperazines
Propanolamines
Quinoxalines
Rats
Rats, Sprague-Dawley
Rhodopsin
Synapses
Time Factors
Transfection
AbstractThroughout the brain, multiple interneuron types influence distinct aspects of synaptic processing. Interneuron diversity can thereby promote differential firing from neurons receiving common excitation. In contrast, Golgi cells are the sole interneurons regulating granule cell spiking evoked by mossy fibers, thereby gating inputs to the cerebellar cortex. Here, we examine how this single interneuron class modifies activity in its targets. We find that GABA(A)-mediated transmission at unitary Golgi cell --> granule cell synapses consists of varying contributions of fast synaptic currents and sustained inhibition. Fast IPSCs depress and slow IPSCs gradually build during high-frequency Golgi cell activity. Consequently, fast and slow inhibition differentially influence granule cell spike timing during persistent mossy fiber input. Furthermore, slow inhibition reduces the gain of the mossy fiber --> granule cell input-output curve, while fast inhibition increases the threshold. Thus, a lack of interneuron diversity need not prevent flexible inhibitory control of synaptic processing.
Languageeng
Pub Type(s)In Vitro
Journal Article
Research Support, N.I.H., Extramural
PubMed ID19778512
  
Advertise on this site.