Neocortical disynaptic inhibition requires somatodendritic integration in interneurons.
In his theory of functional polarity, Ramon y Cajal first identified the soma and dendrites as the principal recipient compartments of a neuron and the axon as its main output structure. Despite notable exceptions in other parts of the nervous system (Schoppa and Urban, 2003; Wässle, 2004; Howard et al., 2005), this route of signal propagation has been shown to underlie the functional properties of most neocortical circuits studied so far. Recent evidence, however, suggests that neocortical excitatory cells may trigger the release of the inhibitory neurotransmitter GABA by directly depolarizing the axon terminals of inhibitory interneurons, thus bypassing their somatodendritic compartments (Ren et al., 2007). By using a combination of optical and electrophysiological approaches, we find that synaptically released glutamate fails to trigger GABA release through a direct action on GABAergic terminals under physiological conditions. Rather, our evidence suggests that glutamate triggers GABA release only after somatodendritic depolarization and action potential generation at GABAergic interneurons. These data indicate that neocortical inhibition is recruited by classical somatodendritic integration rather than direct activation of interneuron axon terminals.
Hull
Court
C
Neurobiology Section, Division of Biology, University of California, San Diego, La Jolla, California 92093-0634, USA.
Adesnik
Hillel
H
Scanziani
Massimo
M
D015761:4-Aminopyridine / Q000494:pharmacology; D000200:Action Potentials / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn; D001703:Biophysics; D000075402:Channelrhodopsins; D003712:Dendrites / Q000502:physiology*; D004558:Electric Stimulation / Q000379:methods; D018274:Electroporation / Q000379:methods; D004622:Embryo, Mammalian; D018698:Glutamic Acid / Q000378:metabolism; D049452:Green Fluorescent Proteins / Q000235:genetics; D066298:In Vitro Techniques; D053444:Inhibitory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D007395:Interneurons / Q000502:physiology*; D051379:Mice; D008813:Mice, Inbred ICR; D008822:Mice, Transgenic; D019579:Neocortex / Q000166:cytology*; D009433:Neural Inhibition / Q000502:physiology*; D010320:Parvalbumins / Q000378:metabolism; D018408:Patch-Clamp Techniques / Q000379:methods; D010775:Photic Stimulation / Q000379:methods; D026902:Potassium Channel Blockers / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D011930:Reaction Time / Q000502:physiology; D026941:Sodium Channel Blockers / Q000494:pharmacology; D013569:Synapses / Q000145:classification / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D000075402:Channelrhodopsins; D010320:Parvalbumins; D026902:Potassium Channel Blockers; D026941:Sodium Channel Blockers; C485184:enhanced green fluorescent protein; D049452:Green Fluorescent Proteins; D018698:Glutamic Acid; D013779:Tetrodotoxin; D005680:gamma-Aminobutyric Acid; D015761:4-Aminopyridine