Excitatory neurons sculpt GABAergic neuronal connectivity in the C. elegans motor circuit.
Belinda BarbagalloAlison PhilbrookDenis TouroutineNavonil BanerjeeDevyn OliverChristopher M LambertMichael M FrancisPublished in: Development (Cambridge, England) (2017)
Establishing and maintaining the appropriate number of GABA synapses is key for balancing excitation and inhibition in the nervous system, though we have only a limited understanding of the mechanisms controlling GABA circuit connectivity. Here, we show that disrupting cholinergic innervation of GABAergic neurons in the C. elegans motor circuit alters GABAergic neuron synaptic connectivity. These changes are accompanied by reduced frequency and increased amplitude of GABAergic synaptic events. Acute genetic disruption in early development, during the integration of post-embryonic-born GABAergic neurons into the circuit, produces irreversible effects on GABAergic synaptic connectivity that mimic those produced by chronic manipulations. In contrast, acute genetic disruption of cholinergic signaling in the adult circuit does not reproduce these effects. Our findings reveal that GABAergic signaling is regulated by cholinergic neuronal activity, probably through distinct mechanisms in the developing and mature nervous system.
Keyphrases
- resting state
- functional connectivity
- white matter
- liver failure
- spinal cord
- genome wide
- drug induced
- respiratory failure
- magnetic resonance
- magnetic resonance imaging
- copy number
- gestational age
- multiple sclerosis
- gene expression
- spinal cord injury
- cerebral ischemia
- hepatitis b virus
- subarachnoid hemorrhage
- extracorporeal membrane oxygenation
- blood brain barrier