Abstract
SummaryThe activity-dependent rules that govern the wiring of GABAergic interneurons are not well understood. Chandelier cells (ChCs) are a type of GABAergic interneuron that control pyramidal cell output through axo-axonic synapses that target the axon initial segment. In vivo imaging of ChCs during development uncovered a narrow window (P12–P18) over which axons arborized and formed connections. We found that increases in the activity of either pyramidal cells or individual ChCs during this temporal window result in a reversible decrease in axo-axonic connections. Voltage imaging of GABAergic transmission at the axon initial segment (AIS) showed that axo-axonic synapses were depolarizing during this period. Identical manipulations of network activity in older mice (P40–P46), when ChC synapses are inhibitory, resulted instead in an increase in axo-axonic synapses. We propose that the direction of ChC synaptic plasticity follows homeostatic rules that depend on the polarity of axo-axonic synapses.
Highlights
An important question in neuroscience is how neurons in the brain wire up and adapt their connectivity to form functional circuits
Mirroring the rapid growth of the axonal arbor, imaging of fixed brain slices at different developmental periods showed that the number of postsynaptic pyramidal cells contacted by an individual Chandelier cells (ChCs) increased during this window (Figures 1D and 1E)
In agreement with these morphological findings, we saw a functional increase in the amplitude (Figure 1J) of GABAergic PSCs recorded from pyramidal cells in response to optogenetic stimulation of ChCs (Figures S1A–S1C) during the period of synaptogenesis, as well as a maturation of the intrinsic firing properties of ChCs themselves (Figures S1D–S1F)
Summary
An important question in neuroscience is how neurons in the brain wire up and adapt their connectivity to form functional circuits. Among the highly heterogeneous population of GABAergic interneurons that provide inhibition in the cortex, Chandelier cells (ChCs) are one of the least well characterized, mainly due to their sparseness and the lack of genetic tools to label them until recently (Taniguchi et al, 2013). They display many morphological features that make them good candidates for controlling both neuronal and circuit activity in the brain (Inan et al, 2013; Somogyi, 1977). Abnormalities in axo-axonic synapses have been associated with developmental brain disorders such as schizophrenia (Fazzari et al, 2010; Lewis, 2011) and epilepsy (DeFelipe, 1999; Marco and DeFelipe, 1997)
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