Abstract
Parvalbumin (PV)-expressing interneurons (PV-INs) mediate well-timed inhibition of cortical principal neurons, and plasticity of these interneurons is involved in map remodeling of primary sensory cortices during critical periods of development. To assess whether bone morphogenetic protein (BMP) signaling contributes to the developmental acquisition of the synapse- and plasticity properties of PV-INs, we investigated conditional/conventional double KO mice of BMP-receptor 1a (BMPR1a; targeted to PV-INs) and 1b (BMPR1a/1b (c)DKO mice). We report that spike-timing dependent LTP at the synapse between PV-INs and principal neurons of layer 4 in the auditory cortex was absent, concomitant with a decreased paired-pulse ratio (PPR). On the other hand, baseline synaptic transmission at this connection, and action potential (AP) firing rates of PV-INs were unchanged. To explore possible gene expression targets of BMP signaling, we measured the mRNA levels of the BDNF receptor TrkB and of P/Q-type Ca2+ channel α-subunits, but did not detect expression changes of the corresponding genes in PV-INs of BMPR1a/1b (c)DKO mice. Our study suggests that BMP-signaling in PV-INs during and shortly after the critical period is necessary for the expression of LTP at PV-IN output synapses, involving gene expression programs that need to be addressed in future work.
Highlights
Parvalbumin (PV)-expressing interneurons (PV-INs) mediate well-timed inhibition of cortical principal neurons, and plasticity of these interneurons is involved in map remodeling of primary sensory cortices during critical periods of development
To investigate whether the developmental acquisition of these functional properties depends on bone morphogenetic protein (BMP)-signaling in PV-INs, we genetically deleted two critical BMP-type 1 receptor subunits, BMP-receptor 1a (BMPR1a) and BMPR1b
We investigated whether the properties of synaptic transmission at inhibitory synapses formed by PV-INs onto L4 principal neurons in auditory cortex are altered in the (c)double KO (DKO) mice
Summary
Parvalbumin (PV)-expressing interneurons (PV-INs) mediate well-timed inhibition of cortical principal neurons, and plasticity of these interneurons is involved in map remodeling of primary sensory cortices during critical periods of development. Earlier genetic studies showed that BMP signaling drives the growth of motor nerve terminals at the Drosophila neuromuscular junction[29,30,31] Together, these studies suggest a role for BMP signaling in guiding the establishment of specific synaptic connectivity at excitatory connections in the mammalian brain and in the periphery. A previous study showed that BMP-signaling in the OLIG lineage of neuronal/oligodendrocyte precursors determines the number of oligodendrocytes and Calbindin-positive interneurons[32], and it was shown that exogenous BMP4 can act on PV-INs or their precursors to contribute to the morphological differentiation of PV-INs33 It is unknown whether BMP signaling in PV-INs is necessary for the development of the functional properties of this class of interneurons.
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