Mounting preclinical and clinical evidence demonstrate that the behavioral and cellular
consequences of stress vary across different stages of development. Cortisol, or corticosterone
(CORT) in rodents, is a major stress hormone and which can rapidly modulate neuronal
excitability in multiple brain regions. However, its short-term effects on the function
of nociceptive circuits in the developing spinal superficial dorsal horn (SDH) are
poorly understood. Here we examined the expression of glucocorticoid receptors (GR)
in the adolescent SDH and explored the effects of CORT on intrinsic membrane excitability
and synaptic transmission in GABAergic and presumed glutamatergic SDH neurons using
Glutamic acid decarboxylase 67-Enhanced Green Fluorescent Protein (Gad67-EGFP) mice.
In situ hybridization revealed that Gad67-EGFP-negative SDH neurons exhibited a significantly
higher number of GR mRNA puncta compared to adjacent Gad67-EGFP-positive SDH neurons.
In vitro patch clamp recordings from spinal cord slices suggested that the acute application
of CORT (100 nM) reduced glutamate or GABA release onto a subset of SDH neurons regardless
of cell type. However, incubation of spinal cord slices with CORT for 90 minutes failed
to influence the intrinsic membrane properties (including rheobase, resting potential
and repetitive firing frequency) or miniature postsynaptic currents (mPSCs) in either
neuronal population compared to the vehicle control. Collectively, while these results
suggest that GR activation fails to exert intermediate effects on the excitability
of the adolescent SDH network, the abundance of GR expression in the region raises
the possibility that CORT can evoke slow changes in the excitability of dorsal horn
neurons via genomic mechanisms. Grant support from NS072202.
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