Abstract
Stress responses are associated with elevations in corticosterone levels and, as a consequence, increases in glutamate in the central nervous system which can lead to neurological impairment. Ceftriaxone promotes glutamate transport and has been used to reduce glutamate toxicity, but so far it is not known whether ceftriaxone is able to reverse the effects of corticosterone administration. Here we describe the separate and combined effects of acute ceftriaxone and acute corticosterone administration in local field potentials (LFPs) recorded from the somatosensory cortex (S1) of anesthetized mice. For this, LFPs were recorded from groups of anesthetized mice injected with saline, corticosterone, ceftriaxone, or both. Comparison of global state maps, and their displacements, as measured by ratios of different frequency bands (Ratio 1: 0.5–20 Hz/0.5–45 Hz; and Ratio 2: 0.5–4.5 Hz/0.5–9 Hz) revealed distinct and opposite effects for corticosterone and for ceftriaxone. Corticosterone specifically increased the displacement in Ratio 2, while ceftriaxone decreased it; in addition, when both corticosterone and ceftriaxone were injected, Ratio 2 displacement values were again similar to those of the control group. The present results suggest that ceftriaxone and corticosterone modulate specific frequency bands in opposite directions and reveal a potential role for ceftriaxone in counteracting the effects of corticosterone.
Highlights
Stress responses are associated with elevations in corticosterone levels and, as a consequence, increases in glutamate in the central nervous system which can lead to neurological impairment
A recent study found no differences in power spectral densities (PSDs) of local field potentials (LFPs) recorded from S1 when chronically stressed and control animals were compared[11]
We asked if the effects of stress could result in changes, not in the power of PSDs in the classical frequency bands, but instead in the dynamics resulting from the combination of specific ratios (Ratio1: 1Center for Interdisciplinary Research in Health, Institute of Health Sciences, Universidade Católica Portuguesa, Porto, Portugal. 2Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, 4710-057, Portugal. 3ICVS/3B’s, PT Government Associate Laboratory, Braga/Guimarães, 4710-057, Portugal. 4Graduate Program in Neuroengineering, Edmond and Lily Safra International Institute of Neuroscience, Santos Dumont Institute, Macaiba, Brazil. 5Clinical Academic Center (2CA-Braga), Braga, Portugal. *email: pvieira@porto
Summary
Stress responses are associated with elevations in corticosterone levels and, as a consequence, increases in glutamate in the central nervous system which can lead to neurological impairment. Our current knowledge about the effects of corticosterone in the primary somatosensory cortex is mostly the result of long term studies in the context of early life stressors and their effects in tactile processing in adult mice (see[13] for a review) These previous studies have identified increases in spine turnover; in basal levels of corticosterone, glutamate, and in microglia motility[9,12,14,15]; little is known about the acute effects of stress/corticosterone in this region. Previous studies have demonstrated that ceftriaxone (a 3rd generation cephalosporin that crosses the blood brain barrier) was able to improve the outcome of traumatic brain injury in rodents[25,26] This suggested that ceftriaxone could potentially be used to treat or prevent the effects of stress responses in the brain, and in the primary somatosensory cortex
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