Acute and chronic corticosterone (CS) elevations after traumatic brain injury (TBI) may be involved in distant hippocampal damage and the development of late posttraumatic behavioral pathology. CS-dependent behavioral and morphological changes were studied 3 months after TBI induced by lateral fluid percussion in 51 male Sprague–Dawley rats. CS was measured in the background 3 and 7 days and 1, 2 and 3 months after TBI. Tests including open field, elevated plus maze, object location, new object recognition tests (NORT) and Barnes maze with reversal learning were used to assess behavioral changes in acute and late TBI periods. The elevation of CS on day 3 after TBI was accompanied by early CS-dependent objective memory impairments detected in NORT. Blood CS levels > 860 nmol/L predicted delayed mortality with an accuracy of 0.947. Ipsilateral neuronal loss in the hippocampal dentate gyrus, microgliosis in the contralateral dentate gyrus and bilateral thinning of hippocampal cell layers as well as delayed spatial memory deficits in the Barnes maze were revealed 3 months after TBI. Because only animals with moderate but not severe posttraumatic CS elevation survived, we suggest that moderate late posttraumatic morphological and behavioral deficits may be at least partially masked by CS-dependent survivorship bias.
Recently, we have shown the differences in the early response of corticosterone and inflammatory cytokines in the hippocampus and frontal cortex (FC) of rats with middle cerebral artery occlusion (MCAO), according to the methods of Longa et al. (LM) and Koizumi et al. (KM) which were used as alternatives in preclinical studies to induce stroke in rodents. In the present study, corticosterone and proinflammatory cytokines were assessed 3 months after MCAO. The most relevant changes detected during the first days after MCAO became even more obvious after 3 months. In particular, the MCAO-KM (but not the MCAO-LM) group showed significant accumulation of corticosterone and IL1β in both the ipsilateral and contralateral hippocampus and FC. An accumulation of TNFα was detected in the ipsilateral hippocampus and FC in the MCAO-KM group. Thus, unlike the MCAO-LM, the MCAO-KM may predispose the hippocampus and FC of rats to long-lasting bilateral corticosterone-dependent distant neuroinflammatory damage. Unexpectedly, only the MCAO-LM rats demonstrated some memory deficit in a one-trial step-through passive avoidance test. The differences between the two MCAO models, particularly associated with the long-lasting increase in glucocorticoid and proinflammatory cytokine accumulation in the limbic structures in the MCAO-KM, should be considered in the planning of preclinical experiments, and the interpretation and translation of received results.
Significance
Cerebral metabolic rate of oxygen (CMRO2) consumption is a key physiological variable that characterizes brain metabolism in a steady state and during functional activation.
Aim
We aim to develop a minimally invasive optical technique for real-time measurement of CMRO2 concurrently with cerebral blood flow (CBF).
Approach
We used a pair of macromolecular phosphorescent probes with nonoverlapping optical spectra, which were localized in the intra- and extravascular compartments of the brain tissue, thus providing a readout of oxygen gradients between these two compartments. In parallel, we measured CBF using laser speckle contrast imaging.
Results
The method enables computation and tracking of CMRO2 during functional activation with high temporal resolution (∼7 Hz). In contrast to other approaches, our assessment of CMRO2 does not require measurements of CBF or hemoglobin oxygen saturation.
Conclusions
The independent records of intravascular and extravascular partial pressures of oxygen, CBF, and CMRO2 provide information about the physiological events that accompany neuronal activation, creating opportunities for dynamic quantification of brain metabolism.
Brain oscillatory patterns of affective prosody perception in children with autism spectrum disorder
Background
Paralinguistic features, such as prosody (tempo, loudness, and timbre), are an essential marker of a speaker’s emotional state. Abnormal processing of emotional prosody may result in the deficient social behavior associated with autism spectrum disorder (ASD).
Method
Two groups of children participated in our study: the ASD group consisted of 30 preschoolers from 4 to 6 years of age and 24 typically developing (TD) peers. An electroencephalogram (EEG) was acquired in response to a combination of syllables uttered with the following types of emotional prosody: joy, anger, sadness, fear, and calmness.
Results
Children with ASD and TD showed a similar EEG oscillatory response to fear and anger prosodies. Significant group differences in power spectral density (PSD) were detected for sad and joy intonations. The PSD differences between pairs of intonations, such as joyful and sad, sad and neutral, or joyful and neutral, were significantly higher in the control group than in the ASD group. EEG responses to affective prosody also demonstrated less hemispheric asymmetry in the ASD than in the TD group.
Conclusions
Our results suggest that difficulties in emotional prosody recognition in autistic children could be based on the atypical processing of specific acoustic features coding differences between sad, neutral, and joyful intonations and could underlie emotional perception deficits in individuals with ASD.