Oscillatory Cortical Activity in an Animal Model of Dystonia Caused by Cerebellar Dysfunction

The synchronization of neuronal activity in the sensorimotor cortices is crucial for motor control and learning. This synchrony can be modulated by upstream activity in the cerebello-cortical network. However, many questions remain over the details of how the cerebral cortex and the cerebellum communicate. Therefore, our aim is to study the contribution of the cerebellum to oscillatory brain activity, in particular in the case of dystonia, a severely disabling motor disease associated with altered sensorimotor coupling. We used a kainic-induced dystonia model to evaluate cerebral cortical oscillatory activity and connectivity during dystonic episodes. We performed microinjections of low doses of kainic acid into the cerebellar vermis in mice and examined activities in somatosensory, motor and parietal cortices. We showed that repeated applications of kainic acid into the cerebellar vermis, for five consecutive days, generate reproducible dystonic motor behavior. No epileptiform activity was recorded on electrocorticogram (ECoG) during the dystonic postures or movements. We investigated the ECoG power spectral density and coherence between motor cortex, somatosensory and parietal cortices before and during dystonic attacks. During the baseline condition, we found a phenomenon of permanent adaptation with a change of baseline locomotor activity coupled to an ECoG gamma band increase in all cortices. In addition, after kainate administration, we observed an increase in muscular activity, but less signs of dystonia together with modulations of the ECoG power spectra with an increase in gamma band in motor, parietal and somatosensory cortices. Moreover, we found reduced coherence in all measured frequency bands between the motor cortex and somatosensory or parietal cortices compared to baseline. In conclusion, examination of cortical oscillatory activities in this animal model of chronic dystonia caused by cerebellar dysfunction reveals a disruption in the coordination of neuronal activity across the cortical sensorimotor/parietal network, which may underlie motor skill deficits

Blood-Brain Barrier and Cognitive Function

The blood-brain barrier (BBB) is the highly specialized and selective crossing area between blood and brain, essential for brain homeostasis and functioning, formed by the endothelial cells of the cerebral microvasculature in a rich and intimate cooperation with the neighboring cells and local signaling factors from both the brain and blood sides. Its distribution throughout the brain is following the brain cytoarchitectonic patterns, each capillary serving the adjacent neurons in a privileged neurovascular interplay that ultimately responds to the manifestation of brain functions, scaled from the cellular to the system level. At the edge of our understanding, cognition stands for what makes us humans and needs the cooperation of the entire body functioning to assist homeostatic favorable conditions for its manifestation. The cerebral endothelial system is operating at this interfacing point, modulating its own phenotype in accordance with various conditions to which the organism and brain are exposed, responding with changes in its permeability and signaling processes. In this chapter we will briefly describe the multicellular assembly of the neurovascular unit from which the BBB emerges, and its contribution to the brain homeostasis by dynamic neurovascular and neurometabolic coupling processes. Further, we will refer to the principal morphologic and functional features of the BBB from which its specific properties arise, making it not just a physical selective barrier, but also a metabolic, neuroimmune and endocrine interface. We will touch on the physiological implications of BBB and neurovascular coupling on high brain functions and cognition, in normal or disease-associated conditions

Temporal–Posterior Alpha Power in Resting-State Electroencephalography as a Potential Marker of Complex Childhood Trauma in Institutionalized Adolescents

The present study explored whether, given the association of temporal alpha with fear circuitry (learning and conditioning), exposure to complex childhood trauma (CCT) is reflected in the temporal–posterior alpha power in resting-state electroencephalography (EEG) in complex trauma-exposed adolescents in a sample of 25 adolescents and similar controls aged 12–17 years. Both trauma and psychopathology were screened or assessed, and resting-state EEG was recorded following a preregistered protocol for data collection. Temporal–posterior alpha power, corresponding to the T5 and T6 electrode locations (international 10–20 system), was extracted from resting-state EEG in both eyes-open and eyes-closed conditions. We found that in the eyes-open condition, temporal–posterior alpha was significantly lower in adolescents exposed to CCT relative to healthy controls, suggesting that childhood trauma exposure may have a measurable impact on alpha oscillatory patterns. Our study highlights the importance of considering potential neural markers, such as temporal–posterior alpha power, to understanding the long-term consequences of CCT exposure in developmental samples, with possible important clinical implications in guiding neuroregulation interventions