Blast-induced temporal alterations in blood-brain barrier properties in a rodent model.

The consequences of blast-induced traumatic brain injury (bTBI) on the blood-brain barrier (BBB) and components of the neurovascular unit are an area of active research. In this study we assessed the time course of BBB integrity in anesthetized rats exposed to a single blast overpressure of 130 kPa (18.9 PSI). BBB permeability was measured in vivo via intravital microscopy by imaging extravasation of fluorescently labeled tracers (40 kDa and 70 kDa molecular weight) through the pial microvasculature into brain parenchyma at 2-3 h, 1, 3, 14, or 28 days after the blast exposure. BBB structural changes were assessed by immunostaining and molecular assays. At 2-3 h and 1 day after blast exposure, significant increases in the extravasation of the 40 kDa but not the 70 kDa tracers were observed, along with differential reductions in the expression of tight junction proteins (occludin, claudin-5, zona occluden-1) and increase in the levels of the astrocytic water channel protein, AQP-4, and matrix metalloprotease, MMP-9. Nearly all of these measures were normalized by day 3 and maintained up to 28 days post exposure. These data demonstrate that blast-induced changes in BBB permeability are closely coupled to structural and functional components of the BBB.

Behavioural laterality in foraging bottlenose dolphins (Tursiops truncatus).

Lateralized behaviour is found in humans and a wide variety of other species. At a population level, lateralization of behaviour suggests hemispheric specialization may underlie this behaviour. As in other cetaceans, dolphins exhibit a strong right-side bias in foraging behaviour. Common bottlenose dolphins in The Bahamas use a foraging technique termed 'crater feeding', in which they swim slowly along the ocean floor, scanning the substrate using echolocation, and then bury their rostrums into the sand to obtain prey. The bottlenose dolphins off Bimini, The Bahamas, frequently execute a sharp turn before burying their rostrums in the sand. Based on data collected from 2012 to 2018, we report a significant right-side (left turn) bias in these dolphins. Out of 709 turns recorded from at least 27 different individuals, 99.44% (n = 705) were to the left (right side and right eye down) [z = 3.275, p = 0.001]. Only one individual turned right (left side and left eye down, 4/4 turns). We hypothesize that this right-side bias may be due in part to the possible laterization of echolocation production mechanisms, the dolphins' use of the right set of phonic lips to produce echolocation clicks, and a right eye (left hemisphere) advantage in visual discrimination and visuospatial processing.

Exposure to Blast Overpressure Impairs Cerebral Microvascular Responses and Alters Vascular and Astrocytic Structure.

Exposure to blast overpressure may result in cerebrovascular impairment, including cerebral vasospasm. The mechanisms contributing to this vascular response are unclear. The aim of this study was to evaluate the relationship between blast and functional alterations of the cerebral microcirculation and to investigate potential underlying changes in vascular microstructure. Cerebrovascular responses were assessed in sham- and blast-exposed male rats at multiple time points from 2 h through 28 days after a single 130-kPa (18.9-psi) exposure. Pial microcirculation was assessed through a cranial window created in the parietal bone of anesthetized rats. Pial arteriolar reactivity was evaluated in vivo using hypercapnia, barium chloride, and serotonin. We found that exposure to blast leads to impairment of arteriolar reactivity >24 h after blast exposure, suggesting delayed injury mechanisms that are not simply attributed to direct mechanical deformation. Observed vascular impairment included a reduction in hypercapnia-induced vasodilation, increase in barium-induced constriction, and reversal of the serotonin effect from constriction to dilation. A reduction in vascular smooth muscle contractile proteins consistent with vascular wall proliferation was observed, as well as delayed reduction in nitric oxide synthase and increase in endothelin-1 B receptors, mainly in astrocytes. Collectively, the data show that exposure to blast results in delayed and prolonged alterations in cerebrovascular reactivity that are associated with changes in the microarchitecture of the vessel wall and astrocytes. These changes may contribute to long-term pathologies involving dysfunction of the neurovascular unit, including cerebral vasospasm.