Blast waves from explosions feature rapid temperature changes due to extreme compression and expansion of air. At the shock front, temperatures can spike to thousands of degrees Kelvin from adiabatic heating, then drop sharply behind the front.[atomicarchive] Shock Front Heating The leading edge of a blast wave compresses air nearly instantaneously, causing temperatures to rise dramatically—often exceeding 3,000–5,000 K for high-explosive blasts, similar to conditions in a nuclear fireball initially. This heating ionizes air and produces luminous effects like fireballs. As the wave propagates, peak temperatures decrease with distance due to energy dissipation.[link.springer +1]

Yes These changes manifest as impaired spatial working memory and fear overgeneralization, with NE depletion models mirroring blast-induced progenitor loss and TDP-43/tau pathology. Enduring hippocampal atrophy emerges at 3 months post-blast, linking NE dysregulation to PTSD-like avoidance and recognition deficits.

Blast exposure triggers locus coeruleus hyperactivity, flooding the hippocampus with NE and elevating basal intracellular calcium levels in CA1 neurons. This causes heterogeneous reductions in fast Ca²⁺ transients tied to spiking activity and slow shifts in basal Ca²⁺, reducing network excitability without neuronal loss. Recovery occurs within ~1 hour, but repeated blasts sustain deficits in hippocampal-dependent tasks like novel object recognition.[pmc.ncbi.nlm.nih +3] Synaptic and Molecular Impacts Excess NE desensitizes α- and β-adrenergic receptors in CA1 and dentate gyrus, downregulating GluR1 phosphorylation at Ser845/Ser831 via PKA/CaMKII inhibition, weakening AMPA trafficking and LTP induction. Proteomic shifts include tau hyperphosphorylation and NLRP3 inflammasome activation, promoting microglial inflammation and progenitor proliferation deficits in dentate gyrus. Mossy fiber pathways show altered NMDA receptor contributions, shifting toward intermediate excitability between sham and moderate injury.[frontiersin +4]