Hypoxic preconditioning in rats with low and high prepulse inhibition of acoustic startle is implemented through topographically different sensory inputs. Working hypothesis

The neurotransmitter and network mechanisms of hypoxic preconditioning are practically unknown. Previously, in rats, we identified the key role of the hippocampus and its cholinergic projections in the preconditioning mechanism of single-exposure of moderate hypobaric hypoxia (HBH) based on the association between the efficiency of HBH and the magnitude of Prepulse Inhibition of Acoustic Startle (PPI). This study presents the first data on PPI-dependent neuronal networks of hypoxic preconditioning and their cholinergic components. The activity of synaptic choline acetyltransferase (ChAT), an indicator of cholinergic function, was used for a correlation analysis of ChAT response to HBH in the hippocampus, cerebral cortex, and caudal brainstem in animals with different levels of PPI. In rats with PPI 40%, ChAT activity was correlated in the hippocampus, cortex and caudal brainstem, while in rats with PPI 40% in the hippocampus and cortex. It is hypothesized that HBH is realized through topographically different sensory inputs, namely through respiratory neurons of the brainstem in rats with low PPI and respiratory neurons of the olfactory epithelium in rats with high PPI.