To improve the pathophysiological understanding of visual changes observed in astronauts, we aimed to use quantitative MRI to measure anatomic and physiological responses during a ground-based spaceflight analog (head-down tilt, HDT) combined with increased ambient carbon dioxide (CO). Six healthy, male subjects participated in the double-blinded, randomized crossover design study with two conditions: 26.5 h of -12° HDT with ambient air and with 0.5% CO, both followed by 2.5-h exposure to 3% CO Volume and mean diffusivity quantification of the lateral ventricle and phase-contrast flow sequences of the internal carotid arteries and cerebral aqueduct were acquired at 3 T. Compared with supine baseline, HDT (ambient air) resulted in an increase in lateral ventricular volume ( = 0.03). Cerebral blood flow, however, decreased with HDT in the presence of either ambient air or 0.5% CO ( = 0.002 and = 0.01, respectively); this was partially reversed by acute 3% CO exposure. Following HDT (ambient air), exposure to 3% CO increased aqueductal cerebral spinal fluid velocity amplitude ( = 0.01) and lateral ventricle cerebrospinal fluid (CSF) mean diffusivity ( = 0.001). We concluded that HDT causes alterations in cranial anatomy and physiology that are associated with decreased craniospinal compliance. Brief exposure to 3% CO augments CSF pulsatility within the cerebral aqueduct and lateral ventricles. Head-down tilt causes increased lateral ventricular volume and decreased cerebrovascular flow after 26.5 h. Additional short exposure to 3% ambient carbon dioxide levels causes increased cerebrovascular flow associated with increased cerebrospinal fluid pulsatility at the cerebral aqueduct. Head-down tilt with chronically elevated 0.5% ambient carbon dioxide and acutely elevated 3% ambient carbon dioxide causes increased mean diffusivity of cerebral spinal fluid within the lateral ventricles.

This study aimed to characterize the excitability changes in peripheral motor axons caused by hindlimb unloading (HLU), which is a model of disuse neuromuscular atrophy. HLU was performed in normal 8-week-old male mice by fixing the proximal tail by a clip connected to the top of the animal's cage for 3 weeks. Axonal excitability studies were performed by stimulating the sciatic nerve at the ankle and recording the compound muscle action potential (CMAP) from the foot. The amplitudes of the motor responses of the unloading group were 51% of the control amplitudes [2.2 ± 1.3 mV (HLU) vs. 4.3 ± 1.2 mV (Control), P = 0.03]. Multiple axonal excitability analysis showed that the unloading group had a smaller strength-duration time constant (SDTC) and late subexcitability (recovery cycle) than the controls [0.075 ± 0.01 (HLU) vs. 0.12 ± 0.01 (Control), P < 0.01; 5.4 ± 1.0 (HLU) vs. 10.0 ± 1.3 % (Control), P = 0.01, respectively]. Three weeks after releasing from HLU, the SDTC became comparable to the control range. Using a modeling study, the observed differences in the waveforms could be explained by reduced persistent Na+ currents along with parameters related to current leakage. Quantification of RNA of a SCA1A gene coding a voltage-gated Na+ channel tended to be decreased in the sciatic nerve in HLU. The present study suggested that axonal ion currents are altered in vivo by HLU. It is still undetermined whether the dysfunctional axonal ion currents have any pathogenicity on neuromuscular atrophy or are the results of neural plasticity by atrophy.

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