Chronic intermittent hypoxia enhances spontaneous synaptic transmission in NTS neurons, providing a potential mechanism for the autonomic dysfunction and hypertension seen in this model.
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Suggests NTS synaptic enhancement as mechanism in CIH hypertension models; leaves open relevance to human sleep apnea.
CIH induces several changes in the cardiovascular system including hypertension. Previous experiments from our laboratory showed that juvenile rats exposed to CIH presented hypertension and an increased sympathoexcitatory response to chemoreflex activation. In the present study we evaluated possible changes in synaptic transmission in NTS neurons of juvenile rats submitted to CIH. 21‐day‐old rats were exposed to 10 days of CIH, and after this period electrophysiological experiments were performed in brainstem slices containing NTS. After CIH, spontaneous synaptic transmission in NTS neurons was enhanced. The frequency of total spontaneous post‐synaptic currents (sPSCs) was significantly increased in NTS neurons of CIH rats (n=21) when compared to NTS neurons of control rats (n=27), (1.84 ± 0.30 Hz vs 1.19 ± 0.17Hz, p<0.05). In addition, amplitude (39.2 ± 4.7 vs 27.0 ± 2.6 pA, p<0.05) and half‐width (3.18 ± 0.30 vs 2.20 ± 0.20 ms, p<0.01) of those spontaneous events were also augmented in NTS neurons of CIH rats. Moreover, half‐width of glutamatergic spontaneous current was increased after CIH (2.49 ± 0.16 vs 1.86 ± 0.14 ms, p<0.01). These data indicate that CIH enhances spontaneous synaptic transmission in NTS neurons, which may explain, at least in part, the autonomic dysfunction and hypertension observed on this experimental model. Supported by FAPESP and CNPq.
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Almado et al. (2008) studied this question.
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