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GABAergic modulation of NTS‐VLM neurons from Wistar Hannover and Sprague Dawley Rats is reduced by sustained hypoxia
Author(s) -
PascoalotiLima Júlio,
Machado Benedito,
AccorsiMendonça Daniela
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2021.35.s1.03921
Subject(s) - gabaergic , inhibitory postsynaptic potential , medulla , postsynaptic current , patch clamp , biology , endocrinology , hypoxia (environmental) , medicine , excitatory postsynaptic potential , electrophysiology , anatomy , neuroscience , chemistry , organic chemistry , oxygen
Short‐term sustained Hypoxia (SH) induces a different pattern of cardiovascular and respiratory responses in rats from Wistar Ribeirão Preto (WRP), Wistar Hannover (WH) and Sprague Dawley (SD) strains. SH induces an increase in the respiratory parameters of rats from these three strains and mean arterial pressure in WRP and SD but not in WH rats. In WRP rats submitted to SH, we documented an increase in the excitability of NTS neurons sending projections to the ventral medulla (NTS‐VLM), which is part of the chemoreflex pathways. However, the role of GABAergic modulation on the neuronal excitability of NTS neurons from different strains of rats submitted to SH was not yet explored. In the present study, we evaluated the inhibitory modulation (GABAergic synaptic activity) onto NTS‐VLM neurons from WH and SD rats previously submitted to SH. The experimental protocols were approved by the Institutional Ethics Committee (#136/2018). NTS‐VLM neurons were labeled with retrograde tracer (Greenbeads) previously microinjected into VLM of WH and SD rats (25‐30 days old). Ten days later, these rats were submitted to SH protocol (24hs, FiO2 0.1). Then NTS slices were obtained, and the evoked and spontaneous inhibitory postsynaptic currents (eIPSCs and sIPSCs, respectively) were recorded in labeled NTS‐VLM neurons using whole‐cell patch‐clamp. SH decreased the amplitude of eIPSCs in NTS‐VLM neurons from WH [‐172 ± 36 (n=7) vs ‐58.1 ± 9.3 pA (n=7), p=0.0100] and also from SD rats [‐231.8 ± 33.9 (n=9) vs ‐48.9 ± 10.5 pA (n=6), p=0.0009]. SH decreased the decay‐time in NTS‐VLM neurons from SD rats (25.4 ± 5.1 vs 9.2 ± 1.2 ms, p= 0.0247) but produced no change in the rise‐time of the events in both rat strains. SH decreased the frequency of sIPSCs in NTS‐VLM neurons from WH [1.7 ± 0.4 (n=8) vs 0.8 ± 0.2 Hz, (n=9), p=0.0290] and from SD rats [2.3 ± 0.17 (n=5) vs 0.51 ± 0.13 ms (n=6), p<0.0001]. No significant changes were observed in amplitude and half‐width of sIPSCs of NTS‐VLM neurons from both rat strains. The data show that SH decreases the evoked and spontaneous GABAergic neurotransmission on NTS‐VLM neurons from WH and SD rats, probably by affecting the presynaptic terminal. The observed change in GABAergic modulation onto the NTS neuronal excitability may explain the observed alterations in the respiratory pattern in WH and SD rats in response to SH.