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Developmental nicotine exposure increases the response to muscimol in hypoglossal motoneurons.
Author(s) -
Wollman Lila,
Levine Richard B,
Fregosi Ralph F
Publication year - 2017
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.31.1_supplement.1055.4
Subject(s) - cnqx , muscimol , strychnine , chemistry , glycine receptor , inhibitory postsynaptic potential , neuroscience , agonist , endocrinology , medicine , tetrodotoxin , glutamate receptor , reversal potential , patch clamp , ampa receptor , receptor , biology , glycine , biochemistry , amino acid
Prenatal nicotine exposure with continued exposure through breast milk over the first week of life (developmental nicotine exposure, DNE) is known to cause complex changes to the brainstem respiratory circuit including increased sensitivity to inhibitory neurotransmitters and increased staining of GABA A R‐1a subunit in the hypoglossal nucleus. Here we test the hypothesis that DNE alters the response of hypoglossal motoneurons (XII MNs) to the GABA A receptor agonist Muscimol. We obtained whole cell patch clamp recordings from XII MNs in medullary slices (700 micron thick) from DNE pups and control pups. Cells were voltage clamped at −75mV. Using a cesium based intracellular solution, and in the presence of the AMPA receptor antagonists 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX), the NMDA receptor antagonist D(‐)‐2‐Amino‐5‐phosphonopentanoic acid (AP‐5), the glycine receptor antagonist Strychnine, and the voltage gated sodium channel blocker Tetrodotoxin, bath application of 0.5 mM Muscimol produces an inward current in these cells. We measured peak inward current from 10 control cells and 10 DNE cells. Our results show that DNE causes in an increased GABA A receptor mediated inward current (Control {n=10} −239.3±30.75 pA, DNE {n=10} −364.4±38.7 pA, P=0.02). This result is consistent with DNE causing increased GABA A receptor expression in XII MNs. Support or Funding Information NIH RO1H071302 AHA 12GRXIT120S0354