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NICOTINE EXCITES CARDIAC VAGAL NEURONS VIA THREE SITES OF ACTION
Author(s) -
Mendelowitz David
Publication year - 1998
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1998.tb02233.x
Subject(s) - sudden infant death syndrome , nicotine , medicine , glutamatergic , brainstem , electrophysiology , neuroscience , autonomic nervous system , neurotransmission , nicotinic agonist , vagal tone , glutamate receptor , anesthesia , receptor , heart rate , biology , blood pressure , pediatrics
SUMMARY 1. Nicotine is involved in many cardio‐respiratory diseases, including hypertension and sudden infant death syndrome (SIDS), which is the most common cause of death in infants between 1 month and 1 year of age. While the aetiology of SIDS remains largely unknown, recent clinical studies suggest maternal cigarette smoking is a major risk factor in SIDS and an abnormality of cardio‐respiratory control, particularly a centrally mediated slowing of the heart that precedes or accompanies apnoea, is involved. 2. Because the sites, mechanisms of action and diverse receptor types of nicotine within the central nervous system are controversial and poorly understood, in the present study we examined the effects of nicotine on specific brainstem neurons that control heart rate. Cardiac vagal neurons were identified in an in vitro slice preparation using a retrograde fluorescent tracer and were studied using both whole‐cell and perforated patch‐clamp electrophysiological techniques. 3. We have found there are different pre‐ and post‐synaptic nicotinic receptors that have dramatic effects on glutamatergic neurotransmission as well as directly activating vagal cardio‐inhibitory neurons.