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1 Pharmacology and Physiology, George Washington University, Washington, DC, USA
* To whom correspondence should be addressed. E-mail: dmendel{at}gwu.edu.
Nicotinic receptors play an important role in modulating the activity of parasympathetic cardiac vagal neurons in the medulla. Previous work has shown nicotine acts via at least three mechanisms to excite brainstem premotor cardiac vagal neurons. Nicotine evokes a direct increase in holding current, and facilitates both the frequency and amplitude of glutamatergic neurotransmission to cardiac vagal neurons. This study tests whether these nicotinic receptor mediated responses are endogenously active, whether [[alpha]}4
2 and 
7 nicotinic receptors are involved, and if prenatal exposure to nicotine alters the magnitude of these responses and the types of nicotinic receptors involved. Application of neostigmine (10 µM) significantly increased the holding current, amplitude and frequency of mEPSC glutamatergic events in cardiac vagal neurons. In unexposed animals the nicotine evoked facilitation of mEPSC frequency, but not mEPSC amplitude or holding current, was blocked by -bungarotoxin (100 nM). Prenatal nicotine exposure significantly exaggerated and altered the types of nicotinic receptors involved in these responses. In prenatal nicotine exposed animals -bungarotoxin only partially reduced the increase in mEPSC frequency. In addition, in prenatal nicotine exposed animals the increase in holding current was partially dependent on -7 subunit containing nicotinic receptors, in contrast to unexposed animals in which -bungarotoxin had no effect. These results indicate prenatal nicotine exposure, one of the highest risk factors for SIDS, exaggerates the responses and changes the types of nicotinic receptors involved in exciting premotor cardiac vagal neurons. These alterations could be responsible for the pronounced bradycardia that occurs during apnea in SIDS victims.
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