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1 Department of Physiology and Biophysics, Howard University, Washington, DC, USA
2 Department of Pediatrics, Case Western Reserve University, Cleveland, OH, USA
3 Department of Pharmacology, Howard University, Washington, DC, USA
4 Department of Physiology and Biophysics, Howard University, Washington, DC, USA; Department of Pediatrics, Case Western Reserve University, Cleveland, OH, USA; Department of Anatomy, Case Western Reserve University, Cleveland, OH, USA
* To whom correspondence should be addressed. E-mail: mhaxhiu{at}howard.edu.
GABA is the main inhibitory neurotransmitter that participates in the regulation of cholinergic outflow to the airways. We have tested the hypothesis that a monosynaptic GABAergic circuit modulates the output of airway-related vagal preganglionic neurons (AVPNs) in the rostral nucleus ambiguus (rNA) using a dual labeling electron microscopic method combining immunocytochemistry for glutamic acid decarboxylase (GAD) with retrograde tracing from the trachea. We also determined the effects of blockade of GABAA receptors upon airway smooth muscle tone. The results showed that retrogradely labeled AVPNs received a significant GAD-immunoreactive (GAD-IR) terminal input. Out of a pooled total of 3161 synaptic contacts with retrogradely labeled somatic and dendritic profiles, 20.2% were GAD-IR. GAD-IR terminals formed significantly more axo-somatic synapses than axo-dendritic synapses (p < 0.02). A dense population of GABAergic synaptic contacts on AVPNs provides a morphological basis for potent physiological effects of GABA upon the excitability of AVPNs. GAD-IR terminals formed exclusively symmetric synaptic specializations. GAD-IR terminals were significantly larger (p < 0.05) in both length and width than unlabeled terminals synapsing on AVPNs. Therefore, the structural characteristics of certain nerve terminals may be closely correlated with their function. Pharmacological blockade of GABAA receptors within the rNA increased activity of putative AVPNs and airway smooth muscle tone. We conclude that a tonically active monosynaptic GABAergic circuit utilizing symmetric synapses regulates the discharge of AVPNs.
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