Abstract

Activation of the trigeminocardiac reflex by airborne irritants or water, stimulates nasotrigeminal sensory fibers eliciting a pronounced bradycardia and increase in parasympathetic cardiac activity. Exaggeration of this response can be fatal, and has been implicated in cardiorespiratory diseases such as sudden infant death syndrome (SIDS). Parasympathetic cardiac vagal neurons (CVNs) in the nucleus ambiguus (NA) play an integral role in mediating this reflex. Stimulation of trigeminal sensory afferents elicits a polysynaptic excitatory glutamatergic neurotransmission to CVNs. We use a UV photo uncaging system to identify the neurons in the spinal trigeminal nucleus (sp5) that project to CVNs by sequential photostimulation of different neuron clusters as well as individual neurons that elicit excitatory glutamatergic neurotransmission to CVNs. Herpes simplex virus 1 expressing GFP was injected into the nasal mucosa of neonatal rats, and, using 2 photon confocal microscopy, areas of the brainstem expressing GFP+ trigeminal sensory afferent fibers within sp5 were identified. Preliminary results indicate scattered neurons in the sp5 that receive sensory afferent synaptic terminals project to and excite CVNs. Further work is necessary to determine if these neurons are located diffusely or in discrete clusters within the sp5.

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