The long term goal of this application is to establish the brainstem circuits through which trigeminal neurons modulate cardiorespiratory activity in mammals. The cardiorespiratory depression (the diving response) seen after stimulation of the upper respiratory tract in the muskrat serves as the model. The aims for this proposal specifically are to 1) demonstrate the role of the nucleus tractus solitarii in the cardiorespiratory depression after URT stimulation; 2) define the efferent projections of the peribrachial region in the muskrat; and, 3) locate cardiomotor neurons in the muskrat. The nasal part of the upper respiratory tract will be stimulated with ammonia vapors, or electrically, while lower parts of the upper respiratory tract will be stimulated with electrical excitation of the superior laryngeal nerve. Experiments in aim 1 documenting the change in the respiratory and cardiovascular responses to URT stimulation after lesions of the dorsomedial medulla will determine if the nucleus tractus solitarii is important in the diving response. No change in the responses would suggest the circuits for the diving response is mediated by other routes. In aims 2 and 3, neuroanatomical methods employing both the anterograde and retrograde transport of tracer substances will determine parabrachial efferent projections, especially those to the ventrolateral medulla, and the location of motor neurons to the heart. Data from these experiments will provide the anatomical substrate tp guide future physiological investigations. Stimulation of the upper respiratory tract in man causes respiratory and cardiovascular depression. Such depression is especially pronounced in infants and could lead to their death. The Sudden Infant Death Syndrome, the etiology which is unknown, is the leading cause of mortality in the neonate. Understanding the brainstem mechanisms governing cardiorespiratory depression after stimulation of the upper respiratory tract may provide a neurological explanation for this syndrome.