Dopamine Modulates Synaptic Transmission in the Nucleus of the Solitary Tract

1 Rammelkamp Center for Education and Research, MetroHealth Medical System and 2 Department of Neuroscience, Case Western Reserve University, Cleveland, Ohio 44109-1998 Kline, David D., Kristin N. Takacs, Eckhard Ficker, and Diana L. Kunze. Dopamine Modulates Synaptic Transmission in the Nucleus...

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Published in:	Journal of neurophysiology Vol. 88; no. 5; pp. 2736 - 2744
Main Authors:	Kline, David D, Takacs, Kristin N, Ficker, Eckhard, Kunze, Diana L
Format:	Journal Article
Language:	English
Published:	United States Am Phys Soc 01-11-2002
Subjects:	Animals Brain Stem - drug effects Brain Stem - physiology Dopamine - pharmacology Electrophysiology Excitatory Postsynaptic Potentials - drug effects Immunohistochemistry In Vitro Techniques Male Membrane Potentials - physiology Microscopy, Fluorescence Neurons, Afferent - drug effects Neurons, Afferent - physiology Patch-Clamp Techniques Rats Rats, Sprague-Dawley Receptors, Dopamine D1 - drug effects Receptors, Dopamine D1 - metabolism Receptors, Dopamine D2 - drug effects Receptors, Dopamine D2 - metabolism Solitary Nucleus - drug effects Solitary Nucleus - physiology Synaptic Transmission - drug effects Synaptophysin - metabolism
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Summary:	1 Rammelkamp Center for Education and Research, MetroHealth Medical System and 2 Department of Neuroscience, Case Western Reserve University, Cleveland, Ohio 44109-1998 Kline, David D., Kristin N. Takacs, Eckhard Ficker, and Diana L. Kunze. Dopamine Modulates Synaptic Transmission in the Nucleus of the Solitary Tract. J. Neurophysiol. 88: 2736-2744, 2002. 10.1152/jn.00224.2002. Dopamine (DA) modulates the cardiorespiratory reflex by peripheral and central mechanisms. The aim of this study was to examine the role of DA in synaptic transmission of the nucleus tractus solitarius (NTS), the major integration site for cardiopulmonary reflexes. To examine DA's role, we used whole cell, voltage-clamp recordings in a rat horizontal brain stem slice. Solitary tract stimulation evoked excitatory postsynaptic currents (EPSCs) that were reduced to 70 ± 5% of control by DA (100 µM). The reduction in EPSCs by DA was accompanied by a decrease in the paired pulse depression ratio with little or no change in input resistance or EPSC decay, suggesting a presynaptic mechanism. The D1-like agonist SKF 38393 Br (30 µM) did not alter EPSC amplitude, whereas the D2-like agonist, quinpirole HCl (30 µM), depressed EPSCs to 73 ± 4% of control. The D2-like receptor antagonist, sulpiride (20 µM), abolished DA modulation of EPSCs. Most importantly, sulpiride alone increased EPSCs to 131 ± 10% of control, suggesting a tonic D2-like modulation of synaptic transmission in the NTS. Examination of spontaneous EPSCs revealed DA reversibly decreased the frequency of events from 9.4 ± 2.2 to 6.2 ± 1.4 Hz. Sulpiride, however, did not alter spontaneous events. Immunohistochemistry of NTS slices demonstrated that D2 receptors colocalized with synaptophysin and substance P, confirming a presynaptic distribution. D2 receptors also localized to cultured petrosal neurons, the soma of presynaptic afferent fibers. In the petrosal neurons, D2 was found in cells that were TH-immunopositive, suggesting they were chemoreceptor afferent fibers. These results demonstrate that DA tonically modulates synaptic activity between afferent sensory fibers and secondary relay neurons in the NTS via a presynaptic D2-like mechanism.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2
ISSN:	0022-3077 1522-1598
DOI:	10.1152/jn.00224.2002