The origin of catecholaminergic nerve fibers in the subdiaphragmatic vagus nerve of rat.

Department of Animal Biology and the Institute of Neurological Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104-6045, USA.
Journal of the Autonomic Nervous System 06/1999; 76(2-3):108-17. DOI: 10.1016/S0165-1838(99)00014-4
Source: PubMed

ABSTRACT It is known that the vagus nerve contains catecholaminergic fibers. However, the origin of these fibers has not been systematically examined. In this study, we addressed this issue using retrograde tracing from the subdiaphragmatic vagus nerve combined with immunocytochemistry. The cervical and thoracic sympathetic trunk ganglia, the nodose ganglia and the dorsal motor nucleus of the vagus nerve were examined following injection of Fluoro-Gold or cholera toxin horseradish peroxidase conjugate into the trunks of the subdiaphragmatic vagus nerve of rats. Numerous retrogradely labeled neurons were seen in the nodose ganglion and the dorsal motor nucleus of the vagus nerve. Very few labeled neurons were found in the sympathetic ganglia (less than 0.06% of the neurons in either superior cervical ganglion or cervicothoracic ganglion were retrogradely labeled). Double labeling with immunofluoresence for catecholamine synthesizing enzymes revealed that: (1) 92% of all Fluoro-Gold retrogradely labeled tyrosine hydroxylase immunoreactive neurons were found in parasympathetic sources (75% in the dorsal motor nucleus of the vagus nerve and 17% in the nodose ganglia), and only 8% in the cervicothoracic sympathetic ganglia; (2) 12% of the retrogradely labeled catecholaminergic neurons in the dorsal motor nucleus of the vagus nerve were also dopamine-beta-hydroxylase immunopositive neurons; (3) 70% of the retrogradely labeled neurons in the sympathetic ganglia were tyrosine hydroxylase immunopositive and 54% of these catecholaminergic neurons contained dopamine-beta-hydroxylase, while 30% of the retrogradely labeled neurons were non-catecholaminergic neurons. These results indicate that catecholaminergic fibers in the abdominal vagus nerve are primarily dopaminergic and of parasympathetic origin, and that only an extremely small number of these fibers, mostly noradrenergic in nature, arise from postganglionic sympathetic neurons.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Innervation of the cervix is important for normal timing of birth because transection of the pelvic nerve forestalls birth and causes dystocia. To discover whether transection of the parasympathetic innervation of the cervix affects cervical ripening in the process of parturition was the objective of the present study. Rats on Day 16 of pregnancy had the pelvic nerve (PnX) or the vagus nerve (VnX) or both pathways (PnX+VnX) transected, sham-operated (Sham) or nonpregnant rats served as controls. Sections of fixed peripartum cervix were stained for collagen or processed by immunohistochemistry to identify macrophages and nerve fibers. All Sham controls delivered by the morning of Day 22 postbreeding, while births were delayed in more than 75% of neurectomized rats by more than 12 h. Dystocia was evident in more than 25% of the PnX and PnX+VnX rats. Moreover, on prepartum Day 21, serum progesterone was increased severalfold in neurectomized versus Sham rats. Assessments of cell nuclei counts indicated that the cervix of neurectomized rats and Sham controls had become equally hypertrophied compared to the unripe cervix in nonpregnant rats. Collagen content and structure were reduced in the cervix of all pregnant rats, whether neurectomized or Shams, versus that in nonpregnant rats. Stereological analysis of cervix sections found reduced numbers of resident macrophages in prepartum PnX and PnX+VnX rats on Day 21 postbreeding, as well as in VnX rats on Day 22 postbreeding compared to that in Sham controls. Finally, nerve transections blocked the prepartum increase in innervation that occurred in Sham rats on Day 21 postbreeding. These findings indicate that parasympathetic innervation of the cervix mediates local inflammatory processes, withdrawal of progesterone in circulation, and the normal timing of birth. Therefore, pelvic and vagal nerves regulate macrophage immigration and nerve fiber density but may not be involved in final remodeling of the extracellular matrix in the prepartum cervix. These findings support the contention that immigration of immune cells and enhanced innervation are involved in processes that remodel the cervix and time parturition.
    Biology of Reproduction 11/2010; 84(3):587-94. · 4.03 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Copper plays an essential role in the function and development of the central nervous system and the exocrine pancreas. Dietary copper limitation is known to result in a non-inflammatory atrophy of pancreatic acinar tissue. Our recent studies have suggested that vagal motoneurons regulate pancreatic exocrine secretion (PES) by activating selective subpopulations of neurons within vago-vagal reflexive neurocircuits. In this study, we used a combination of in vivo, in vitro and immunohistochemistry techniques in a rat model of copper deficiency to investigate the effects of a copper deficient diet on vago-vagal reflexes controlling PES. Duodenal infusions of Ensure ® or casein as well as microinjections of cholecystokinin (CCK-8s) into the dorsal vagal complex (DVC) resulted in an attenuated stimulation of PES in copper deficient animals compared to controls. Immunohistochemistry of brainstem slices revealed that copper deficiency reduced the number of tyrosine hydroxylase (TH) immunoreactive, but not the number of neuronal nitric oxide synthase (NOS)- or choline acetyltransferase (ChAT)-immunoreactive neurons in the dorsal motor nucleus of the vagus (DMV). Moreover, copper deficient diet reduced the number of large (>11 neurons), but not small intrapancreatic ganglia, particularly in the tail of the pancreas. Electrophysiological recordings showed that DMV neurons from copper deficient rats are less responsive to CCK-8 or PP than DMV neurons from control rats. Our results demonstrate that copper deficiency decreases efferent vagal outflow to the exocrine pancreas. These data suggest that selective loss of acinar pancreatic tissue results in a decreased excitability of efferent vagal neurons that regulate PES.
    AJP Gastrointestinal and Liver Physiology 12/2012; · 3.65 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Vasopressin (VP)-, neuropeptide FF (NPFF)-, and tyrosine hydroxylase (TH)-expressing neurons were studied by means of single and double immunocytochemistry in the human brainstem of controls who died suddenly due to trauma and of patients who suffered from essential hypertension and died due to acute myocardial infarction, while in one case there was brain hemorrhage. In the control and hypertensive groups VP fibers and NPFF neurons and fibers were the most abundantly present in the dorsal vagal complex, especially in the dorsal motor nucleus of the vagus. Numerous VP and NPFF fibers formed synaptic-like contacts with neuronal profiles in the dorsointermediate, centrointermediate, ventrointermediate, caudointermediate, and caudal parts of the dorsal motor nucleus of vagus as well as adjacent medial and intermediate subnuclei of the solitary nucleus. VP, but not NPFF, positive fibers were found to vastly contact TH-positive neuronal profiles in A2/C2, A2, and ambiguus nucleus (Amb). The density of VP fibers in the dorsal motor nucleus of the vagus and Amb did not differ between hypertensive patients and controls, whereas the density of NPFF fibers in hypertensives was 3.19 times lower in the dorsal motor nucleus of vagus and markedly decreased in the Amb. In both groups, VP and NPFF were scarcely present in the pain pathways, suggesting that these peptides are not crucially involved in nociceptive control in human. The reduction of NPFF release within the dorsal motor nucleus and Amb could serve as a possible cause of the impairment of cardiac vagal control in hypertensive patients.
    The Journal of Comparative Neurology 01/2011; 519(1):93-124. · 3.66 Impact Factor