Neural regulation of inflammation: no neural connection from the vagus to splenic sympathetic neurons.

The 'inflammatory reflex' acts through efferent neural connections from the central nervous system to lymphoid organs, particularly the spleen, that suppress the production of inflammatory cytokines. Stimulation of the efferent vagus has been shown to suppress inflammation in a manner dependent on the spleen and splenic nerves. The vagus does not innervate the spleen, so a synaptic connection from vagal preganglionic neurons to splenic sympathetic postganglionic neurons was suggested. We tested this idea in rats. In a preparatory operation, the anterograde tracer DiI was injected bilaterally into the dorsal motor nucleus of vagus and the retrograde tracer Fast Blue was injected into the spleen. On histological analysis 7-9 weeks later, 883 neurons were retrogradely labelled from the spleen with Fast Blue as follows: 89% in the suprarenal ganglia (65% left, 24% right); 11% in the left coeliac ganglion; but none in the right coeliac or either of the superior mesenteric ganglia. Vagal terminals anterogradely labelled with DiI were common in the coeliac but sparse in the suprarenal ganglia, and confocal analysis revealed no putative synaptic connection with any Fast Blue-labelled cell in either ganglion. Electrophysiological experiments in anaesthetized rats revealed no effect of vagal efferent stimulation on splenic nerve activity or on that of 15 single splenic-projecting neurons recorded in the suprarenal ganglion. Together, these findings indicate that vagal efferent neurons in the rat neither synapse with splenic sympathetic neurons nor drive their ongoing activity.

Intraspecific variability of the pulse-type discharges of the African electric fishes, Pollimyrus isidori and Petrocephalus bovei (Mormyridae, Teleostei), and their dependence on water conductivity.

The electric organ discharge (EOD) of the mormyrid Pollimyrus isidori is a short pulse with three phases: (1) weak head positive (P1); (2) strong head negative (N); (3) weak head positive (P2). 1. At a stable water conductivity (100 microS/cm), which is near the upper end of the natural range in tropical Africa, there was a statistically significant difference between the sexes only in one of five EOD parameters, the P-ratio. The P1-amplitude was lower than the P2-amplitude (i.e. P1/P2 less than 1) in males (N = 10), while, on average, the opposite (P1/P2 greater than 1) was true for females (N = 14). Because of wide overlapping we do not consider this sex difference to be a sexual dimorphism. The difference between males and females could be due to well-known biophysical and physiological reasons (discussed later) and need not be the result of intraspecific selection (such as female choice). 2. Water conductivity seriously affected the EOD waveform. The P-ratio decreased in 2/3 of our fish (16 out of 24), as conductivity increased from 5 to 200 microS/cm, causing 6 out of 14 females to change from a P-ratio of greater than 1 to a P-ratio of less than 1, becoming more "male-like". P1 amplitude increased with decreasing conductivity in the EODs of 5 out of 10 males to a more "female-like" shape (P-ratio greater than 1). The P-ratio changed only slightly when above a conductivity of 200 microS/cm. The N-wave duration increased with decreasing conductivity, while the peak amplitude frequency of an EOD amplitude spectrum decreased. 3. Long-term stability was found to be poor in the EOD of 1 female (better in 2 other fish), which changed from a "female-like" waveform (P-ratio greater than 1) to a "male-like" waveform (P-ratio less than 1 over the whole conductivity range) without apparent reason within 120 days. 4. The EOD waveform of Petrocephalus bovei did not show a sex difference. Decreasing conductivity affected the EOD of P. bovei in a similar way to most P. isidori: the P1-wave increased and the P2-wave decreased, while the N-wave broadened strongly. 5. The occurrence of multiple discharges per primary neural command signal at very low conductivities, indicates that P. isidori is adapted to conductivities above 17 microS/cm, and P. bovei to those above 5 microS/cm.(ABSTRACT TRUNCATED AT 400 WORDS)

Immunohistochemical demonstration of calbindin-D 28K (CABP28K) in the spinal cord motoneurons of teleost fish.

The distribution and localization of the calcium-binding protein, calbindin-D 28K (CaBP28K), in the spinal cord motoneurons of larvae of the teleost fish, Apteronotus leptorhynchus (Gymnotidae) and Pollimyrus isidori (Mormyridae), and in the adult goldfish, Carassius auratus (Cyprinidae), were determined by means of immunohistochemistry. Sections of whole larvae and goldfish spinal cord were reacted with a polyclonal antibody to rat renal CaBP28K. CaBP28K was located by the PAP technique (Sternberger). It was found in the soma, dendrites, axons and axon terminals of spinal motoneurons but not in those of electromotoneurons of Apteronotus leptorhynchus, whereas it occurred in both motoneurons and electromotoneurons of the larval electric organ of Pollimyrus isidori. In these species CaBP28K was also present in the electromotoneuron axon terminals that make synaptic contacts with the pedicles of the electrocytes. In adult Carassius auratus, CaBP28K was found in the soma, dendrites and axons of certain spinal motoneurons. The results indicate that, in teleosts, the motoneurons containing CaBP28K may represent a well-defined population within the spinal cord; the role of this protein in these cells remains to be determined.