Neurturin has multiple neurotrophic effects on adult rat sacral parasympathetic ganglion neurons

2005 ◽  
Vol 22 (3) ◽  
pp. 595-604 ◽  
Author(s):  
Yewlan Wanigasekara ◽  
Janet R. Keast
1987 ◽  
Vol 58 (2) ◽  
pp. 276-287 ◽  
Author(s):  
M. D. Womble ◽  
S. Roper

1. To study the retrograde effects of changes in target tissue upon the innervating nerve supply, we have examined the parasympathetic submandibular ganglion of the adult rat. Neurons of this ganglion innervate the submandibular and sublingual salivary glands. 2. Ligating the salivary ducts leads to rapid and prolonged salivary gland cell atrophy. 3. Duct ligations, without direct injury to the glandular nerve supply, initially produced few alterations in the ganglion. After 8 wk, however, neuron number was reduced by 50%. The numbers of presynaptic inputs/neuron and synapses/neuron perimeter were not affected by the cell loss. 4. After 1 wk of duct ligation in which the glandular nerve supply was intentionally damaged, some ganglionic neurons have lost all presynaptic inputs, suggesting synaptic disjunction. This is followed at 3 wk by a 40% decrease in neuron number and an increase in the number of inputs per (remaining) ganglion cell. However, the number of synapses/neuronal profile was unchanged. 5. Thus axotomy plus target atrophy causes synaptic disjunction, neuron cell death, and input rearrangement, presumably due to a combination of direct injury effects and an abrupt loss of peripheral trophic supplies. 6. In contrast, target atrophy alone produced more gradual changes in submandibular ganglion neurons. Only prolonged target atrophy leads to a decrease in the number of ganglionic neurons, perhaps due to the gradual loss of peripheral trophic supplies. However, other features, such as the number of inputs/cell and the number of synapses/neuron perimeter, remain unaltered. Evidently, the gradual loss of trophic support does not result in synaptic disjunction to the degree needed to produce presynaptic input rearrangement.


2000 ◽  
Vol 278 (3) ◽  
pp. L485-L491 ◽  
Author(s):  
Radhika Kajekar ◽  
Allen C. Myers

The effect of bradykinin on membrane properties of parasympathetic ganglion neurons in isolated guinea pig bronchial tissue was studied using intracellular recording techniques. Bradykinin (1–100 nM) caused a reversible membrane potential depolarization of ganglion neurons that was not associated with a change in input resistance. The selective bradykinin B2 receptor antagonist HOE-140 inhibited bradykinin-induced membrane depolarizations. Furthermore, the cyclooxygenase inhibitor indomethacin attenuated bradykinin-induced membrane depolarizations to a similar magnitude (∼70%) as HOE-140. However, neurokinin-1 and -3 receptor antagonists did not have similar inhibitory effects. The ability of bradykinin to directly alter active properties of parasympathetic ganglion neurons was also examined. Bradykinin (100 nM) significantly reduced the duration of the afterhyperpolarization (AHP) that followed four consecutive action potentials. The inhibitory effect of bradykinin on the AHP response was reversed by HOE-140 but not by indomethacin. These results indicate that bradykinin can stimulate airway parasympathetic ganglion neurons independent of sensory nerve activation and provide an alternative mechanism for regulating airway parasympathetic tone.


1994 ◽  
Vol 72 (6) ◽  
pp. 2796-2815 ◽  
Author(s):  
M. A. Rizzo ◽  
J. D. Kocsis ◽  
S. G. Waxman

1. Voltage-dependent Na+ conductances were studied in small (18-25 microns diam) adult rat dorsal root ganglion (DRG) neurons with the use of the whole cell patch-clamp technique. Na+ currents were also recorded from larger (44-50 microns diam) neurons and compared with those of the small neurons. 2. The predominant Na+ conductance in the small neurons was selective over tetramethylammonium by at least 10-fold and was resistant to 1 microM external tetrodotoxin (TTX). Na+ conductances in many larger DRG neurons were kinetically faster and, in contrast, were blocked by 1 microM TTX. 3. The Na+ conductance in the small neurons was kinetically slow. Activation half-times were voltage dependent and ranged from 2 ms at -20 mV to 0.7 ms at +50 mV. Approximately 50% of the activation half-time was comprised of an initial delay. Inactivation half-times were voltage dependent and ranged from 11 ms at -20 mV to 2 ms at +50 mV. 4. Peak slow Na+ conductances were near maximal with conditioning potentials negative to -120 mV and were significantly reduced or eliminated with conditioning potentials positive to -40 mV. The slow Na+ conductance increased gradually with test potentials extending from -40 to +40 mV. In some cells the conductance could be saturated at +10 mV. Peak conductance/voltage relationships, although stable in a given neuron, revealed marked variability among neurons, spanning > 20- and 50-mV domains for steady-state activation and inactivation (current availability), respectively. 5. Kinetics remained stable within a given neuron over the course of an experiment. However, considerable kinetic variation was exhibited from neuron to neuron, such that the half-times of activation and of inactivation spanned an order of magnitude. In all small neurons studied there appeared to be a singular kinetic component of the current, based on sensitivity to the conditioning potential, voltage dependence of activation, and inactivation half-time. 6. Unique closing properties were exhibited by Na+ channels of the small neurons. Hyperpolarization following a depolarization-induced fully inactivated state resulted in tail currents that appeared to be the consequence of reactivation of the slow Na+ conductance. Tail currents recorded at various times during a fixed level of depolarization revealed that the underlying channels accumulated into a volatile inactivated state over the course of the preceding depolarization.(ABSTRACT TRUNCATED AT 400 WORDS)


2004 ◽  
Vol 113 (1-2) ◽  
pp. 32-42 ◽  
Author(s):  
Rainer Viktor Haberberger ◽  
Nadia Bernardini ◽  
Michaela Kress ◽  
Petra Hartmann ◽  
Katrin Susanne Lips ◽  
...  

2015 ◽  
Vol 144 (3) ◽  
pp. 249-259 ◽  
Author(s):  
Masami Tsukamoto ◽  
Naoko Niimi ◽  
Kazunori Sango ◽  
Shizuka Takaku ◽  
Yasushi Kanazawa ◽  
...  

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