Sensory ganglia as a target of autonomic and sensory nerve fibres in the guinea-pig

Neuroscience ◽  
1994 ◽  
Vol 59 (3) ◽  
pp. 739-754 ◽  
Author(s):  
W. Kummer
Development ◽  
1985 ◽  
Vol 86 (1) ◽  
pp. 109-124
Author(s):  
Gavin J. Swanson

What constrains growing nerves to follow the paths they take during the development of peripheral nerve patterns? This paper examines two, related, topics concerning the pathways taken by sensory nerve fibres in the embryo chick wing: the constraints imposed on the nerves by limb tissues; and the timing of axon outgrowth. Sensory ganglia from 7-day-old chick embryos were grafted into younger host embryo wing buds which had been previously denervated. The resultant nerve patterns revealed that, first, nerve fibres could grow almost anywhere within the wing bud, with the exceptions of cartilage and a region just beneath the growing tip. Secondly, the younger the host wing bud at the time of grafting, the more likely the neurites were to form a thick fascicle which followed the limb's normal nerve pathways. The wing apparently does not impose a rigid restraint on nerves to grow only along certain routes; however, if a nerve fibre reaches a normal nerve pathway, it prefers to follow it.


1967 ◽  
Vol 46 (1) ◽  
pp. 63-84
Author(s):  
K. M. CHAPMAN ◽  
J. H. PANKHURST

1. Conduction velocities of individual afferent nerve fibres from tactile spines and proprioceptive campaniform sensilla have been measured in situ over the temperature range 5-42° C., in leg preparations of the cockroach Periplaneta americana. 2. Conduction velocities at 20° C. (u20) averaged 3.3±1.4 m./sec., ranging from 1.6 to 11.0 m./sec. 3. Temperature coefficients, expressed as Q10 for the interval 20-30° C., averaged 1.7±0.24, ranging from 1.3 to 2.6. 4. The length of the propagated disturbance is about 2-3 mm., and is nearly temperature-independent. 5. Fibre diameters, estimated from conduction velocity, must be about 10 µ. 6. There is no correlation between conduction velocity and distance from the sensillum to the thoracic ganglion. Conduction delays in fibres conducting within one standard deviation of mean u20 range from about 2 to 15 msec., from the most proximal to the most distal tactile spines. 7. The effect of conduction delay on temporal and spatial sensory encoding is probably unimportant from a behavioural point of view. It contributes a factor of the form exp(-sd/u) to the sensory transfer function, and may be appreciable at upper physiological frequencies of impulse frequency modulation.


2008 ◽  
Vol 155 (4) ◽  
pp. 547-557 ◽  
Author(s):  
M G Belvisi ◽  
H J Patel ◽  
V Freund-Michel ◽  
D J Hele ◽  
N Crispino ◽  
...  

1986 ◽  
Vol 11 (1) ◽  
pp. 125-130
Author(s):  
M. SAKURAI

Sympathetic nerve fibres innervating the sweat glands in the skin are known to accompany sensory nerve fibres closely. Examination of sudorific function, therefore, is a useful aid in making a diagnosis of severed peripheral nerve and also provides valuable information on nerve function in the recovery stage following injury and surgery such as neurorrhaphy. Among the many methods which have been used clinically, the one employing bromphenol blue is thought to be the most simple and accurate.


2000 ◽  
Vol 29 (6) ◽  
pp. 387-391 ◽  
Author(s):  
C. Cavallotti ◽  
M. Artico ◽  
N. Pescosolido ◽  
F. M. Tranquilli Leali ◽  
E. Pacella

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.


1995 ◽  
Vol 269 (2) ◽  
pp. G203-G209 ◽  
Author(s):  
S. Vanner ◽  
W. K. MacNaughton

This study examined whether capsaicin-sensitive sensory nerves regulate intestinal ion transport using both Ussing chamber and intracellular recording techniques in in vitro submucosal preparations from the guinea pig ileum. In Ussing chamber studies, serosal application of capsaicin (20 nM-20 microM) evoked a biphasic dose-dependent increase in short-circuit current (Isc) (maximal effective concentration 200 nM and 2 microM, respectively). In chloride-free buffer, capsaicin responses were significantly reduced. Capsaicin evoked little or no response when extrinsic sensory nerve fibers had been surgically removed and tetrodotoxin and low-calcium and high-magnesium solutions blocked responses to capsaicin. In epithelial preparations devoid of submucosal neurons, capsaicin had virtually no effect, suggesting that responses evoked by capsaicin-sensitive nerves result from activation of submucosal secretomotor neurons. Intracellular recordings from single submucosal neurons demonstrated that superfusion with capsaicin (2 microM) depolarized neurons with an associated decreased conductance. Depolarizations were completely desensitized when capsaicin was reapplied, but synaptic inputs were unaffected. This study suggests that capsaicin-sensitive nerves can regulate ion transport in the gastrointestinal tract by release of neurotransmitter(s) that activate submucosal secretomotor neurons.


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