PubMed · 11388543
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S S Liu, S B McDonald. 2001. Current issues in spinal anesthesia.. https://doi.org/10.1097/00000542-200105000-00030
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Clonidine, an alpha(2)-adrenoceptor agonist, has been reported to inhibit gastric and small intestinal motility in rats. Whether clonidine also inhibits colonic motility is still not clear. The aim of this study was to examine the effect of clonidine on colonic motility and its possible site of action in adult Wistar rats. Colonic motilities in anesthetized rats in vivo or motilities of the isolated colon of rats in vitro were recorded. Clonidine was administered intravenously (i.v.) and intracerebroventricularly (i.c.v.) in vivo while bath administration was used in in vitro study. Clonidine i.v. or i.c.v. significantly inhibited colonic motility. This inhibitory effect was antagonized by pre-administration of yohimbine, an alpha(2)-adrenoceptor antagonist, but not by pre-administration of prazosin, an alpha(1)-adrenoceptor antagonist. Also, we have unpublished data indicating that the sympathectomy antagonized the inhibitory effect of systemically administered clonidine. A significant depression of colonic motility on the isolated colon was induced by bath administration of noradrenaline, while no such inhibition was seen by clonidine. The results of the present study suggested that clonidine inhibits colonic motility in rats through activation of central alpha(2)-adrenergic receptor.
The goal of these experiments was to define the contribution of hindpaw cutaneous inputs in the expression of spinal locomotion in cats. In 3 cats, some (n = 1) or all (n = 2) cutaneous nerves were cut bilaterally at ankle level before spinalization. This denervation caused small deficits that were gradually compensated as reported in the companion study. After spinalization, the completely denervated cats never recovered plantar foot placement or weight bearing of the hindquarters despite more than 35 days of treadmill training. Although normal electromyographic rhythmic activity developed at the hip and knee, ankle flexors and extensors were abnormally coactivated during stance. In contrast, the partially denervated cat regained foot placement and weight support 15 days after spinalization. However, after completing the denervation, foot placement and weight bearing were lost as in previous cats. In a 4th cat, spinalization was performed before denervation and the cutaneous nerves were cut sequentially in the right hindlimb only. Rapid locomotor adaptation occurred after cutting the deep peroneal, saphenous, and sural nerves. Later, cutting the superficial peroneal nerve produced paw drag, which was compensated within 8 days. On cutting the last cutaneous nerve (tibial), plantar foot placement was lost despite another 71 days of training. On the one hand, these experiments show that some cutaneous inputs are necessary for appropriate plantar foot placement and weight bearing of the hindquarters during spinal locomotion and, on the other hand, that locomotor compensation to partial cutaneous denervation after spinalization reveals important adaptive capacities of the spinal cord.
The dorsal motor nucleus of the vagus (DMV) receives more noradrenergic terminals than any other medullary nucleus; few studies, however, have examined the effects of norepinephrine (NE) on DMV neurons. Using whole cell recordings in thin slices, we determined the effects of NE on identified gastric-projecting DMV neurons. Twenty-five percent of DMV neurons were unresponsive to NE, whereas the remaining 75% responded to NE with either an excitation (49%), an inhibition (26%), or an inhibition followed by an excitation (4%). Antrum/pylorus- and corpus-projecting neurons responded to NE with a similar percentage of excitatory (49 and 59%, respectively) and inhibitory (20% for both groups) responses. A lower percentage of excitatory (37%) and a higher percentage of inhibitory (36%) responses were, however, observed in fundus-projecting neurons. In all groups, pretreatment with prazosin or phenylephrine antagonized or mimicked the NE-induced excitation, respectively. Pretreatment with yohimbine or UK-14304 antagonized or mimicked the NE-induced inhibition, respectively. These data suggest that NE depolarization is mediated by alpha(1)-adrenoceptors, whereas NE hyperpolarization is mediated by alpha(2)-adrenoceptors. In 16 neurons depolarized by NE, amplitude of the action potential afterhyperpolarization (AHP) and its kinetics of decay (tau) were significantly reduced vs. control. No differences were found on the amplitude and tau of AHP in neurons hyperpolarized by NE. Using immunohistochemical techniques, we found that the distribution of tyrosine hydroxylase fibers within the DMV was significantly different within the mediolateral extent of DMV; however, distribution of cells responding to NE did not show a specific pattern of localization.