Distribution of rat facial motoneurons and its reorganization following nerve reinnervation]

OBJECTIVE: To examine the distribution of rat facial motoneurons contributing different branches under normal situation and when nerve reinnervation occurred following facial nerve axotomy. METHODS: The normal distribution of motoneurons innervated both buccal and marginal mandibular branches and its reorganization after facial nerve reinnervation was observed using retrograde labeling with fluorescein. RESULTS: Under normal situation, the motoneurons contributing buccall and marginal mandibular branches were primarily distributed in the intermedial and lateral subnucleus in facial nucleus and almost completely overlapped. The two types labeled neurons organized closely, but there were no double-labeled neurons. Although the motoneurons contributing buccall and marginal mandibular branches were primarily overlapped 4 month post-anastomosis, the number of the labeled neurons obviously decreased and the organization got more scattered. There were 10% of buccall branches, 5% of marginal mandibular motoneurons in the dorsal subnuleus, 1% of buccall and 4% of marginal mandibular in dorsal ventral and medial subnucleus. The distribution pattern of the motoneurons 6 month post-anastomosis was similar to that of 4 month post-anastomosis, but the number of the labeled neurons increased, and there were 1%-2% double-labeled neurons. CONCLUSION: The distribution pattern of motoneurons innervated both buccal and marginal mandibular branches indicates that it should exist wide-spread communicating branches, and its reorganization after facial nerve reinnervation suggests that misdirected regeneration occurs among motoneurons innervating different branches.     

Excitation of locus coeruleus neurons by an adenosine 3',5'-cyclic monophosphate-activated inward current: extracellular and intracellular studies in rat brain slices

The firing rate of locus coeruleus (LC) neurons in rat brain slices was increased reversibly by agents that either elevate intracellular levels of adenosine 3',5'-cyclic monophosphate (cAMP) or mimic its actions (e.g., forskolin, and activator of adenylate cyclase, 8-Br-cAMP, a membrane permeable analog of cAMP, and Ro20-1724, a preferential inhibitor of cAMP-phosphodiesterase). Intracellular recordings showed that 8-Br-cAMP and forskolin induce a depolarization of LC neurons, accompanied by a decrease in input resistance. The 8-Br-cAMP- and forskolin-elicited depolarization persisted in the presence of cobalt, a calcium channel blocker. Steady-state current-voltage curves revealed that in the voltage range of -50 to -120 mV, 8-Br-cAMP and forskolin induced an inward current, which did not reverse at the potassium equilibrium potential and could not be blocked by tetrodotoxin. Partial replacement of sodium with Tris or choline markedly reduced the depolarization elicited by 8-Br-cAMP. We conclude that 8-Br-cAMP and forskolin act through a common mechanism to increase the firing rate of locus coeruleus neurons by inducing a cAMP-activated inward current, carried out at least in part by sodium ions.     

The interaction between the activator agents batrachotoxin and veratridine and the gating processes of neuronal sodium channels

The depolarization of frog sciatic nerves by the Na channel-activating toxins, batrachotoxin and veratridine, was studied using the sucrose-gap technique. To study the interaction between the activators and the gating processes of Na channels, we measured the depolarizations of unstimulated nerves, of nerves during repetitive stimulation, and of nerves whose Na channel inactivation process had been pharmacologically modified. Stimulation enhanced the rates of depolarization by the activators but did not effect the steady state depolarization values. Of the three inhibitors of Na channel inactivation that were tested (Leiurus alpha-scorpion toxin, chloramine T, and Ni2+), only Leiurus toxin enhanced the potencies of the activators. Neither chloramine T nor Ni2+ had any effect on the steady state level of depolarization produced by either activator. Both chloramine T and Ni2+, however, enhanced the rate of batrachotoxin action, although neither affected the rate of veratridine action. Leiurus toxin also potentiated the effects of the activators in chloramine T-treated nerves. We tested the interaction between the Na channel activators and a class of agents, local anesthetics, that stabilize a non-conducting state of the Na channel. The presence of lidocaine inhibited the depolarization produced by addition of either activator, although the addition of lidocaine subsequent to the development of batrachotoxin-induced depolarization produced repolarization very weakly and slowly. We also found that the lidocaine homologue, RAC 109I, was about 3 times as potent as its stereoisomer, RAC 109II, in its ability both to reduce the compound action potential amplitude and to inhibit the veratridine-induced depolarization.     

提壶揭盖法治疗前列腺增生症82例

笔者自1995年以来，宗提壶揭盖法，用补中益气汤加减治疗前列腺增生82例疗效满意，报告如下。