Immediate-early gene expression in the inferior mesenteric ganglion and colonic myenteric plexus of the guinea pig. (1/416)

Activation of neurons in the inferior mesenteric ganglion (IMG) was assessed using c-fos, JunB, and c-Jun expression in the guinea pig IMG and colonic myenteric plexus during mechanosensory stimulation and acute colitis in normal and capsaicin-treated animals. Intracolonic saline or 2% acetic acid was administered, and mechanosensory stimulation was performed by passage of a small (0.5 cm) balloon either 4 or 24 hr later. Lower doses of capsaicin or vehicle were used to activate primary afferent fibers during balloon passage. c-Jun did not respond to any of the stimuli in the study. c-fos and JunB were absent from the IMG and myenteric plexus of untreated and saline-treated animals. Acetic acid induced acute colitis by 4 hr, which persisted for 24 hr, but c-fos was found only in enteric glia in the myenteric plexus and was absent from the IMG. Balloon passage induced c-fos and JunB in only a small subset of IMG neurons and no myenteric neurons. However, balloon passage induced c-fos and JunB in IMG neurons (notably those containing somatostatin) and the myenteric plexus of acetic acid-treated animals. After capsaicin treatment, c-fos and JunB induction by balloon passage was inhibited in the IMG, but there was enhanced c-fos expression in the myenteric plexus. c-fos and JunB induction by balloon stimulation was also mimicked by acute activation of capsaicin-sensitive nerves. These data suggest that colitis enhances reflex activity of the IMG by a mechanism that involves activation of both primary afferent fibers and the myenteric plexus.  (+info)

Cytochemical studies on golgi apparatus, GERL, and lysosomes in neurons of dorsal root ganglia in mice. (2/416)

Cytochemically demonstrable thiamine pyrophosphatase activity is present in the innermost Golgi element in both small and large neurons of the dorsal root ganglia in CF1, C57 black, and C57 beige mice, thus resembling the neurons of rat dorsal root ganglia. The localization of acid phosphatase (EC 3.1.3.2) activity in the large neurons of dorsal root ganglia in these mice is also similar to that in rats; it is not demonstrable in Golgi elements but is present in GERL and in three types of lysosomes apparently derived from GERL. However, the small neurons of the mouse differ from those of the rat in showing acid phosphatase activity in all elements of the Golgi apparatus. In the mouse neurons the acid phosphatase activity of residual bodies is "latent," i.e., it is not demonstrable in well-preserved cells.  (+info)

Functional vagal input to chemically identified neurons in pancreatic ganglia as revealed by Fos expression. (3/416)

The importance of neural elements in the control of both endocrine and exocrine pancreatic secretory functions and their coordination with gastrointestinal, hepatic, and general homeostatic functions is increasingly recognized. To better characterize the vagal efferent input to the pancreas, the capacity of electrical vagal stimulation to induce expression of c-Fos in neurochemically identified neurons of intrapancreatic ganglia was investigated. At optimal stimulation parameters, unilateral stimulation of either the left or right cervical vagus induced Fos expression in approximately 30% of neurons in the head and 10-20% of neurons in the body and tail of the pancreas. There was no Fos expression if no stimulation or stimulation with a distally cut vagus was applied. Large proportions of neurons contained nitric oxide synthase as assessed with NADPH diaphorase histochemistry (88%) and choline acetyltransferase. The proportion of nitrergic and nonnitrergic neurons receiving vagal input was not different. It is concluded that a significant proportion of pancreatic neurons receives excitatory synaptic input from vagal preganglionic axons and that many of these vagal postganglionic neurons can produce nitric oxide and acetylcholine.  (+info)

Central regulation of sympathetic neuron development. (4/416)

The sixth lumbar (L-6) ganglion has been used to study the central regulation of peripheral sympathetic neuron development. During post-natal ontogeny, tyrosine hydroxylase [tyrosine 3-monooxygenase, L-tyrosine, tetrahydropteridine: oxygen oxidoreductase (3-hydroxylating), EC 1.14.16.2] activity increased 60-fold, while total protein rose 10-fold in the ganglion. Transection of the spinal cord at the fifth thoracic (T-5) segment in neonatal rats prevented the normal developmental increase in tyrosine hydroxylase activity of the L-6 ganglion. However, spinal transection did not alter the ontogeny of tyrosine hydroxylase in the superior cervical ganglion, which derives its innervation from spinal segments rostral to the surgical lesion. Thus, spinal transection interfered with the maturation of sympathetic neurons distal to, but not proximal to, the lesion. The effect of transection on the L-6 ganglion persisted for at least one month, the longest time tested. Our observations suggest that trans-synaptic regulation of adrenergic maturation in the periphery is governed by suprasegmental mechanisms in the central nervous system.  (+info)

Effects of persistent selective suppression of ganglionic butyrylcholinesterase on steady state and regenerating levels of acetylcholinesterase: implications regarding function of butyrylcholinesterase and regulation of protein synthesis. (5/416)

Persistent selective suppression of the butyrylcholinesterase (cholinesterase; acylcholine acyl-hydrolase, EC 3.1.1.8) activity of the superior cervical, stellate, and ciliary ganglia of cats by the daily administration of tetramonoisopropyl pyrophosphortetramide, 3.0 mumol/kg, intravenously, for 6 days produced a significant elevation in the levels of ganglionic acetylcholinesterase (acetylcholine hydrolase, EC 3.1.1.7). When the same procedure was preceded by the inactivation of over 95% of the ganglionic acetylcholinesterase by sarin, 2.0 mumol/kg, intravenously, the rate of regeneration of acetylcholinesterase was decreased. Results are interpreted as evidence that ganglionic butyrylcholinesterase may serve as a precursor to acetylcholinesterase, and that the level of butyrylcholinesterase may regulate the rate of acetylcholinesterase synthesis.  (+info)

Rat sympathetic neurons and cardiac myocytes developing in microcultures: correlation of the fine structure of endings with neurotransmitter function in single neurons. (6/416)

Microcultures containing single sympathetic principal neurons and small numbers of dissociated heart myocytes were prepared from newborn rats. After the transmitter properties of the neuron were studied by electrophysiological experiments, the microculture was examined with the electron microscope. Single neurons of either putative cholinergic or putative adrenergic character made morphological synapses on themselves (autapses), although only cholinargic autapses were detected electrophysiologically. Numerous axonal varicosities were present adjacent to the myocytes but no synaptic specializations were evident. After permanganate fixation to localize endogenous norepinephrine, the endings of neurons which appeared to secrete catecholamines contained many small granular vesicles, while the endings of neurons which appeared to secrete acetylcholine contained none. The endings of neurons which apparently secreted both catecholamines and acetylcholine contained only occasional small granular vesicles.  (+info)

Neurally mediated depressor hemodynamic response induced by intracoronary catheter balloon inflation in pigs. (7/416)

OBJECTIVES: To assess whether intracoronary catheter balloon inflation triggers a neurally mediated hemodynamic response that interacts with the ischemia-induced myocardial dysfunction. METHODS: Forty-eight chloralose anesthetized pigs underwent a 60 s intraluminal catheter balloon inflation of the proximal left anterior descending (LAD) coronary artery before and after one of these treatments: disruption of LAD pericoronary nerves with phenol (n=6), bilateral stellectomy (n=8), bilateral cervical vagotomy (n=6), atropine (n=5), and ganglionic blockade with hexamethonium (n=10). In 13 other pigs, we assessed the reproducibility of two balloon inflations spaced 15 min (n=6) or 60 min (n=7). The ECG, left ventricular (LV) pressure, and LV dP/dt were recorded during each intervention. Right ventricular (RV) pressure, RV dP/dt, and aortic blood flow were also measured in a subset of pigs. RESULTS: Balloon inflation induced an early (10 s) and reproducible (ANOVA, P<0.001) drop in systolic pressure and peak dP/dt; a decrease in aortic blood flow; a rise in end-diastolic pressure; and elevation of the ST segment. Pericoronary denervation, stellectomy and ganglionic blockade attenuated (P<0.001) the drop in LV parameters during coronary inflation, but atropine and vagotomy did not. CONCLUSIONS: A depressor hemodynamic response subserved by pericoronary nerves worsens the LV dysfunction induced by brief coronary catheter balloon inflation in anesthetized pigs. Cholinergic fibers do not appear to play a major role.  (+info)

Ciliary ganglion stimulation. I. Effects on aqueous humor inflow and outflow. (8/416)

Stimulation of the ciliary ganglion in an enucleated, arterially perfused cat eye preparation produced a sustained increase in aqueous humor formation and an increase in the rate of aqueous humor outflow. The increased aqueous humor formation induced by ciliary ganglion stimulation has been found to be pressure-dependent and therefore suggests that ultrafiltration may be the underlying mechanism of action. No change in capillary permeability of the ciliary body could be demonstrated.  (+info)