On the involvement of tachykinin neurons in the secretory nervous reflex elicited by cholera toxin in the small intestine

The possible involvement of tachykinins in the nervous reflex activated by exposing the intestinal mucosa to cholera toxin was investigated in cats and rats. Three types of experiments were performed. In cats the release of tachykinins into blood was followed after placing cholera toxin in the intestinal lumen. In rat experiments a tachykinin receptor antagonist (Spantide II) was given close i.a. and its effect on cholera toxin-evoked fluid secretion was studied. Finally, in rats the effect of cholera toxin on the SP contents in the intestinal mucosa was studied. No release of tachykinins could be demonstrated. Spantide II did not change the rate of cholera toxin induced secretion. The SP content in the intestinal mucosa was not influenced by placing the toxin in the intestinal lumen. Hence, no experimental evidence was obtained for the involvement of a tachykinin neuron in the intestinal secretory nervous reflex activated by cholera toxin. Based on observations reported in the literature the involvement of an acetylcholine/tachykinin neuron in the reflex is tentatively discussed.     

Neuronally mediated anion secretion induced by short-chain fatty acids in the rat distal small intestine

The short-chain fatty acids acetate, propionate and butyrate induced a concentration-dependent increase of short-circuit current (I_sc) in the rat distal small intestine in vitro. They were ineffective in the proximal small intestine. The increase of I_sc in the distal small intestine was dependent on the presence of Cl^- and HCO^-₃ ions. It was blocked by the inhibitor of the Na⁺-K⁺-Cl^--cotransporter, bumetanide, and by the Cl^- channel blocker, 5-nitro-2-(3-phenylpropylamino)-benzoate, indicating that short-chain fatty acids evoke an anion secretion. The secretion induced by propionate was blocked by the neurotoxin, tetrodotoxin, and inhibited by the muscarinic antagonists, atropine. In contrast, indomethacin, a cyclooxygenase inhibitor, or nordihydroguaiaretic acid, a lipoxygenase inhibitor, were ineffective. These results indicate that short-chain fatty acids stimulate chemosensitive neurones in the rat small intestine in a region-specific manner, which induce anion secretion by the release of mainly acetylcholine.     

Light and electron microscopic studies of pituitary adenylate cyclase-activating peptide (PACAP) – immunoreactive neurons in the enteric nervous system of rat small and large intestine

 Pituitary adenylate cyclase-activating peptide (PACAP)-immunoreactive (IR) neurons in the myenteric and submucosal plexus of the rat small and large intestine were examined by immunostaining with purified polyclonal antiserum against PACAP (1–15), using both light and electron microscopy. Many PACAP-IR neuronal cell bodies and fibers were found in the myenteric and submucosal plexus. Many of the PACAP-IR fibers originated from the cell bodies of the myenteric and submucosal ganglia. The ganglia were also innervated by PACAP-IR fibers. PACAP-IR fibers penetrated both the circular and longitudinal muscle layers, confirming the previous observations indicating that PACAP neurons act as motor neurons. Ultrastructural study demonstrated that PACAP-IR nerve terminals formed synaptic contacts with PACAP-IR nerve cell bodies or dendritic processes. This observation suggests that PACAP-IR neurons innervate other PACAP-IR neurons, and that PACAP neurons work as interneurons in the enteric nervous system. PACAP-IR nerve cells received not only PACAP-positive nerve terminal input also PACAP-negative nerve terminal input. It also suggests that PACAP neurons are regulated not only by PACAP-IR enteric neurons, but also by neurons originating elsewhere. Our observations support the view that PACAP-IR neurons are involved in the control of gut motility. Accepted: 20 April 1998     

Effects of stimulation of the parasympathetic and sympathetic innervations in bursts on the syntheses of polyamines,DNA and protein in salivary glands of the rat: non-adrenergic,noncholinergic responses

The increase in the activity of ornithine decarboxylase, the key enzyme in the formation of polyamines, in the sublingual glands of the chloralose-anaesthetized rat in response to stimulation of the parasympathetic innervation was enhanced by employing an intermittent pattern of nerve stimulation. 20 Hz in bursts delivered for 1 second every 10th second over a period of 3 hours increased the activity 1000-fold, whereas a frequency of 2 Hz delivered continuously, and thus giving rise to the same total number of impulses as the burst stimulation, increased the enzyme activity only 50-fold. Already 2 Hz in bursts caused the ornithine decarboxylase activity to increase. A parasympathetic non-adrenergic, non-cholinergic regulation of ornithine decarboxylase activity was shown in response to the two modes of stimulation. The increase to 2 and 20 Hz in bursts was 2- and 80-fold, respectively, whereas it was 29-fold to 2 Hz continuously. Increases in the concentration of the polyamine putrescine in response to burst stimulation of the parasympathetic nerve were found both in the absence and in the presence of atropine. The ornithine decarboxylase activity of the submaxillary gland was not affected by the parasympathetic stimulation. Stimulation of the sympathetic innervation was more effective in both types of glands, as to increases in the ornithine decarboxylase activity, when employing the continuous mode. In cultured tissue of the sublingual glands which, in vivo, had been subjected to parasympathetic stimulation in bursts (20 Hz), the syntheses of DNA and protein were increased as judged by the incorporation of radio-labelled thymidine and leucine; in the presence of atropine the stimulation resulted only in increased synthesis of protein.