VPB 121: Veterinary Physiology - II (2+1)

ENTERIC NERVOUS SYSTEM

• Innervations are from sympathetic and parasympathetic divisions of ANS, which control on intramural plexus (myenteric/auerbach plexus and meissner’s plexus)
• Intramural plexus made up of 10⁸ neurons which is almost equal to number of neurons in spinal cord.
• Sympathetic division made of thoracolumbar outflow has got preganglionic cholinergic nerve fibres.
• They end upon coeliac ganglia , superior and inferior mesenteric ganglia or hypogastric plexus.
• From these ganglia, post ganglionic adrenergic nerve fibres arise these nerves end up on intramural plexus and bring about inhibitory action (secretion & motility reduced). Some branches of post sympathetic nerves end upon sphincters and when sympathetic is stimulated it will inhibit the myenteric plexus in sphincters. As a result sphincters relax-defaecation occurs.
• Inhibitory action includes reduced glandular secretion, reduced blood supply (constricted blood vessel), reduced motility, (when there is sympathetic dominance).
• Parasympathetic outflow is from cranio sacral division (3,7,9,10 cranial nerves and sacral) has got preganglionic cholinergic nerves which are long enough to reach intramural plexus (ganglia).

• The post ganglonic parasympathetic nervous system arise from these ganglia and thus are present within the structure or organ.
• Post ganglionic PSNS use Acetyl choline  as neurotransmitter .
• Post ganglonic SNS use Nor epinenephrine as neurotransmitter.
• Sympathetic stimulation decreases  GI function and Parasympathetic stimulation increases GI function. 
• Organo phosphorous compounds are parasympathomimetics.
• In case of Organophosphorous poisoning in animals, there will be excess salivation, shooting of diarrhoea, body temperature is reduced.
• Sympathetic post ganglonic nerves act on neural circuits in the intra mural plexus that provide signals to smooth muscles of GI tract.
• Intramural (intrinsic) plexus can control much of the coordinated activity in the absence of extrinsic innervation of GI tract.
• Parasympathetic nervous division (Vagus and Sacral spinalcord outflow) with  their cholinergic preganglionic fibres act up on intramural plexus (i.e. Intramural plexus act as ganglia for preganglionic PSNS).
• From intramural plexus, postganglionic nerves arise which are seen within the structure of innervation. On stimulation motor and sensory activities are improved.
• There are local and central reflex pathways that affect the functioning of GI tract organs.
• Meissners plexus contains neurons with are intimately attached with circular muscles and glands and blood vessels of GI tract (Synaptic cleft is very much shortened). The neurons of their synaptic cleft is widened. So it takes more time for axon potential to reach post synaptic structure. The circular muscles of GI tract contract ahead of longitudinal muscles as a result gut becomes longer and thinner. When longitudinal muscles contract, gut becomes shorter and wider. Preganglionic parasympathetic nerves sometimes get innervations from post ganglionic sym nerves and adrenoreceptors are present on both pre or post ganglionic sympathetic nerves and α₁ adrenoceptors are present on both pre and post ganglionic PSNS. In such cases Ach (acetyl choline) will not be discharged thereby Parasympathetic activity getting reduced. NE (norepinephrine) inhibits Ach release through its interference via α₁ adrenoceptors on axon terminals of PSNS.
• Atropine is the cheapest and effective antidote for OP (Organo phosphorous) poisoning. (Atropin- from Atropa belladonna)
•  In OP poisoning -excess PSNS dominance.
• Atropine inhibits Ach to occupy post synaptic membrane receptors. In these two ways (ie NEP and Atropine) the vagal refex can be controlled.
• The Vagovagal reflex (generally is stimulating in nature (i.e. Increase motility, secretory and vasodilatory) carries both afferent and efferent through vagus, whereas only ENS is independent of CNS generally inhibitory involving only ENS and is intestine intestinal reflex is generally inhibitory involving only ENS and is independent of CNS.
• Central reflex pathway eg. Vagovagal reflex.
• Local reflex pathway eg. intestino intestinal reflex.
• Most of the reflexes are mediated by Ach and NE There are other neuromodulatory substances/neuro transmittors which include enkephalins, 5-hydrooxytryptophan (5HT), cholecystokinin (CCK), glycine, motilin, angiotensin, secretin, galanin, somatostatin, VIP (vasoactive intestinal polypeptide), substance-P, GABA, bombesin, gastrin, histamine, GRP (Gastrin releasing polypeptide) PG (Prostaglandin), GIP (Gastrin inhibitory polypeptide), enteroglucagon etc. Out of these, 7 are produced from enteroendocrine cells whereas others are produced from gut cells as well as from nerve endings, so called brain gut peptides.
• The chief neurotransmitters of ENS are Ach , NEP, enkaphalin (or opioid compounds) and VIP (Vasoactive intestinal peptide).
• Enkephalins decreases gastro intestinal motility by inhibiting release of Ach.
• VIP acts directly on smooth muscles to cause muscle relaxation. It is localised with cholinergic nerves in vagus.
• VIP is in local neurons (ENS) and is released when vagal fibres excite these inhibitory neurons to cause relaxation. 
• Enkephalins, VIP, nitric oxide (NO-only gaseous neuro transmitter) serotonin are all neurotransmitters produced by specialised neurons which are localized along with Ach or NEP secreting neurons in ANS.
• Depending on the nerve, whenever Ach or NEP are released, these neurons release their neurotransmitters.