This is a lab report on Coordination Gastric Muscle Activity.
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The main aim of this practical lab report is about autonomic and enteric nervous systems and how they control gastric motility of a guinea pig ileum. The enteric nervous system abbreviated as ENS refers to the intrinsic nervous system of the gastrointestinal tract. ENS is composed of complete reflex circuits whose main purposes are to; integrate information about the state of the gastrointestinal tract, detect the physiological condition of the gastrointestinal tract, and provide outputs to control gut movement, fluid exchange between the gut and its lumen, and local blood flow ( Furness J.B., 2006). The enteric nervous system is the only part of the peripheral nervous system that contains extensive neural circuits that are capable of local and autonomous function in most living animals. The ENS has extensive, two-way, connections with the central nervous system (CNS), that facilitates the control the digestive system in the context of local and whole body physiological demands (Gershon M.D., 2005). The ENS is one of the main part of the autonomic nervous system. The autonomic nervous system also contains the sympathetic and parasympathetic which form extensive connections.
Control of Motility
One of the main functions of ENS is motility control. The gastrointestinal tract has an external muscle coat whose purposes are to mix the food so that it is exposed to digestive enzymes and to the absorptive lining of the intestine, and to propel the contents of the digestive tube. The muscle also relaxes to accommodate increased bulk of contents, notably in the stomach. The ENS reflex circuit helps in regulating the movement through control of the activity of both excitatory and inhibitory neurons that innervate the muscle. The neurons have co-transmitters, for the excitatory neurons, acetylcholine and tachykinins, and for the inhibitory neurons nitric oxide, vasoactive intestinal peptide (VIP) and ATP. There is also evidence that pituitary adenylate cyclase activating peptide (PACAP) and carbon monoxide (CO) contribute to inhibitory transmission (Spiller R, Grundy D , 2004).
Patterns of small and large intestine motility are mainly generated by the intrinsic reflexes of the enteric nervous system with the major movement in the ileum being; mixing activity, the migrating myoelectric complex; peristaltic rushes; and retropulsion associated with vomiting and propulsive reflexes that travel for only small distances.
Smooth muscle is found in the gastrointestinal tract of many animals and is responsible for peristaltic movements. Smooth muscle is also present in the walls of arteries and arterioles, where it helps to regulate blood pressure and flow. As illustrated in the figure 1 below, smooth muscle unlike other muscles found in animal body, they are not striated and have single nuclei. Although they do not have the highly ordered arrangement of actin and myosin filaments that are seen in skeletal muscle, both actin and myosin are present and involved in the contractile process. These muscles exhibit unstructured contractile activity that is modulated and modified by the autonomic nervous system. Hence, the smooth muscles do not contract voluntarily instead they contract and relax slowly. It does not exhibit the characteristic “twitch” as in the case of skeletal muscle.
Figure1: Smooth Muscle structure
On the other hand, the smooth muscle sphincters restrict and regulate the passage of the luminal contents between regions. In general, reflexes that are initiated proximal to the sphincters relax the sphincter muscle and facilitate the passage of the contents, whereas reflexes that are initiated distally restrict retrograde passage of contents into more proximal parts of the digestive tract. In addition, smooth muscle is not prone to muscle fatigue, making it an ideal component of sphincter muscles.
Mineral elements plays a major role contractile activity of smooth muscles for instance, the depolarizing phase of the action potential involves an increase in calcium (Ca2+) permeability rather than in sodium (Na+) permeability. This influx of very tiny calcium causes calcium release from cellular stores and this cell calcium concentration is responsible for triggering contractile activity. The muscle relaxes when the calcium is stored again. Also, Changes in extracellular potassium (K+) ion concentration have a great influence on the resting membrane potential of the cell; rising potassium concentration depolarizes the membrane and brings it closer its threshold, while decreasing potassium concentration hyperpolarizes the membrane and thereby decreases muscle excitability
The arrangement of smooth muscle in the guinea pig is the same as its arrangement in human gut and in rat small intestine whereby the smooth muscle is arranged in two layer namely; circular and longitudinal layers as shown in figure 2 below. It has an extensive enteric nervous system in its wall and, as in mammalian gut, the neurotransmitters acetylcholine and adrenaline are among the chemicals that can affect gut smooth muscle activity. Neurotransmitters affect different types of smooth muscle differently, depending on the association of the smooth muscle with excitable cells. In general, acetylcholine increases the muscle cell’s permeability to calcium, while adrenaline decreases the cell’s permeability to calcium.
Figure 2: Guinea-pig ileum
The main aim of this lab report is to investigate the function of the enteric and autonomic nervous systems in controlling the smooth muscle of guinea pig small intestine and its influence on the gastrointestinal tract motility. The other aims of this lab report include the following;
- To identify the neurotransmitter which will yield the greatest force of contraction of the smooth muscle located in the guinea-pig ileum;
- To identify the neurotransmitter that gives the highest frequency of contraction of the smooth muscle located in the guinea-pig ileum;
- To identify the receptor sub-type that is involved in the stimulatory effects using inhibitory compounds as specific antagonists;
- To identify which branch of autonomic nervous system that is responsible for gastrointestinal motility stimulatory and inhibitory; and
- To understand the process of making physiological measurements using various techniques such as Chart, Powerlab and isolated tissue preparations.
The hypothesis of this practical lab report is:
The force and frequency of contraction of the guinea-pig ileum can be changed by using specific agonists and antagonists of neurotransmitter chemicals involved in the enteric and autonomic nervous systems.
For this practical experiment to achieve its main aim, the following solutions were provided to help in testing the neurotransmitters and antagonists
Tyrode – a homeostatic solution that will maintain the sample of guinea-pig ileum in a suitable state for you to make your measurements.
Neurotransmitters (or agonists):Carbachol (acetylcholine mimic), Adrenaline, Histamine, Nicotine (agonist)
Antagonists: Atropine, Hexamethonium bromide Pyrilamine maleate salt
The following method was used in this practical experiment;
- The pots were marked especially on the lowermost chamber to indicate the points for 18 and 19ml.
- A small volume of each of the neurotransmitters and receptor agonists was put into the pots.
- 1ml of either the neurotransmitters or antagonists was added to the pots using two separate syringes.
- The forces of contraction and frequency of contraction was measured using a tissue connected via a transducer to the powerlab and Chart.
- The following strategy was worked out with an aim of fulfilling the aims of this practical experiment. This strategy involved adding each antagonist first to the pot and the followed by the neurotransmitter.
- Each antagonist was tested with each neurotransmitter until an inhibition occurred to the action of the neurotransmitter. For instance, Carbachol was tested against each antagonist.
- Pyrilamine maleate salt was added to the bath and then carbachol but its action was not inhibited by Pyrilamine maleate salt and the same with Phentolamineand and Hexamethonium bromide. However, an inhibition occurred when Atropine was added with carbachol.
- The same strategy was done with each neurotransmitter, until an inhibition was achieved. Each time the lowermost chamber was drain and re-filled with fresh Tyrode, 5-10 minutes had to be waited between each refill.
The following results were obtained from this practical experiment; Each of the receptor antagonists is effective against one of the following receptors: nicotinic cholinergic receptors, muscarinic cholinergic receptors, a-adrenergic receptors and an H2 receptor antagonist. There is no relationship between the order in which the receptor antagonists are listed above and the order of the receptors that they inhibit is listed. Three of the neurotransmitters or agonists are involved in the autonomic or enteric nervous system, whilst the other exerts a local effect. In summary, the results of this practical experiment can be represented as; Atropine inhibits carbachol; Hexamethonium bromide inhibits Nicotine; Pyrilamine maleate salt inhibits Histamine and Phentolamine inhibits Adrenaline.
This practical experiment did give the expected results that greatly support the already stated hypothesis. Through this practical experiment, the force and frequency of contraction of the guinea-pig ileum can be changed by using specific agonists and antagonists of neurotransmitter chemicals involved in the enteric and autonomic nervous systems. In this respect, the aims of this practical lab experiment were achieved by the results obtained. The reliability of this experimental results greatly depends on the procedures used in performing this experiment hence, the easier the procedures, the greater the experimental reliability and vice versa.
It is evident that the control of smooth muscle activity, particularly how smooth muscle in the gastrointestinal tract is regulated through the enteric and autonomic nervous system.
Gershon M.D., (2005). Nerves, reflexes, and the enteric nervous system. J. Clin. Gastroenterol. 184-193.
Furness J.B., (2006). The Enteric Nervous System. Blackwell, Oxford. 274.
Spiller R, Grundy D . (2004). Pathophysiology of the enteric nervous system, a basis for understanding functional diseases. Blackwell, Oxford.