November 22, 2019

The is a tube that runs from mouth to

The digestive system is
composed by the gastrointestinal track (GI), accessory glands and organs. The
gastrointestinal tract is a tube that runs from mouth to rectum and it is
divided into seven parts: mouth, pharynx, esophagus, stomach, small and large
intestine, and rectum. The purpose of the GI track is to conduct, and digest
food into absorbable units that the body can use as energy; it does so by
performing four basic processes to the food we ingest: motility, secretion,
digestion and absorption (Sherwood, 2016). The GI track’s wall consists of the
mucosa, submucosa, muscularis externa and serosa layers. The mucosa is the
innermost layer of the GI track and its main function is to absorb nutrients. On
top of the mucosa layer is the submucosa, which is a layer of connective tissue
that contains blood vessels and provides support and elasticity to the GI
track; it also contains the submucosal plexus, which is composed of several
nerves. The muscularis externa layer is composed of two layers of smooth muscle
layers: the inner layer is circular and contracts inwards, while the outer
layer is longitudinal and contracts in length (makes it shorter); these layers
provides motility to the GI track. When combining the movement of both circular
and longitudinal smooth muscle, segmentation and peristalsis occur. Segmentation
is a circular movement which allows mixing of the bolus, and peristalsis is the
longitudinal movement which pushes the bolus forward (Sherwood, 2016).   The
outermost layer of the GI track wall is the serosa which prevents friction with
organs surrounding the GI track. In this lab, we focused on the small intestine
and its muscularis externa layer of smooth muscle.

            The
smooth muscle found in the GI track wall has several anatomical and
physiological properties, which combined, give rise to intestinal motility. Smooth
muscle is not striated, meaning it does not have z lines and it is not
organized into sarcomeres; instead, it has dense bodies and intermediate
filaments. In addition, smooth muscle does not contain t-tubules and has a
poorly developed sarcoplasmic reticulum with little calcium (SR); its activity requires
the influx of extracellular calcium (Sherwood, 2016). Smooth muscle cells are
activated by calcium dependent phosphorylation of myosin (Clinton, 2003). There
are two types of smooth muscle: multiunit, smooth muscle cells innervated independently
by neurons for small movements, and unitary, where there is a collection of
them innervated by one neuron. Unitary smooth muscle is found in the GI track.
Also, smooth muscle has gap junctions which allow the propagation of electrical
activity. Smooth muscle receives inputs from the autonomic central nervous
system (ACS), and the enteric nervous system (ENS), these two have different
nerves which contact multiple parts of smooth muscle cells (Sherwood, 2016). The
GI’s smooth muscle has its own peacemaking activity; its pacemaker cells.
called interstitial cells of Cajal (ICC), have a slower rate than the pacemaker
cells of the heart; about 12 cycles per minute (Sherwood, 2016). ICC create slow
waves, or also called Basal electric rhythm (BER), which depend on the opening
and closing of calcium channels and calcium-dependent potassium channels. When
calcium gated channels open, there is an extracellular calcium influx into the
cell’s cytosol, calcium concentration increases inside the cell and this leads
to an action potential spike (Kito et al, 2015). Once the concentration of
calcium inside the cell is high enough, calcium induces the opening of
potassium channels, and potassium causes the hyperpolarization of the cell. Then
calcium channels close and calcium concentration inside the cell decreases. The
closing of calcium-dependent-potassium channels is necessary before another
action potential spike takes place. There are two sources of calcium in smooth
muscle: extracellular, and from the sarcoplasmic reticulum (SR). In response a stimulus,
voltage gated channels in caveoli open and allow the influx of extracellular
calcium following its concentration gradient; this calcium binds to calmodulin
(Ca-CAM). Ca-CAM activates MLC kinase which phosphorylates myosin, and leads to
contraction (Sherwood, 2016). Muscle relaxation occurs when intracellular
calcium levels decrease and MLC phosphatase activity increases (Clinton, 2003).
Calcium release from the SR occurs by calcium-induced-calcium releases
mechanism or by IP3 activation of the SR calcium channels. The later mechanism
involves the binding of an agonist, into the G-protein complex which activates
phospholipase C and causes IP2 to become IP3; IP3 then binds to SR receptors
which causes calcium channels in SR to open, leading to calcium efflux (Nowak, 1985).

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The ACS also influences
the activity of the smooth muscle of the GI tract wall. The sympathetic nervous
system suppresses the GI system, while the parasympathetic, through the vagus
nerve, stimulates it (Sherwood, 2016). The sympathetic nervous system’s
neurotransmitter is typically norepinephrine, an adrenergic agent, which stimulates
adrenergic receptors. The stimulation of these receptors activates adenyl
cyclase and activates MLC phosphatase, which dephosphorylates myosin, leading to
a decrease of cross-binding and muscle tension. On the other hand,
parasympathetic activity relies on the cholinergic agent acetylcholine, which
stimulates muscularis receptors activating phospholipase C. These cause the
depolarization of IP2 to IP3 which activate MLC kinase; myosin then is
phosphorylated and increases cross-binding activity (Nowak, 1985). Tension in
the smooth muscle increases. Frequency of contraction is not affected by either
parasympathetic nor sympathetic activity.

            In
this lab we measured the motility of the intestinal segment while being treated
with different substances: epinephrine, methacholine, Adenosine-5’diphosphate
(ADP) and Ca2+-free Ringer-Tyrode’s solution. The purpose of this lab was to
observe and examine the effect these substances have on the motility of the
small intestinal segment, and what effect does an environment with no calcium
has on smooth muscle. We measured three parameters to compare activity of “baseline”
(control) and “with-substance” motility: tension, frequency and wave amplitude.
We expected to see the following results on each trial: In trial 1, if we treat
the intestinal segment with epinephrine, an adrenergic agent, we expect to see
a decrease in tension and wave amplitude, but no effect in frequency. In trial
2, if we apply methacholine, a cholinergic agent, to the intestinal segment, we
expected an increase in tension and wave amplitude, and no change in frequency.
In trial 3, if the segment is treated with ADP, a purinergic agent, we expect
to see a decrease in tension and wave amplitude and no effect on frequency. Lastly,
if we submerge the intestinal segment into Ca2+-free Ringer-Tyrode’s solution,
we expected to see a decrease in tension, amplitude and frequency.

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