Muscle tissue 2 Flashcards
A. Neuromuscular junction (NMJ)
As mentioned previously, muscles contract due to a rapid release of CALCIUM (Ca+2) from the Sarcoplasmic reticulum (SR).
Recall how Ca+2 binds to the troponin/tropomyosin complex which allows sliding of the filaments (contraction).
This rapid influx of Ca+2 into the muscle fiber is due to an electrical impulse called an action potential (AP) (more on APs next module).
For now, just understand that it’s an electrical signal that causes changes to the membrane which causes different ion channels to open/close which in turn causes Ca+2 to be released.
Somatic motor neurons
– nerves that extend from the brain & spinal cord (both part of the central nervous system) that are responsible for somatic movements. These terminate at the sarcolemma of a muscle fiber (the plasma membrane of the muscle fiber). Thus the junction between the neuron and the muscle fiber is called the neuromuscular junction.
Synaptic cleft
– the space between the end of the somatic neuron (axon terminal) and the muscle. The synapse is how different nerves communicate with one another (this includes the cleft).
Neurotransmitter (NTs). APs CANNOT jump across this gap. Instead, chemicals called neurotransmitters are used to propagate the signal across the cleft. There are hundreds of naturally occurring NTs in the body. Some may have an excitatory effect, while others will be inhibitory (depending on the specific synapse). NB: NTs are discussed extensively in chapters 12-17.
Acetylcholine (ACh)
– the neurotransmitter that is released at the NMJ (stored in vesicles in the pre-synaptic terminal).
Motor endplate
– the side of the synapse which consists of the muscle sarcolemma containing ACh receptors (ligand-gated receptors). This is also known as the post-synaptic membrane/terminal.
B. Generation of the action potential at the NMJ:
- Release of ACh – nervous impulse arrives at the axon terminal causing the stored ACh inside vesicles to be exocytosed into the cleft and migrate to the motor endplate.
- Activation of ACh receptors
– ACh binds to their corresponding receptors on the motor endplate, which in turn opens sodium (Na+) channels, causing Na+ to flow into the sarcolemma (membrane) of the muscle.
- Production of the AP
– the rapid influx of Na+ into the muscle fiber causes an increase in positive charge within the cell. This generates a further action potential which is propagated along the sarcolemma into the T-tubule system, causing a secondary release of Ca+2 that ultimately causes the muscle to contract.
- Termination of ACh
– ACh is broken down by an enzyme acetylcholinesterase (AChE), and the end products are recycled back into the axon terminal to make new ACh molecules for the next time it’s needed.
Steps involved in initiating muscle contraction
AP arrives at the pre-synaptic terminal
ACh (neurotransmitter) is released
3. ACh travels across the NMJ via fast diffusion
4. ACh binds to & stimulates receptors on the post-synaptic membrane
5. Na+ channels open up and Na+ rapidly enters the muscle cell
6. An action potential is generated at the post-synaptic membrane (post-synaptic action potential)
7. AP travels along the sarcolemma (all directions) and down the T-tubules
8. This triggers the release of Ca+2 from the sarcoplasmic reticulum
7. Ca+2 binds to troponin in the sarcoplasm causing tropomyosin to change position (revealing the myosin-binding sites on actin)
8. Myosin can now bind with actin
9. ATP attached to myosin heads is hydrolyzed to ADP + phosphate
10.Muscle contraction occurs
Note
: NMJs tend to be located at the middle of muscle fibers. This allows the APs to reach both ends of the muscle cells more quickly (travelling in both directions). In other words, the APs travel towards the origin and insertion of a muscle and thus allow the most forceful contraction.
REMEMBER! Muscle fibers contract evenly throughout the entire length of the muscle!!!
Botox
is the clinical use of botulinum toxin – the poison derived from clostridium botulism (anaerobic bacteria).
This substance has the effect of blocking the release of ACh from axon terminals in the NMJ.
When ACh isn’t released, corresponding ACh receptors aren’t stimulated and no muscle AP is generated (thus no muscle contraction!).
C. Cardiac muscle tissue:
Recall that cardiac muscle tissue is striated and involuntary.
Ca+2 ions are found in the SR and the interstitial fluid. High levels of Ca+2 in cardiac muscle tissue allows prolonged contraction (up to 10-15 times longer than skeletal muscle). More on this in AP200.
Cardiac muscle tissue has auto-rhythmicity (it contracts in response to its own self-generated action potentials).
In the heart there are 2 nodes:
Sinoatrial (SA) node
Atrioventricular (AV) node
These nodes are responsible for the automatic rhythmic contractions of the upper and lower portions of the heart, which results in the characteristic “lubb dubb” we hear as heart sounds.
The average heart contracts about 75 times/minute during rest.
Recall that between heart cells are intercalated discs (increased/thickened areas of the sarcolemma made up of gap junctions & desmosomes). What was the purpose of these?
D. Smooth Muscle Tissue:
Recall: smooth muscle tissue is non-striated and involuntary
Like cardiac muscle tissue, it also has auto-rhythmicity; an AP sent to one smooth muscle fiber will in turn be transmitted to neighbouring fibers (allowing them to contract in unison).
E.g. When the digestive control centers in the brain send nerve signals to the stomach and small intestines to begin contraction, only one or a few action potentials are needed to stimulate the entire organ to contract.
There are 2 types of smooth muscles:
Visceral (single unit) – more common – more like cardiac fibers
Multi unit – less common
Very similar to physiology of skeletal except:
Much slower contractions (onset and duration) It takes much longer for a contraction to initiate and the duration may be for hours.
Has the ability to stretch and distend to much greater lengths.
E. Muscle metabolism:
There are 3 ways in which muscles can generate ATP for
contraction.
- Creatine phosphate (CP)
High-energy molecule found only in muscles
Creatine is produced in the liver, kidneys & pancreas, then transferred to muscles.
Creatine kinase (CK), an enzyme, transfers a phosphate (PO4) group from ATP to creatine making creatine phosphate (this is a reversible reaction). ATP + creatine creatine phosphate + ADP ATP + creatine This readily accessible form of energy provides maximum muscle contraction for up to 15 secs of activity. The breakdown product of creatine is creatinine, a metabolite excreted in the urine.
- Anaerobic glycolysis
Occurs in the absence of oxygen
Takes place in the sarcoplasm
This is the BREAKDOWN of glucose (glycolysis) in a series of steps to form ATP
This process results in 2 molecules of ATP & 2 molecules of pyruvic acid (which go on to aerobic respiration to form lots more ATP)
During heavy exercise when not enough oxygen is available, the pyruvic acid is converted into LACTIC ACID, which travels to the liver and is converted back to glucose (however in high doses this contributes to the temporary rise in the blood acidity and is thought to cause muscle soreness).
Produces enough ATP for maximum muscle contraction for 30-40 secs of activity (i.e. 400 meter dash).