BIOM2011 (2022) Exam SAQs Flashcards
You are on the last stretch of a rollercoaster, the cart goes downhill, makes a hard turn to the
left before braking and stopping for you to get down. Describe which parts of the vestibular
system are stimulated, and how they are stimulated during each stage:
a. Downhill
b. Hard turn to the left
c. Braking and stopping
a. Downhill: During the downhill phase of the rollercoaster ride, the vestibular system is primarily stimulated by changes in linear acceleration and gravitational forces. The otolith organs, which include the utricle and saccule located in the inner ear, are responsible for detecting linear acceleration and changes in head position relative to gravity. As the rollercoaster goes downhill, the otolith organs sense the forward acceleration, tilting the otolith crystals and activating hair cells in response to the change in head position.
b. Hard turn to the left: During the hard turn to the left, the vestibular system is stimulated by angular acceleration and changes in rotational forces. The semicircular canals, which are also part of the inner ear, detect angular acceleration and rotational movements. As the rollercoaster makes a sharp left turn, the fluid in the semicircular canals is set into motion, stimulating the hair cells within the canals. This activation provides information about the direction and magnitude of the rotational movement, allowing the brain to perceive the change in direction.
c. Braking and stopping: During the braking and stopping phase of the rollercoaster ride, the vestibular system experiences a decrease in acceleration and movement. The otolith organs continue to detect changes in linear acceleration, but as the rollercoaster comes to a stop, the sensations of motion and acceleration diminish. The stimulation of the vestibular system decreases as the rollercoaster comes to a complete halt.
You are walking down the street and hear the low rumble of your neighbour putting out their
wheelie bin, describe the mechanism by which your brain can locate the direction the sound is
coming from (along the horizontal plane/azimuth).
The brain can locate the direction from which a sound is coming using several mechanisms, particularly for sounds along the horizontal plane or azimuth. One of the primary mechanisms involved in sound localization is the interaural time difference (ITD) and interaural level difference (ILD).
Interaural Time Difference (ITD): The ITD refers to the difference in the time it takes for a sound to reach each ear. As sound waves propagate through the air, they reach one ear slightly earlier than the other if the source of the sound is off-center. The brain detects this time difference and uses it to localize the sound.
For low-frequency sounds, the wavelengths are relatively long, and the head acts as a barrier, causing a phase delay in the sound wave reaching the ear on the opposite side of the sound source. This phase delay creates a significant ITD. The brain processes the ITD and compares the timing of the sound wave reaching each ear to determine the direction from which the sound is coming.
Interaural Level Difference (ILD): The ILD refers to the difference in sound intensity or level between the two ears. When a sound source is off-center, the head creates an acoustic shadow, attenuating the sound reaching the ear on the side opposite the sound source. As a result, the ear closer to the sound source receives a higher sound intensity compared to the ear on the other side. The brain utilizes this difference in sound intensity to localize the sound source.
ILD is more effective for high-frequency sounds as their short wavelengths allow them to be diffracted by the head. This diffraction causes a reduction in sound intensity reaching the ear on the opposite side of the sound source. The brain processes the ILD and compares the sound levels reaching each ear to determine the direction of the sound.
By comparing the information received from both ears regarding the ITD and ILD, the brain can determine the direction from which a sound is coming along the horizontal plane. These mechanisms allow us to accurately perceive and locate sounds in our environment, enabling us to turn our attention toward the source of the sound.
List a total of 5 essential roles of the L-type Ca2+ channel in the heart for excitability and
initiating Ca2+ release from sarcoplasmic reticulum?
The L-type Ca2+ channel in the heart plays several essential roles in excitability and initiating Ca2+ release from the sarcoplasmic reticulum. Here are five of its key roles:
Initiation of cardiac action potential: The L-type Ca2+ channel, also known as the voltage-gated Ca2+ channel, is responsible for the influx of Ca2+ ions during the depolarization phase of the cardiac action potential. It contributes to the initiation of the action potential and is crucial for the electrical excitability of cardiac cells.
Triggering Ca2+-induced Ca2+ release (CICR): The influx of Ca2+ through the L-type Ca2+ channel triggers the release of Ca2+ from the sarcoplasmic reticulum (SR) through a mechanism called Ca2+-induced Ca2+ release (CICR). The released Ca2+ further activates the contractile machinery of the cardiac muscle, leading to muscle contraction.
Excitation-contraction coupling: The L-type Ca2+ channel is a key component of the excitation-contraction coupling process in the heart. It acts as the primary pathway for the entry of extracellular Ca2+ into the cardiac muscle cells, which allows the Ca2+ ions to interact with the proteins involved in muscle contraction, including troponin and tropomyosin.
Regulation of cardiac contractility: The L-type Ca2+ channel is involved in regulating the contractile strength of the cardiac muscle. The influx of Ca2+ through the channel modulates the intracellular Ca2+ concentration, which directly impacts the force of cardiac muscle contraction. Changes in the activity or expression of L-type Ca2+ channels can affect contractility.
Modulation of heart rate: The L-type Ca2+ channel also contributes to the regulation of heart rate. It plays a role in the generation and modulation of the pacemaker activity in the sinoatrial (SA) node, which is responsible for initiating the electrical impulses that coordinate the contraction of the heart. Alterations in L-type Ca2+ channel activity can influence the rate and rhythm of cardiac beating.
These are just a few essential roles of the L-type Ca2+ channel in the heart, highlighting its significance in cardiac excitability, contraction, and overall heart function.
Ca2+ release during excitation-contraction coupling is terminated by different means in skeletal
and cardiac muscle. How is termination of Ca2+ release regulated in skeletal and cardiac muscle
cells?
In skeletal muscle cells and cardiac muscle cells, the termination of Ca2+ release during excitation-contraction coupling is regulated through different mechanisms.
Skeletal muscle:
In skeletal muscle cells, the termination of Ca2+ release is primarily regulated by the decline in the depolarization of the transverse tubules (T-tubules). During excitation-contraction coupling, an action potential propagates along the T-tubules, leading to the opening of L-type Ca2+ channels (dihydropyridine receptors, DHPRs). The depolarization of the T-tubules triggers the opening of the ryanodine receptors (RYRs) located on the sarcoplasmic reticulum (SR), resulting in the release of Ca2+ from the SR into the cytoplasm.
To terminate Ca2+ release in skeletal muscle, the action potential repolarizes, causing the closure of the L-type Ca2+ channels. This repolarization prevents further influx of Ca2+ into the T-tubules and, subsequently, the closure of the RYRs on the SR membrane. As a result, the release of Ca2+ from the SR ceases, and the Ca2+ concentration in the cytoplasm decreases. The decline in cytoplasmic Ca2+ concentration leads to the reuptake of Ca2+ into the SR through the Ca2+-ATPase pump (SERCA), effectively terminating Ca2+ release during excitation-contraction coupling in skeletal muscle cells.
Cardiac muscle:
In cardiac muscle cells, the termination of Ca2+ release is regulated by a process called Ca2+-induced Ca2+ inactivation (CICI). During excitation-contraction coupling, the depolarization of the T-tubules activates the L-type Ca2+ channels (DHPRs), resulting in the influx of Ca2+ into the cytoplasm. This Ca2+ entry triggers the opening of the RYRs on the SR membrane, leading to the release of additional Ca2+ from the SR into the cytoplasm.
However, unlike in skeletal muscle, the termination of Ca2+ release in cardiac muscle cells is primarily regulated by the binding of cytoplasmic Ca2+ to the RYRs. As the cytoplasmic Ca2+ concentration increases, Ca2+ binds to the RYRs, causing them to undergo a conformational change and enter an inactivated state. This inactivation prevents further Ca2+ release from the SR, effectively terminating the release of Ca2+ during excitation-contraction coupling in cardiac muscle cells. The decline in cytoplasmic Ca2+ concentration, along with the action of SERCA, leads to the reuptake of Ca2+ into the SR, further contributing to the termination of Ca2+ release.
In summary, the termination of Ca2+ release during excitation-contraction coupling is regulated by different mechanisms in skeletal and cardiac muscle cells. In skeletal muscle, it is primarily controlled by the repolarization of the T-tubules, while in cardiac muscle, it is regulated by the binding of cytoplasmic Ca2+ to the RYRs, leading to their inactivation.
Describe the steps involved in neurotransmitter release from a synapse and generation of a
postsynaptic excitatory postsynaptic current.
Action potential propagation: An action potential is generated in the presynaptic neuron and travels down its axon towards the synapse.
Calcium influx: Arrival of the action potential at the presynaptic terminal triggers the opening of voltage-gated calcium channels, allowing calcium ions to enter the presynaptic terminal.
Neurotransmitter release: The influx of calcium triggers the fusion of synaptic vesicles with the presynaptic membrane, leading to the release of neurotransmitter molecules into the synaptic cleft.
Diffusion of neurotransmitters: The released neurotransmitters diffuse across the synaptic cleft and bind to receptors on the postsynaptic membrane.
Receptor activation: The binding of neurotransmitters to postsynaptic receptors activates ion channels, resulting in the influx of positive ions, such as sodium or calcium, into the postsynaptic neuron.
Excitatory postsynaptic current (EPSC) generation: The influx of positive ions depolarizes the postsynaptic membrane, generating an EPSC. This brings the postsynaptic neuron closer to its threshold for generating an action potential.
The overall process involves the propagation of an action potential, calcium influx triggering neurotransmitter release, diffusion of neurotransmitters across the synapse, binding to postsynaptic receptors, and the generation of an EPSC, which allows for communication between neurons.
Describe the steps involved in neurotransmitter release from a synapse and generation of a
postsynaptic excitatory postsynaptic current
Action potential propagation: An action potential is generated in the presynaptic neuron and travels down its axon towards the synapse.
Calcium influx: Arrival of the action potential at the presynaptic terminal triggers the opening of voltage-gated calcium channels, allowing calcium ions to enter the presynaptic terminal.
Neurotransmitter release: The influx of calcium triggers the fusion of synaptic vesicles with the presynaptic membrane, leading to the release of neurotransmitter molecules into the synaptic cleft.
Diffusion of neurotransmitters: The released neurotransmitters diffuse across the synaptic cleft and bind to receptors on the postsynaptic membrane.
Receptor activation: The binding of neurotransmitters to postsynaptic receptors activates ion channels, resulting in the influx of positive ions, such as sodium or calcium, into the postsynaptic neuron.
Excitatory postsynaptic current (EPSC) generation: The influx of positive ions depolarizes the postsynaptic membrane, generating an EPSC. This brings the postsynaptic neuron closer to its threshold for generating an action potential.
The overall process involves the propagation of an action potential, calcium influx triggering neurotransmitter release, diffusion of neurotransmitters across the synapse, binding to postsynaptic receptors, and the generation of an EPSC, which allows for communication between neurons.
Consider this hypothetical scenario: a person is born with a mutation in the prolactin receptor
that results in severely reduced (only 20% of normal) signalling via the Jak/STAT signal
transduction pathway.
Based on your understanding of the regulation of prolactin, what would you expect as an
outcome in this individual in terms of
A. prolactin concentrations in blood, in a non-lactating state
B. milk production in the mammary gland, in a lactating state
For each answer explain your reasoning.
A. Prolactin concentrations in blood, in a non-lactating state:
In a non-lactating state, prolactin levels are typically low. However, the reduced signaling via the Jak/STAT pathway due to the mutation in the prolactin receptor may lead to a compensatory mechanism in the body. The reduced signaling could result in decreased negative feedback regulation of prolactin production and secretion. As a result, the individual may exhibit higher-than-normal prolactin concentrations in their blood even in a non-lactating state.
B. Milk production in the mammary gland, in a lactating state:
Prolactin is the key hormone responsible for initiating and maintaining milk production in the mammary glands during lactation. The reduced signaling via the Jak/STAT pathway due to the mutation in the prolactin receptor would impair the activation of downstream signaling pathways involved in milk production. Therefore, the individual with the mutation would likely have significantly reduced milk production in the mammary glands during lactation compared to individuals with normal prolactin receptor signaling.
First explain the somatomedin hypothesis for the endocrine regulation of growth.
Then describe how this hypothesis has been modified since its inception many decades ago.
In your answer use endocrine terms to differentiate where growth signals act.
In summary, the somatomedin hypothesis suggests that GH stimulates the liver to produce IGF-1, which acts as a mediator of GH’s growth-promoting effects. However, modifications to the original hypothesis have recognized the involvement of multiple IGFs, the local actions of IGFs, feedback regulation, and tissue-specific effects. These modifications have enhanced our understanding of the intricate endocrine mechanisms involved in the regulation of growth and development.
Compare and contrast lateral junction complexes in terms of composition and function
Lateral junction complexes are specialized structures found between adjacent epithelial cells, playing crucial roles in cell adhesion, barrier formation, and tissue integrity. Here is a brief comparison and contrast of three types of lateral junction complexes in terms of their composition and function:
Tight junctions (zonula occludens):
Composition: Tight junctions are composed of transmembrane proteins called claudins and occludins, which interact with corresponding proteins on adjacent cells. These proteins are connected to the actin cytoskeleton inside the cell.
Function: Tight junctions form a barrier that restricts the movement of molecules between cells, effectively sealing the intercellular space. They maintain cell polarity, regulate paracellular transport, and prevent leakage of substances between epithelial cells.
Adherens junctions (zonula adherens):
Composition: Adherens junctions contain transmembrane proteins called cadherins, which interact homophilically with cadherins on neighboring cells. The cytoplasmic domain of cadherins binds to catenins, which link to the actin cytoskeleton.
Function: Adherens junctions mediate cell-cell adhesion by connecting the actin cytoskeletons of adjacent cells. They provide mechanical stability to tissues, transmit mechanical forces, and participate in cell signaling.
Desmosomes (macula adherens):
Composition: Desmosomes consist of desmogleins and desmocollins as transmembrane proteins, which interact homophilically between adjacent cells. Intracellularly, desmogleins and desmocollins bind to desmoplakin, which anchors intermediate filaments.
Function: Desmosomes provide strong adhesion between cells, distributing mechanical stress and resisting mechanical forces. They are particularly important in tissues that undergo mechanical stress, such as the skin and cardiac muscle.
In summary, tight junctions primarily form a barrier, adherens junctions mediate cell-cell adhesion, and desmosomes provide strong adhesion and mechanical stability. While they share the common goal of maintaining tissue integrity, their compositions and specific functions differ, reflecting their distinct roles in epithelial tissues.
Name three antibody isotypes that dominate a secondary immune response and describe a
unique feature of each isotype
a) Individual roles of MHC I and MHC II in antigen presentation:
MHC I:
Role: MHC I molecules present antigens derived from intracellular pathogens, such as viruses, to cytotoxic CD8+ T cells (also known as cytotoxic T lymphocytes or CTLs).
Recognition: CD8+ T cells recognize antigens presented by MHC I molecules through their T cell receptors (TCRs).
Function: When a CD8+ T cell recognizes a foreign antigen presented on MHC I, it becomes activated and initiates an immune response against infected cells by inducing their destruction.
MHC II:
Role: MHC II molecules present antigens derived from extracellular pathogens, such as bacteria, to helper CD4+ T cells.
Recognition: CD4+ T cells recognize antigens presented by MHC II molecules through their T cell receptors (TCRs).
Function: Upon recognition of an antigen presented on MHC II, CD4+ T cells become activated and provide help to other immune cells, such as B cells and cytotoxic CD8+ T cells. This help includes cytokine secretion, promoting antibody production, and enhancing the cytotoxic activity of CD8+ T cells.
b) Name three antibody isotypes that dominate a secondary immune response and describe a unique feature of each isotype
Three antibody isotypes dominating a secondary immune response and their unique features:
IgG:
Unique feature: IgG is the most abundant antibody isotype in the bloodstream and tissues. It has a longer half-life compared to other isotypes and can cross the placenta, providing passive immunity to the fetus.
Function: IgG plays a major role in opsonization, neutralization of toxins and viruses, and complement activation.
IgA:
Unique feature: IgA is primarily found in mucosal secretions, such as saliva, tears, and breast milk. It can exist as a dimer, allowing it to effectively neutralize pathogens at mucosal surfaces.
Function: IgA provides immune defense at mucosal sites, preventing pathogen colonization and infection.
IgE:
Unique feature: IgE is involved in allergic and hypersensitivity reactions. It has a low concentration in the bloodstream but is bound to mast cells and basophils.
Function: IgE triggers the release of inflammatory mediators upon exposure to allergens, leading to immediate hypersensitivity reactions, such as allergic asthma or anaphylaxis.
These antibody isotypes play essential roles in the immune response, each with unique features and functions that contribute to the overall defense against pathogens and regulation of immune reactions.
