Week 2 Flashcards
how does the body exert fine control over tissues and organs?
Through a huge diversity of regulatory molecules and receptors. There are millions of receptor proteins, alternative splicing, and posttranslational mods
what determines where a receptor is located?
The type of regulatory molecule. If it is a non polar signal, it can easily diffuse through the membrane so the receptor is intracellular. If it is polar it cannot diffuse through membrane so receptor is on the membrane
*examples of non polar regulatory molecules
steroid hormones
thyroid hormones
nitric oxide gas
intracellular receptors!!
*examples of polar regulatory molecules
epinephrine (hormones)
acetylcholine (amine neurotransmitter)
insulin (hormone)
receptor on plasma membrane!
if a polar molecule binds to the outside of a cell, how does it affect intracellular processes?
Through second messengers. These are intermediates in the cytoplasm that are activated by the receptor and which cause some other response in the cell
Common second messengers
- Ions such as Ca2+ that enter the cell from the extracellular fluid
- Cyclic adenosine monophosphate which is a molecule produced within the cytoplasm in response to the signal binding the receptor
describe cyclic adenosine monophosphate activation pathway and an example
An important second messenger with the following sequence of events: a polar regulatory molecule binds its receptor in the PM. this indirectly activates an enzyme in the PM that produces cAMP from ATP in the cytoplasm. cAMP then activates other enzymes which change cell activities.
Example: epinephrine (adrenaline) uses cAMP as a second messenger in stimulation of the heart
Why are G proteins necessary?
the binding of a polar regulatory molecule to its receptor activates an enzyme protein in the PM indirectly because the receptor and enzyme are in different locations. Something has to travel in the plasma membrane between receptor and enzyme. This is the G protein!
what would you call a receptor that binds a polar molecule and thus acts through a specific intracellular intermediary to produce a second messenger?
G protein COUPLED receptor
describe the process of G protein activation
Regulatory molecule reaches PM and binds receptor. Alpha subunit dissociates from beta-gamma. Alpha dissociation occurs because of GDP release and GTP binding. The alpha then moves through membrane and binds to effector protein (enzyme or ion channel) and activates it. Then alpha hydrolyzed GTP to GDP and Pi, causing the three subunits to reaggregate and move back to the receptor protein.
2 examples of 2 types of effector proteins activated by G proteins
Enzyme: epinephrine and norepinephrine activate cAMP producing enzyme and stimulates heart
Ion channel: acetylcholine causes heart rate to slow by opening channels
two divisions of the nervous system
Central nervous system (CNS): brain and spinal cord
Peripheral nervous system (PNS): cranial nerves arising from the brain and the spinal nerves arising from spinal cord. Everything that is NOT the brain and spinal cord
two principle types of cells in the nervous system
neurons: basic structural and functional unit of the system. They respond to physical and chemical stimuli, conduct electrochemical impulses, and release chemical regulators.
Supporting cells: aid the functions of neurons and are 5x more abundant than neurons. Also commonly called NEUROGLIA or GLIAL CELLS
why are brain tumors in adults usually composed of glial cells?
Neurons cannot divide by mitosis while glial cells (neuroglia, supporting cells) can. So in a cancerous overgrowth situation, glial cells will be the ones dividing too much.
three principle regions of all neurons
Cell body: Enlarged portion that contains the nucleus. nutritional center.
Dendrites: Processes, or extensions from cell body, which are thin and branched. Provides receptive area that transmits impulses TO the cell body
Axon: Longer process that conducts impulses AWAY from the cell body
what are nissl bodies
Dark stained granules in the cell body and larger dendrites (not axons). They are composed of large stacks of rough endoplasmic reticulum needed for synthesis of membrane proteins
terms for clusters of cell bodies in the CNS and PNS
CNS clusters of cell bodies are nuclei (singular nucleus)
PNS clusters of cell bodies are ganglia (singular ganglion)
Parts of the axon
The origin of the axon near the cell body is called the axon hillock, this is where the excitement threshold must be reached. Adjacent to that is the axon initial segment, where first action potentials are generated. Axons can be a millimeter to over meter in length. Towards the ends are lots of branches called axon collaterals, and each of those can divide many more times.
why is axonal transport necessary?
Axons can be very long, over a meter, and special mechanisms are required to transport organelles and proteins from the cell body to the axon terminals. This is accomplished by energy dependent axonal transport
classifications of neurons based on direction in which they conduct impulses
Sensory or Afferent neurons: conduct impulses from sensory receptors INTO the CNS
Motor or Efferent neurons: conduct impulses OUT of the CNS to effector organs
Interneurons: located entirely within CNS and serve integrative functions
Afferent = adding to CNS Efferent = exiting CNS
types of motor neurons
Somatic motor neurons: responsible for reflex and voluntary control of skeletal muscles
Autonomic motor neurons: innervate the involuntary effectors like smooth muscle, cardiac muscle, and glands. Includes the Sympathetic (speeds up, except GI tract) and Parasympathetic (slows down, except GI tract) subdivisions.
classifications of neurons based on structure and examples of each type
Pseudounipolar neurons: single short process that branches like a T to form a pair of longer processes. Includes sensory neurons where one branch receives sensory stimuli and the other delivers impulses to CNS
Bipolar neurons: two process, one at either end. Found in retina of the eye
Multipolar neurons: most common type, have several dendrites and one axon extending from the cell body. Includes motor neurons
What activity is the gray matter of the spinal cord often associated with?
reflexes
Term for a bundle of axons in the PNS and the CNS
Nerve is a bundle of axons in the PNS. Most nerves are composed of motor and sensory fibers and are called mixed nerves. Some cranial nerves are only sensory, such as for sight, hearing, taste, and smell.
Tract is a bundle of axons in the CNS
types of neuroglia in the PNS
- Schwann cells or Neurolemmocytes: form the myelin sheaths around peripheral axons
- Satellite cells: support neuron cell bodies within the ganglia of the PNS by movement of nutrients and waste
types of neuroglia in the CNS
- Oligodendrocytes: form myelin sheaths around multiple nearby axons of the CNS (like octopus)
- Microglia: migrate through CNS and phagocytose foreign and degenerated material. “Sculpts” the CNS
- Astrocytes: regulate the external environment of neurons in the CNS and wrap blood capillaries to create the Blood Brain Barrier
- Ependymal cells: epithelial cells that line the ventricles of the brain and central canal of spinal cord. They have cilia which move cerebrospinal fluid and maintain it’s homeostasis
what makes microglia unique among CNS neuroglial cells
They are derived from cells that were produced in the embryonic yolk sac and migrated into the developing neural tube. They are thus related to macrophages found elsewhere in the body (but are replaced only by replication of microglial cells not like macrophages made from blood monocytes)
describe the function of microglia
They have many fine processes that constantly wave and survey the environment to maintain healthy neuronal and synaptic function. Microglial Activation results from infection or trauma. The cells become amoeboid in shape and are transformed into phagocytic, motile cells that sense damage by ATP receptors. They kill exogenous pathogens and remove damaged debris in the CNS. They also shape neural circuits by pruning axons
All PNS cells (myelinated or not!) are surrounded by a continuous living ______ which the CNS lacks
sheath of Schwann cells or neurilemma.
CNS lack a neurilemma because Schwann cells are found only in the PNS (CNS has oligodendrocytes)
What forms the myelin sheath and on which cells?
Some axons (not all) in the PNS have a myelin sheath formed by successive wrappings of the cell membrane of Schwann cells.
In the CNS, some axons have a sheath formed by oligodendrocytes.
Axons smaller than 2 micrometers in diameter are usually unmyelinated and those that are larger are likely to be myelinated.
In myelinated PNS axons, is the entire axon covered by a neurilemma?
Yes, but not all parts of the axon are myelinated. The myelination is composed of Schwann cells that wrap multiple times around only a millimeter of axon, so there are gaps of unmyelinated (but still has neurilemma/schwann cell!) axon between adjacent Schwann cells called Nodes of Ranvier.
Unmyelinated axons also have neurilemma but lack the multiple wrappings that compose the myelin sheath.
how is myelination accomplished in the CNS
oligodendrocytes have multiple extensions that form myelin sheaths around several axons. They also provide lactate for energy needs as well as rapid conduction.
explain white and gray matter
White matter is area in the CNS with a high concentration of myelinated axons. It is located in the inner brain and outer spinal cord
Gray matter is area in the CNS with a high concentration of cell bodies and dendrites which lack myelin sheaths. It is located in the outer brain and inner spinal cord
*How are PNS axons regenerated?
After the cut, the distal portion of the axon is degenerated and phagocytose by Schwann cells. These Schwann cells, and the basement membrane, form a regeneration tube. They secrete chemicals that attract the growing axon tip and guide the regenerating axon to its proper destination.
*describe regeneration in CNS axons
Central axons have a much more limited ability to regenerate. Injury stimulates growth of axon collaterals but regeneration is prevented by inhibitory proteins (Nogo) in the membranes of myelin sheaths. Regeneration may also be physically blocked by a glial scar (astrocytes) or the scar might aid, we don’t know.
Describe the proteins that prevent axon regeneration
In the CNS, Nogo proteins are produced by oligodendrocytes and have been shown in rodents to inhibit axon regeneration.
In the PNS, Schwann cells also produce myelin proteins that can inhibit axon regeneration. But, after axon injury these are removed and Schwann cells stop producing the inhibitory proteins, creating an environment conducive to axon regeneration in PNS
What features of the brain capillaries create the blood-brain barrier
Brain capillaries do not have pores between adjacent endothelial cells, all are joined by tight junctions. Astrocytes wrap around the capillaries to regulate permeability. Therefore, the brain cannot obtain molecules from the blood plasma by nonspecific filtering process. Molecules must be moved through the endothelial cells by diffusion and active transport, also endocytosis and exocytosis. This is the blood-brain barrier
Some molecules that can pass through the blood-brain barrier
Nonpolar O2 and CO2 and some organic molecules like alcohol and barbiturates.
How does glucose get into the brain?
GLUT1 is a specialized glucose carrier that is always present in the brain
How is the degree of “tightness” and selectivity of the blood-brain barrier regulated?
Astrocytes release regulatory molecules that stimulate the capillary endothelial cells to produce the proteins of the tight junctions. These regulatory molecules can also stimulate production of carrier proteins, channels, etc. that are required for rapid transport into CNS. The CNS capillaries are also periodically surrounded by cells called pericytes which are tightly associated and produce important transporters.
Communication between astrocytes and CNS capillaries (with pericytes) controls “tightness”
How does the blood-brain barrier pose a problem for treatment of brain diseases? One example of this
Because drugs that can enter other organs may not be able to enter the brain. In Parkinson’s disease, patients need dopamine in the brain but this cannot cross the blood-brain barrier. It’s precursor, levodopa (L-dopa) can cross the barrier so it is often used.
Review what creates the Resting Membrane Potential
- The sodium potassium pump moves unequal amounts of sodium and potassium in/out the cell creating an imbalance (K high inside, Na high outside)
- Large anions are trapped in the cell and attract a positive charge, BUT
- The membrane is more permeable to certain ions. K is the most permeable and so is drawn in by the anions.
what kind of cells alter their membrane potential?
Neurons and muscle cells. Alterations in membrane potential are achieved by varying membrane permeability to specific ions.
The ability to alter potential is termed excitability or irritability
define depolarization and hyperpolarization and their effect on nerve impulses
depolarization (hypopolarization) is when positive charges flow into the cell and the potential difference is reduced. This is excitatory activity on an impulse
Hyperpolarization is when the inside of the cell becomes more negative as positive charges leave or negative charges enter the cell. This is inhibitory activity on an impulse
how are changes in membrane potential caused? What are the specific proteins that accomplish this action?
Caused by changes in the net flow of ions through ion channels. Gated Channels are the controllers of ion flow through the plasma membrane. The gates are proteins that open and close according to stimuli. There are ion channels for Na+ (all gated but sometime flicker and leak) and K+ (one type gated and one type always open - leakage channel)
explain the depolarization threshold
adding positive charge to the inside of the cell causes depolarization. If only a little is added, the cell quickly return to normal resting potential. If a certain level is reached (-55 mV) a sudden and very rapid change in membrane potential is observed. -55 mV is the threshold level that causes Na+ channels to open, making the membrane freely permeable to Na+ and letting it rush into the cell
What causes K+ channels to open during an action potential?
Depolarization. After threshold is reached and Na+ rushes into the cell, the depolarization causes the gated K+ channels to open just before Na+ channels close. This makes the membrane more permeable to K+ and it diffuses out of the cell, moving the membrane potential back toward potassium equilibrium potential
Describe an entire action potential event
- Axon membrane is depolarized to a threshold level of -55 mV and some Na+ gates open, increasing Na+ permeability.
- Na+ rushes into cell and causes further depolarization, opening more channels, increasing permeability. (positive feedback loop)
- Increase in Na+ results in rapid reversal of membrane potential to +30 mV which causes Na+ channels to inactivate
- K+ channels open and K+ diffuses out of the cell, making the inside of the cell less positive, restoring resting membrane potential. Repolarization is a negative feedback loop
what are the structures that will eventually produce sperm within the testes? When do they appear?
seminiferous tubules. Appear very early, about 43-50 days after conception
Types of cell in the seminiferous tubules and what they do
Germinal cells: cells that eventually become sperm through meiosis and specialization
Sertoli, nurse, or sustentacular cells: nongerminal cells that appear about day 42 of development
Leydig cells: Appearing about day 65, these cells are clustered in the interstitial tissue that surrounds seminiferous tubules. Constitutes the endocrine tissue of the testes, so also called interstitial endocrine cells. They secrete ANDROGENS (testosterone)
What are the functional units of the ovaries and when do they appear?
ovarian follicles. Appear during second trimester of pregnancy, about day 105
What secretes testosterone and why is it important? When is it secreted?
Leydig cells (in the seminiferous tubules) secrete androgens about 8 weeks after conception and peak secretion at 12 to 14 weeks, then declines by 21 weeks. Testosterone levels rise again in newborns until 3 months then are undetectable from 7-12 months. At 12 months until adolescence, sex hormones are at the same level in both sexes.
Testosterone secretion is important because it masculinizes embryonic structures
Describe descent of the testes and why it is important
Testes develop within the abdominal cavity and gradually descend into the scrotum, sometimes this isn’t complete until shortly after birth. Descent is stimulated by Leydig cells secretion of hormones (testosterone).
This is important because the temp of the scrotum is maintained 3 degrees C below normal body temp. The cooler temp is needed for spermatogenesis!
What is cryptorchidism
When the testes do not descend properly. Spermatogenesis does not occur (infertile) and there is a higher risk of testicular cancer
*What are the two systems of embryonic ducts
Wolffian (mesonephric) ducts: derive male accessory organs
Mullerin (paramesonephric) ducts: derive female accessory organs
Both systems are present in male and female embryos between day 25 to 50!
What happens after castration of an embryo? What does this indicate about sex organ development?
Castration results in regression of wolffian ducts and development of mullerian ducts and development of female accessory organs (uterus and Fallopian tubes). This tells us that the absence of the testes and their secretions is required to allow the female accessory sex organs to develop
What causes regression of mullerian tubes
Mullerian inhibition factor (MIF) secreted by Sertoli cells. Then Leydig cells secrete testosterone which causes growth of the wolffian ducts into male accessory organs
Common external genitalia of males and females during first 6 weeks of development
urogenital sinus
genital tubercle
urethral folds
labioscrotal swellings
What are some homologous structures between male and female reproductive structures
Penis and Clitoris: both are formed from the genital tubercle
Scrotum and Labia Majora: both are formed from the labioscrotal swellings
*How does testosterone cause masculinization of the embryonic structures
Once inside target cells, testosterone is converted by 5a-reductase into the active hormone dihydrotestosterone (DHT). DHT is the molecule that is needed for development of penis, spongy urethra, scrotum, and prostate.
Testosterone directly stimulates the Wolffian duct derivatives: epididymis ductus deferens, ejaculatory duct, and seminal vesicles
Describe the general pattern of sex determination and development from fertilization to genitalia and why it makes sense
General Pattern: genetic sex is determined by whether the sperm is X or Y bearing. The presence or absence of the Y determines the gonads development into testes or ovaries. The presence or absence of testes then determines whether accessory sex organs and external genitalia form male or female.
Makes sense because embryos develop within a high estrogen environment secreted by mother. If ovary secretions determined sex, all embryos would be female!
Explain hermaphroditism cause and result
Condition in which both ovarian and testicular tissue is present in the body. Can be one ovary and one testis, an ovotestes, or both.
Caused when only SOME embryonic cells receive the short arm of the Y chromosome with its SRY gene while others don’t.
What is a pseudohermaphrodite
Disorder involves individuals with either testes or ovaries (not both) who have accessory sex organs and external genitalia that are incompletely developed or inappropriate for their chromosomal sex
How does hormone concentration (and therefore endocrine regulation) change before and after puberty?
Before puberty there are equally low concentrations of sex steroids (androgens and estrogens). During puberty, gonads secrete increased amounts of sex steroid hormones as a result of increased stimulation by gonadotrophic hormones from the anterior pituitary
Types of gonadotrophic hormones
Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH). named according to female actions, but are the same hormones in males.
LH sometimes called interstitial cell stimulating hormone ICSH
Effects of Gonadotrophic hormones
- Stimulation of spermatogenesis or oogenesis
- Stimulation of gonadal hormone secretion
- Maintenance of the structure of the gonads
What stimulates the secretion of Luteinizing Hormone and Follicle Stimulating Hormone
Secretion of gonadotrophic hormones from anterior pituitary is stimulated by Luteinizing Hormone- Releasing Hormone (LHRH) produced by the hypothalamus and secreted into the hypothalamo-hypophyseal portal vessels
LHRH stimulates both hormones, so is often called Gonadotropin-Releasing Hormone (GnRH)
*What happens to hormone levels in castrated (neutered) animals? What does this indicate about the gonads?
When gonads are removed, FSH and LH secretion increases to very high level. This demonstrates that gonads secrete products that exert a negative feedback effect on gonadotrophin secretion. The negative feedback is largely exerted by testosterone and estrogen in males and females respectively
What are the mechanisms of negative feedback effects of steroid hormones on gonadotropin release?
- inhibition of gonadotropin-releasing hormone secretion from the hypothalamus
- inhibition of the pituitary’s response to gonadotropin-releasing hormone. This is accomplished via INHIBIN secreted by Sertoli cells (males) and granulose cells (females) which inhibits FSH but not LH
Differences between males and females in hypothalamus-pituitary-gonadal regulation
Males have constant secretion of gonadotropins and sex hormones. Always on
Females show cyclic variations in secretion of gonadotropins and sex hormones during the menstrual cycle. *ALSO shortly before ovulation, estrogen exerts a positive feedback effect on Luteinizing Hormone secretion!
Is secretion of Gonadotropin-releasing hormone continuous? Why?
Secretion of GnRH from hypothalamus is PULSATILE, stimulating a similar pulse secretion of FSH and LH from anterior pituitary.
Needed to prevent desensitization and down regulation of the target glands. Frequency and amplitude affect target gland’s response
Example: slow frequency of GnRH pulses in females stimulate FSH secretion while faster pulses favor LH secretion.
Describe the overshooting that occurs in an action potential
When the depolarization threshold is reached and Na+ flows into the cell, the membrane overshoots so that it is actually positively charged (+30) inside. Then, when repolarization occurs and K+ flows into the cell it overshoots the resting membrane potential (more negative than -70) producing an after-hyperpolarization. Neither of these overshoots reaches the Na+ of K+ equilibrium potentials because channels close before then.
What is the Na+ / K+ pump doing during an action potential event?
It is constantly going! Pumping 3 Na+ out and 2 K+ in and restore the normal resting potential (because only a small amount of Na+ and K+ ions actually move during an action potential)
Is an action potential the product of active transport processes? What chemical helps show this fact?
Active transport is not directly involved in action potentials, all ions flow down their concentration gradients. However, the maintenance of the Na+ and K+ gradients requires the pump which is active transport. Cyanide poisoning demonstrates this because a neuron can still produce action potentials for a period of time after halting ATP production.
What does it mean that impulses are all or none?
Once threshold is reached, all action potentials are the same. The amplitude and length of time are independent of the strength of the stimulus. A stronger stimulus does not make a stronger action potential
Why are channels only open for a fixed period of time during an action potential
They are soon inactivated by either a ball and chain polypeptide blockage or a conformational shape change. This inactivates the channel but is different from closing it. Inactivation ends once the membrane repolarizes
*What codes for stimulus strength?
- Frequency. A greater stimulus causes more frequent action potentials, NOT high amplitude impulses. It is frequency modulated (FM) not amplitude modulated (AM)
- Recruitment. As intensity of stimulation increases, more and more axons will become activated (some have higher thresholds)
Explain what the absolute refractory period is and how it is are caused molecularly
The interval between successive action potentials will never be so short that a new action potential can be produced before one has finished. During the time that a patch of axon is producing an impulse, it is incapable of responding to any stimulus - it is in an absolute refractory period!
Caused by the inactive state produced by the ball and chain molecular construct or shape alterations of the channel.
Explain what causes the relative refractory period
This is the period while repolarization is taking place and K+ channels are open, making the membrane potential more negative than usual (hyperpolarized). It is still possible to depolarize the cell and trigger another action potential but it would take a very strong signal during the relative refractory period.
*Why do action potentials only move forward and not backwards?
- The refractory period makes it impossible to stimulate an action potential in the previous area but the next adjacent area can be stimulated.
- Chemical synapse transmission only moves in one direction, from presynaptic to postsynaptic
How does the strength of a signal change as an action potential moves along an axon?
It stays the same! Each action potential remains a separate all-or-nothing event so the strength of the signal is always the same, it either triggers or it doesn’t
How are relative concentrations of Na+ and K+ affected by a large number of action potentials?
They are not very affected at all. Action potentials really don’t require that much of a change in ion concentrations and the Na+ K+ pump quickly corrects any changes that do occur.
*Explain cable properties of axons
Cable properties are neurons abilities to conduct charges through their cytoplasm. The axon is a very poor conductor and a change in potential is localized within 1 to 2 mm. It is poor because there is a high internal resistance to the spread of charges and many charges leak out.
Because cable properties are not good, this suggests that conduction of nerve impulses does not rely on the cable properties of an axon
How is stimulation conducted through unmyelinated neurons?
When threshold is reached at the INITIAL SEGMENT of the axon a depolarization will occur and positive Na+ ions are injected at that segment. The ions are conduced by cable properties to an adjacent region 1 to 2 mm away. This region reaches threshold and depolarizes and the cycle continues like this.
Action potentials are produced along the entire length of the axon in an unmyelinated neuron.
What influences the rate of conduction in neurons?
Thickness and myelination. Thicker is faster because they have less resistance to the flow of charges (better cable properties). Myelination is faster because fewer action potentials are produced along the axon as channels are only really present at the nodes of Ranvier
*Describe the spacing of nodes of ranvier
Nodes cannot be separated by more than 1 to 2 mm because that is how far cable properties of axons can conduct depolarizations. The node itself is then 1 to 2 µm wide.
What is the name for conduction on a myelinated axon?
Saltatory conduction, meaning leaping from node to node
What role does Calcium play in generation of action potentials?
A decrease in Ca2+ (hypocalcemia) decreases the threshold of excitation of neurons by increasing permeability of sodium channels. Basically hypocalcemia increases neuron excitability and leads to paresthesia (tingling), tetany, and even psychiatric disorders
What is a synapse? What are some other names for a synapse
Synapse: the functional connection between a neuron and a second cell (in the CNS it’s another neuron, in PNS may be neuron or effector cell)
If a neuron-muscle synapse, can be called neuromuscular synapses or neuromuscular junctions
Explain the two potential modes of synaptic transmission
Electrical: action potentials conducted directly from one cell to the next. original thought because they appeared to touch and the delay was so short.
Chemical: presynaptic nerve endings release chemicals (neurotransmitters) that then change the membrane potential of the postsynaptic cell. Revealed to be the more accurate picture after seeing the tiny gaps in synapses and that actions of nerves could be duplicated by certain chemicals
Explain the experiment that suggested synaptic transmission was chemical. Who conducted the study?
Otto Loewi isolated the heart of a frog with the vagus nerve attached and stimulated the nerve to innervate the heart in a solution. (Vagus nerve was known to slow heart rate.) This solution was then given to a second heart with no vagus nerve stimulation and the second heart also slowed it’s beat! Loewi concluded a chemical called Vagusstoff was released by the vagus. Vagusstoff is now identified as acetylcholine
where to electrical synapses exist?
In some nervous system cells, within smooth muscles, and in cardiac cells in the heart. Electrical synaptic conduction is only possible when adjacent cells are joined by gap junctions
Explain gap junctions structure and function
Structure: 6 connexins form a transmembrane structure with an aqueous core. Each of these are half the gap junction, called hemichannels. Two hemichannels dock together to complete the gap junction that spans both cell’s membranes
Function: allow cardiac muscle cells to contract as a unit, smooth muscles to contract together such as uterus in labor, and in neuroglial cells to allow Ca2+ passage and other molecules.
*Compare tetanus toxin and botulinum toxin
Both are proteases that block the release of neurotransmitters by destroying SNARE complex proteins.
Tetanus toxin reduces glycine or GABA release from INHIBITORY synapses by attacking synaptobrevin-2 causing muscle rigidity
Botulinum toxin reduces ACh release from EXCITATORY synapses by attacking SNAP-25 causing flaccid paralysis.
How do local anesthetics work? What are three common anesthetics and what additional compound is often added?
Anesthetics bind to Na+ channels in the axon and prevent them from opening and causing depolarization. So, they block a sensory axons ability to produce action potentials.
Cocaine, Procaine, Lidocaine
Epinephrine (Vasopressors) are often added to counteract the vasodilation which limits the duration of the drugs action.
What are two demyelinating diseases?
Guillain-Barré syndrome: T cells attack the myelin sheath of the PNS. causes muscle weakness, cardiac and blood pressure problems
Multiple Sclerosis: T cells attack CNS myelin sheath. Causes inflammation, demyelination, axon degeneration. Highly variable symptoms from sensory impairment to bladder/intestinal problems. Drugs that reduce autoimmune activity can help treat symptoms, but there is no cure.
How can hypokalemia affect the heart?
Hypokalemia is low blood K+ concentration (can be caused by diuretics). Low K+ hyperpolarizes the membrane potential and so the heart is less responsive to stimulus.
Two nondisjunction diseases and what do they demonstrate about sex determination?
Kleinfelter’s syndrome: person has the genotype XXY, develops male
Turner’s syndrome: person has the X genotype, develops female
Illustrate the Y chromosome determines the sex.
What is the test done to determine if testicular torsion (twisting of the spermatic cord) has occurred? Explain the function of the muscle being tested
The cremasteric reflex involves the contraction of the cremaster muscles and is absent if testicular torsion has occurred.
Cremaster muscles have the function of maintaining the correct temperature of the testes optimal for spermatogenesis. They contract and elevate testes closer to the body in cold weather (or when frightened or during intercourse) and lower them in cold weather.
What is endometriosis? How do we treat?
The presence of endometrial tissue outside of its normal location, which is the inner layer of the uterus. Can be though of as “retrograde menstruation” where endometrial implants flow from the uterus backward into the ovaries and then develop and bleed like normal. Causes inflammation, scar tissue, pain, and infertility.
Treatment is nafarelin (synarel), a GnRH analog that stimulates FSH and LH secretion BUT continuously instead of pulsatile. This down regulates GnRH receptors and reduces FSL and LH secretion. This stops ovarian steroid secretion and growth of endometrium. May require birth control pills of estrogen and progesterone to combat menopause mimicking effect.
