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Biology 5 Test 2 Study Guide
Chapter 7 – Hormonal Signaling
A. Hormones
a. Characteristics
i. Produced by endocrine cells and secreted into blood stream
ii. Act at long distances
iii. Potent – low quantities have a large effect
iv. Bind to specific receptors – only target cells contain the specific receptor
b. Types
i. Peptide – small proteins. Signal extracellularly (lipophobic) (Fig. 7.4)
ii. Steroid – cholesterol derived. Signals intracellularly (lipophilic) (Fig. 7.5)
iii. Amino acid derivatives – signals intracellularly (Fig. 7.6)
c. Reflex systems involve negative feedback loops
i. High blood glucose levels signal the pancreas to release insulin. (Fig. 7.7b)
B. The Endocrine System
a. Controlling Glands (Fig. 7.8a)
i. Hypothalamus – master controller. Sends releasing hormones or inhibiting
hormones to pituitary.
1. Releasing
a. Prolactin releasing hormone (PRH)
b. Thyrotropin releasing hormone (TRH)
c. Corticotropin releasing hormone (CRH)
d. Growth hormone releasing hormone (GHRH)
e. Gonadotropin releasing hormone (GnRH)
2. Inhibiting
a. Dopamine
b. Somatostatin
ii. Pituitary – sends signals to turn on other glands or to inhibit hypothalamus.
1. Anterior – produces hormones in the hypothalamic-hypophyseal portal
system (Fig. 7.8b, 7.9)
a. Prolactin (PRL) for milk production
b. Thyroid-stimulating hormone (TSH)
c. Adrenocorticotropic hormone (ACTH) for adrenal function
d. Growth hormone (GH)
e. Follicle-stimulating hormone (FSH) and luteinizing hormone
(LH) for ovary and testes function
2. Posterior – releases hormones sent from hypothalamus (Fig. 7.8c)
a. Vasopressin or antidiuretic hormone (ADH) slows urine
production
b. Oxytocin (OT) involved in childbirth and lactation
b. Some Pituitary Responding Glands
i. Thyroid – under voicebox
1. Functions: regulates metabolism by controlling oxygen consumption
during cellular respiration
2. T3 (triiodothyronine) and T4 (thyroxine) require iodine for production.
Goiter can be formed from too little iodine causing hypothyroidism.
ii. Adrenal – on top of kidneys
1. Functions: response to stress
2. Adrenal cortex (outside) responds to long-term stress. ACTH 
corticosteroids. Cortisol – increases breakdown of proteins and fats
leading to increase glucose. (Fig. 7.11b)
C. Endocrine Pathologies
a. Hypersecretion – too much hormone released
b. Hyposecretion – too little released (Fig. 7.15)
c. Receptor or signal transduction problems – signal is not relayed properly in cells
d. Diagnosis
i. Primary pathology – the last gland in the reflex is faulty
ii. Secondary pathology – another gland upstream of primary is faulty
iii. Example – hypercortisolism (Fig. 7.14)
1. Cushing’s Syndrome is caused by hypercortisolism. Symptoms similar to
diabetes (high glucose). Also, obesity in trunk and face, muscle loss.
2. Caused by pituitary tumor (secondary) or adrenal tumor (primary)
iv. Example - Addison’s Disease is caused by hypocortisolism. Symptoms are
muscle weakness, fatigue, weight loss, skin darkening, low blood pressure, and
low blood sugar
Chapter Problems: 1, 2, 6, 10, 11, 13, 16, 17, 20, 21, 24, 25, 27-29, 31
Chapter 8 – Neuronal Signaling
A. Overview
a. Organization (Fig. 8.1)
i. Central Nervous System (CNS) – brain and spine
ii. Peripheral Nervous System (PNS)
1. Afferent – sensory nerves going towards CNS
2. Efferent – away from CNS
a. Autonomic – involuntary control
b. Somatic Motor Division – skeletal muscles: voluntary control
b. Cell Types
i. Neurons – dendrites, cell body, axon, myelin sheath, synapse (Fig. 8.2).
ii. Glial – support nerves by providing nutrients, forming myelin sheath, taking
away wastes, and providing structure. (Fig. 8.5)
B. Electrical Signals in Neurons
a. Graded Potentials
i. Occurs on dendrite and cell body of the neuron
ii. Strength is proportional to stimulation. Caused by influx of an ion. Decreases as
it travels away from site of stimulation (Fig. 8.7a)
iii. If signal that reaches trigger zone of axon is above a certain threshold, an action
potential will be triggered. (Fig. 8.7b, c)
b. Action Potentials (Fig. 8.8)
i. An axon has positive charges outside of membrane and negative charges inside
of the membrane.
ii. Intensity of impulse is always the same. When “on” it is fully turned on. This is
called “all-or-none”.
iii. An action potential begins by letting positive charge in through gates and this
triggers adjacent gates to open. Gates behind the action potential close. This
causes “the wave” (Fig. 8.13)
iv. Sodium (Na) and Potassium (K) control action potentials (Fig. 8.12)
1. Sodium starts out high outside, low inside. Potassium starts out high
inside and low outside.
2. Sodium rushes in at the “front” of the action potential.
3. Potassium rushes out at the “back” of the action potential. This restores
original charge quickly.
4. Both gates close and cannot be opened for a brief period (refractory
period).
5. Na-K pumps restore original gradients.
v. Cycle of voltage gated Na+ channel
1. Resting potential is -70mV. Once threshold of -55mV is reached,
activation gates open (Fig. 8.10)
2. Ions rush through. Inactivation gate closes. After a period, gates reset.
vi. Summary of action potentials (Fig. 8.14)
vii. Conduction in myelinated axons is faster
1. Myelin sheaths act as insulation. No need for gated channels in these
regions.
2. Only need gates in nodes between the myelinated axons. Therefore
action potential jumps from node to node. This is saltatory conduction
(Fig. 8.16)
3. Multiple sclerosis is an autoimmune disease where myelin is destroyed.
C. Synaptic Communication Between Neurons
a. Junction between two cells. Focus on chemical synapses (Fig. 8.18)
b. Mechanism (Fig. 8.19a)
i. Action potential reaches axon terminus.
ii. Calcium channels open and let in calcium from cleft.
iii. This allows binding of vesicles containing neurotransmitter to bind membrane.
iv. Neurotransmitter is released and binds to receptor across cleft on postsynaptic
cell.
v. Response occurs in postsynaptic cell.
c. Neurotransmitters (Tab 8.4)
i. A subcategory of neurocrines
ii. Fall into 7 subcategories.
iii. Each bind to specific receptors
iv. Competitors
1. Antagonists bind to receptor and block it.
2. Agonists bind to receptor and activate it.
v. Action terminates by being broken down, reuptake, or diffusion away from cleft.
(Fig. 8.19b)
vi. Drug Abuse
1. Cocaine – binds to dopamine reuptake transporters. Dopamine stays for
too long in synaptic cleft.
2. LSD (lysergic acid diethylamide) – a hallucinogen that acts as an
antagonist or agonist for serotonin receptors.
3. THC – found in marijuana. Is an agonist to cannabinoid receptors that
produce inhibitory neurocrines for dopamine release.
4. Alcohol – a sedative. Is an agonist of GABA receptors and an antagonist
of glutamate receptors.
D. Integrated Neural Communication
a. Pathway branching (Fig. 8.22)
i. Divergence – when pathways split
ii. Convergence – when pathways merge
1. Sometimes graded potentials from many cells can add up to trigger an
action potential. This is summation (8.24)
2. Inhibitory neurons can negate a signal. (8.25)
iii. The cell body or axon terminus can be modulated (Fig. 8.26)
b. Long-term Potentiation and Depression
i. Potentiation increases signaling, depression decreases signaling.
ii. These may partially explain addiction to drugs.
iii. Mechanisms
1. Turn on a second messenger system (Fig. 8.27)
2. Increase or decrease number of receptors.
3. Change the form of receptors.
c. Nerve Development
i. Growth of nerves depends on chemical signals that tell it where to extend.
Growth cones are projections that reach until target cells are found (Fig 8.4)
ii. Growth and connections are increased by usage. Babies deprived of neural
stimulus have fewer connections and smaller brain size.
iii. Neural injury in the brain does not repair easily. Damaged PNS nerves can mimic
embryonic growth. Severed areas usually die (Fig. 8.6). Stem cell research may
result in the ability to re-grow neurons.
Chapter Problems: 2-5, 7, 8, 11-14, 16, 17, 19, 21-23, 25-29, 31
Chapter 11 – Efferent Nerves
A. Autonomic Division
a. Sympathetic and parasympathetic branches work opposite of one another. Generally,
sympathetic is for “fight-or-flight” activities and parasympathetic is for “rest-and-digest”
activities. (Fig. 11.1)
b. Control
i. Autonomic control centers in the brain maintain homeostasis (Fig. 11.3)
ii. Control is antagonistic between two branches.
iii. Pathways have two nerves: preganglionic neuron and postganglionic neuron.
They connect in the autonomic ganglion. (Fig. 11.4). They use acetylcholine in
the ganglia (Fig. 11.6)
iv. Sympathetic and parasympathetic branches exit spinal cord in different regions
(Fig. 11.5)
c. Sympathetic Pathways
i. Activate smooth muscle, cardiac muscle, glands, and other tissues.
ii. Neuroeffector junction uses norepinephrine to bind to adrenergic receptors (Fig.
11.9). Norepinephrine is removed by reuptake and diffusion.
iii. Adrenal medulla – activated by sympathetic neurons. Releases epinephrine for
fight-or-flight response. (Fig. 11.8)
d. Parasympathetic Pathways
i. Neuroeffector junction uses acetylcholine to bind to muscarinic receptors. (Fig.
11.9) Acetylcholine is removed by enzymatic breakdown and diffusion.
B. Somatic Motor Division
a. Controls skeletal muscle only.
b. Uses one neuron only
c. Neuromuscular junction uses acetylcholine to bind to nicotinic receptors (Fig. 11.10c-e)
i. Depolarization of axon terminus opens voltage gated Ca+ channels.
ii. This causes binding of vesicles to terminus, releasing acetylcholine.
iii. Nicotinic receptors are bound. This opens them, allowing ions to pass.
Chapter Problems: 1, 3, 4, 8, 10, 11, 12a, 15ac, 16-19
Chapter 12 – Muscle Function
A. Skeletal Muscle
a. Skeletal Muscle Structure (Fig. 12.3)
i. Fascia is the covering of the muscle. It extends to form the tendon which attaches
to a bone
ii. Fascicle is a bundle of fibers
iii. Each muscle fiber is a single cell
iv. Striations are from muscle filaments that overlap
1. Actin filaments are thin
2. Myosin filaments are thick
3. Sarcomere is a functional unit (Fig. 12.5)
a. Z disks – connects actin
b. I band – exposed actin only
c. A band – myosin
d. H zone – exposed myosin only
e. M line – connects myosin
4. T-tubules bring impulse from a motor neuron to sarcoplasmic reticulum.
This will cause sarcomere to contract. (Fig. 12.4)
b. Contraction
i. Sliding filaments (Fig. 12.9)
1. Rigor state – myosin head is bound to actin
2. Release – ATP binds myosin
3. Cocked state – ATP hydrolysis causes head shape to change
4. Power stroke –Myosin head changes back to original state. ADP and
phosphate are released.
ii. Calcium initiates contraction (Fig. 12.8)
1. Power stroke occurs because myosin binding sites on actin are exposed.
2. Calcium binds troponin. This causes tropomyosin to be pulled away from
actin.
iii. Excitation (Fig. 12.10)
1. Action potential travels down motor neuron. This releases ACh into
neuromuscular junction.
2. Na gates let Na through. This initiates action potential in T-tubules
3. DHP (dihydropyridine) receptor opens RyR (ryanodine receptor).
Calcium exits sarcoplasmic reticulum
c. Twitches
i. Contraction-relaxation cycle (Fig. 12.11)
1. Latent period – between muscle action potential and tension
development
2. Contraction phase – tension develops
3. Relaxation phase – loss of tension
ii. ATP Supply
1. Muscles do not have high ATP supply. Only enough for 8 twitches.
2. ATP is restored from cellular respiration
3. Phosphocreatine donates phosphate to ADP as a backup source (Fig.
12.12)
iii. Fatigue
1. Central – due to CNS. Usually psychological because low pH from
muscle overuse signals feelings of tiredness.
2. Peripheral – occurs at neuromuscular junction or muscle itself. Many
potential causes, such as depletion of glycogen or buildup of acid. (Fig.
12.13)
3. Muscle types (Table 12.2)
a. Slow-twitch – aerobic and slow tension buildup. Used for
posture, standing, walking. Fatigue resistant.
b. Fast-twitch oxidative-glycolytic – aerobic and medium tension
buildup. Used in moderate activity. Fatigue resistant.
c. Fast-twitch glycolytic – anaerobic and fast tension buildup. Used
in quick or heavy movements. Fatigues easily.
iv. Force
1. Tension – greatest when a sarcomere is at optimal length. (Fig. 12.15)
2. Summation – each twitch generates a small amount of tension. When
added together, tension is greater (summation). (Fig. 12.16)
3. Tetanus – sustained maximum tension
4. Number of motor units – one neuron and the fibers it innervates. Smaller
muscles have fewer (face, fingers), larger muscles have many (leg).
d. Dysfunction
i. Cramps – painful sustained contraction by over-firing of the motor neuron. Many
causes such as: overuse, old age, injury, electrolyte imbalance, medications.
ii. Poisons – botulism toxin from Clostridium infection causes muscle paralysis by
blocking ACh release. Botox reduces wrinkles by paralyzing facial muscles that
pull skin into folds.
iii. Duchenne muscular dystrophy – dystrophin is a protein important in
development of the proper arrangement of muscle fibers. Patients have weak
muscle activity and die prematurely.
B. Smooth Muscle
a. Found in linings of many organ systems (e.g. GI tract, urinary, respiratory), on blood
vessels, and in the eye. Controls involuntary movements.
b. Structure
i. Small size (Fig. 12.23)
1. Single unit – cells contract together. Action potential spread to adjacent
cells through gap junctions. Found on vessels and GI tract.
2. Multi-unit – cells contract individually. Each cell receives signals
independently. Found in the eye and reproductive tract. Allows fine
control of contractions.
ii. Variation in filaments – actin and myosin are longer. Myosin has an extra light
chain for regulation.
iii. Arranged in bundles, not sarcomeres. No striations. Contraction causes cell to
become round (Fig. 12.25)
c. Contraction (Fig. 12.26a)
i. Calcium enters cytoplasm from sarcoplasmic reticulum or extracellularly
ii. Calcium binds calmodulin. They activate myosin light chain kinase (MLCK)
iii. MLCK phosphorylates myosin light chain
iv. Myosin can cleave ATP and begin sliding filament cycle.
d. Relaxation (Fig. 12.26b)
i. Calcium is pumped out of the cytoplasm
ii. Calmodulin is released
iii. Myosin phosphatase dephosphorylates myosin light chain
e. Calcium initiates contraction
i. Calcium is stored and enters from extracellular fluid or sarcoplasmic reticulum
ii. Signals for calcium influx (Fig. 12.29)
1. Decreased sarcoplasmic reticulum stores
2. Stretch – stretch activated receptors open when vessels dilate.
3. Depolarization – action potential similar to skeletal muscle, although
potentials are much more varied
4. Chemicals – neurotransmitters, hormones, and paracrines
Chapter Problems: 1, 3, 6, 7, 9, 11-20, 22-25, 28, 29a-d,g, 30-32, 34