Exercises: The nervous and endocrine systems

Compare nerve and hormonal signals in terms of their speed, duration, transmission pathway and destination precision, and give an example of a typical response for each.

Describe the parts of a neuron (dendrites, cell body or soma, axon, and axon terminals) and explain the function of each in receiving, conducting, and transmitting nerve impulses.

What is a hormone and where is it produced? Name two human endocrine glands, the hormone secreted by each, and its main effect.

Distinguish between the central and the peripheral nervous systems: which organs each includes, what general function it fulfils and how they communicate with each other.

1. a) Name the three main parts of the brain.
2. b) State a characteristic function of each of them.

What is a synapse? Explain why the signal does not pass electrically from one neuron to another in most of them and what advantage using a chemical messenger can have (modulation, amplification).

Distinguish between sensory and motor nerves, and discuss what functional loss the injury of each type produces in a hand (what happens to sensation and to movement?).

Name three human hormones (insulin, thyroxine, adrenaline, growth hormone), the gland that secretes each and the main effect of each one.

When you touch a very hot object, you pull your hand away before feeling pain. Describe the pathway of the nerve impulse in this reflex arc, naming the neurons involved and explaining why the response does not pass through the brain first.

Look at the image of the neuron and the chemical synapse. a) Describe the pathway of the signal from structure 2 to 8, explaining what happens at each step. b) Reason what advantage structure 4 provides to the conduction speed. c) Explain why the signal at the synapse can only travel from 5 to 8 and never in reverse.

Explain what negative feedback is in hormonal regulation, describing a specific example: the regulation of blood glucose by insulin and glucagon, or that of the thyroid axis.

Explain qualitatively what the action potential is: which ions enter and leave the neuron, why it is said to work in an "all-or-nothing" way, and how the myelin sheath allows the saltatory conduction that speeds up the impulse.

The spinal cord is at once a reflex centre and a motorway for information. Explain what happens after a complete spinal cord injury depending on its height (paraplegia if it is lumbar or thoracic, tetraplegia if it is cervical) and discuss why the neurons of the central nervous system hardly regenerate.

Goitre is the growth of the thyroid due to lack of iodine. Explain, using the negative feedback of the pituitary-thyroid axis, why the gland grows when it cannot make thyroid hormone, and why iodised salt almost eradicated this problem.

Melatonin regulates the circadian rhythm. Explain which environmental signal controls it (light), what happens to its secretion when we use bright screens at night, and what consequences chronic jet lag has for sleep and performance.

Compare the sympathetic and the parasympathetic nervous systems: effects on the heart, digestion, the pupils and the bronchi, and explain why they are summarised as "fight or flight" and "rest and digest", indicating in which situations each one dominates.

In a diagnostic oral glucose tolerance test, blood glucose levels and plasma insulin concentrations are monitored in two individuals (subject A and subject B) while fasting, and at 60 and 120 minutes after ingesting 75 g of dissolved glucose:

• Subject A: starts at 85 mg/dL of glucose; reaches 135 mg/dL at 60 min and returns to 90 mg/dL at 120 min. Their plasma insulin rises from 8 µU/mL to 70 µU/mL and then drops to 12 µU/mL.

• Subject B: starts at 170 mg/dL of glucose; rises to 290 mg/dL at 60 min and stands at 265 mg/dL at 120 min. Their insulin remains constant and undetectable (< 2 µU/mL) across all measurements.

1. a) Justify which of the two subjects has type 1 diabetes mellitus, relating the data to negative feedback mechanisms and glucose transporters in muscle and liver tissue.
2. b) If subject B mistakenly injects three times their prescribed dose of exogenous insulin without ingesting carbohydrates, predict what will happen in adipose tissue, muscle tissue, and the brain. Justify why severe hypoglycemia is life-threatening within minutes, unlike sustained moderate hyperglycemia.

A neurophysiology team electrically stimulates a presynaptic motor neuron and records the activity in the muscle fiber it innervates after independently applying two different neurotoxins:

• With Toxin 1: the action potential propagates along the axon at 75 m/s to the terminal bouton without alteration, but no potential change is recorded in the muscle membrane, nor is acetylcholine detected in the synaptic cleft.

• With Toxin 2: the axonal action potential slows down drastically and its amplitude decays until it disappears before reaching the synaptic terminal; however, if the researchers apply acetylcholine directly onto the muscle membrane using a micropipette, it depolarizes and contracts completely normally.

1. a) Deduce and justify which specific type of voltage-gated ion channel is blocked by each toxin, distinguishing between axonal electrical propagation and the molecular steps of chemical synaptic transmission.
2. b) If purely electrical transmission (via gap junctions) is virtually instantaneous and experiences no synaptic delay, argue what decisive adaptive advantage led the central nervous system of vertebrates to base most of its circuitry on chemical synapses with a delay.

During an acute stress response experiment, two groups of individuals are subjected to an unexpected 30-minute stress test:

• Control Group: experiences an immediate increase in heart rate (from 70 to 135 bpm in just 6 seconds), pupillary dilation, and an early spike in blood glucose, followed from 15-20 minutes onward by a sustained increase in hepatic gluconeogenesis and a decrease in protein synthesis.

• Treated Group: has previously received a specific beta-adrenergic receptor-blocking drug.

1. a) Predict with justification what differences the Treated Group will show compared to the Control Group in heart rate, blood pressure, and blood glucose during the first 60 seconds after stimulus onset.
2. b) Explain why the adrenaline-mediated response (sympathetic nervous system and adrenal medulla) triggers cellular effects within seconds, whereas the response coordinated by cortisol (hypothalamic-pituitary-adrenal cortex axis) takes tens of minutes to establish itself. Base your reasoning on the chemical nature of each hormone and their respective cellular transduction mechanisms.

During a neurological examination of a 28-year-old female patient with suspected multiple sclerosis, visual evoked potentials in the optic nerve are recorded and compared with a healthy individual:

• Healthy individual: P100 wave latency = 98 ms; axonal conduction velocity = 55 m/s.

• Patient: P100 wave latency = 148 ms; axonal conduction velocity = 18 m/s, with a marked loss of signal amplitude. Furthermore, the patient reports that when taking a hot shower or engaging in strenuous physical exercise, her vision becomes much blurrier for a few minutes (Uhthoff's phenomenon).

1. a) Explain at the molecular and biophysical levels why the autoimmune destruction of the myelin sheath causes both signal slowing and the possible complete extinction of the action potential, taking into account the typical localization of voltage-gated Na+ channels and current leaks across the axonal membrane.
2. b) Formulate a reasoned hypothesis as to why a moderate increase in body temperature can completely interrupt nerve conduction in a demyelinated axon, and reason why two individuals with multiple sclerosis may present completely different initial clinical pictures.

In a study on the mesocorticolimbic reward circuit in laboratory rodents, microdialysis is used to measure dopamine concentrations in the nucleus accumbens, and autoradiography techniques are used to assess the density of D2 receptors in postsynaptic neurons under three conditions:

• Condition 1 (natural appetitive stimulus: sugar solution): dopamine increases by 45% above baseline for 20 minutes; D2 receptor density remains unchanged (100%).

• Condition 2 (acute amphetamine injection): plasma dopamine at the synapse spikes by 650% for more than 90 minutes.

• Condition 3 (after 4 weeks of daily amphetamine use, following 24 hours of deprivation): baseline dopamine levels drop 35% below normal, and the density of active D2 receptors falls to 40% of the initial level.

1. a) Interpret the data from Condition 3 to explain the molecular mechanisms of drug tolerance and anhedonia (the inability to experience pleasure from natural stimuli). What adaptive synaptic plasticity phenomenon explains the reduction in D2 receptors?
2. b) Based on these biological data, refute the claim of someone who argues that "overcoming an addiction requires no medical or pharmacological support, but merely a firm act of willpower."

A patient suffers a traumatic brain injury that results in the complete traumatic transection of the pituitary stalk (infundibulum), severing both the vascular network of the hypothalamic-hypophyseal portal system and the axonal nerve fibers originating from the supraoptic and paraventricular nuclei.

1. a) Predict with reasoning how the blood concentration (will increase, drop drastically, or remain the same) will change for each of the following hormones:

1. Thyroid-stimulating hormone (TSH) and Growth Hormone (GH).

2. Prolactin (considering that the hypothalamus exerts a tonic inhibitory control mediated by dopamine).

3. Oxytocin and Antidiuretic Hormone (ADH or vasopressin).

1. b) During the first 24 hours of hospital admission, the patient excretes more than 12 liters of very dilute urine (specific gravity 1,002 g/mL, similar to pure water) and reports extreme, insatiable thirst. Identify the specific endocrine disorder they suffer from, justify which hormone is responsible for this fluid balance, and describe the homeostatic feedback failure that has occurred.

In the medical treatment of children with central precocious puberty (abnormal pubertal development before age 8 due to premature activation of the hypothalamic axis), a potent gonadotropin-releasing hormone (GnRH) agonist administered via a continuous-release subcutaneous implant is used as a drug.

1. a) Knowing that under normal physiological conditions the hypothalamus secretes GnRH in intermittent pulses every 60 to 90 minutes to induce the synthesis of LH and FSH in the anterior pituitary, explain the apparent contradiction: why does the uninterrupted and constant administration of a GnRH activator (agonist) halt puberty instead of accelerating it? Justify the cellular mechanism undergone by the anterior pituitary receptors.
2. b) In recent decades, the age of pubertal onset has significantly advanced in populations with high-calorie diets and higher rates of childhood obesity. Formulate a biological hypothesis relating body adipose tissue mass, the hormone leptin, and the GnRH pulse generator, and predict why a youth athlete with an extremely low body fat percentage may present with amenorrhea or delayed puberty.

A 23-year-old male presents to a medical clinic due to a one-year history of infertility and gynecomastia (breast tissue development). Blood tests and a semen analysis yield the following results:

• Plasma androgens (total testosterone): 36 ng/mL (normal reference range: 3,0 to 10,0 ng/mL).

• LH (luteinizing hormone): < 0,1 mIU/mL (normal range: 1,5 to 9,0 mIU/mL).

• FSH (follicle-stimulating hormone): < 0,1 mIU/mL (normal range: 1,4 to 14,0 mIU/mL).

• Semen analysis: total azoospermia (zero viable sperm in the ejaculate) and marked bilateral testicular atrophy.

1. a) Interpret these results by deducing whether the origin of the androgens is endogenous or exogenous (use of synthetic anabolics). Justify how the hypothalamic-pituitary negative feedback loop responds and why, despite having an androgen concentration four times higher than normal, the patient produces no sperm.
2. b) If the patient abruptly stops using anabolics without medical supervision, predict with reasoning what hormone levels and physical and emotional symptoms he will experience in the subsequent weeks. Justify why the endocrine axis does not normalize instantaneously.