Exam 4 Practice Flashcards

(65 cards)

1
Q

Explain what is the resting membrane potential of a cell and how it gets established in a neuron

A

Resting potential is the membrane potential of a cell in its resting or unstimulated state. It is established by a difference in concentrations inside and outside of the cell. Neurons have a high intracellular concentration of K+ and low intracellular concentrations of Na+ and Cl-

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2
Q

What are the similarities between a cell membrane and a battery?

A

Batteries have different charges on each side (positive vs negative), creating a voltage difference or electrical potential. Similar to the separation of charges in membrane potential that also cause electrical potential. They both also store chemical energy and convert it into electrical energy

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3
Q

How does an action potential propagate along the axon?

A

Step 1 - at the start of an action potential, the influx of Na+ attracts intracellular negative charges and repels positive charges, causing cations to spread away from the sodium channels
Step 2 - as cations are pushed farther from the initial sodium channels, they depolarize adjacent “downstream” portions of the membrane
Step 3 - downstream voltage-gated Na+ channels open when the adjacent membrane reaches threshold, resulting in a new action potential there
They always propagate down the entire length of the axon

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4
Q

What are the phases of an action potential, describe the changes in permeability for Na and K that occur in each phase

A

An action potential has three phases: depolarization, repolarization, and hyperpolarization. Na+ and K+ permeability is initially low in the resting phase (Na+ channels were closed) but the Na+ permeability quickly increases during depolarization because the voltage-gated Na+ channels rapidly opened (K+ remains the same). During repolarization, Na+ permeability is low and K+ is high (potassium channels open with delay), cell returns to being negative. Lastly, during hyperpolarization, Na+ gated channels close so permeability is low but K+ stay open longer than necessary then close. Permeability is high but decreases when channel closed

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5
Q

What are the key features of an action potential. What does it mean that it is a “all or none event?”

A

Action potential is a rapid, temporary change in a membrane potential. They have three phases and MUST reach the threshold potential to initiate. They all have the same general characteristics in all species and all types of neurons. It being all or none indicates there is no such thing as “partial” action potential. All action potentials for a given neuron are identical in magnitude and duration. Action potentials are propagated down the length of the axon and again the threshold potential must be reached for action potential to occur at all.

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6
Q

Calculate the equilibrium potential of K+ in the squid axon using the Nernst equation if the concentration of this ion inside the cell is known to be 400mM and the concentration in the extracellular medium is 20mM. Assume that the temperature is 20 degrees

A

Nernst Equation: E_ion = 2.3 RT/zF(ln([ion]_o/[ion]_i))
E=equilibrium potential in VOLTS
R = universal gas constant 8.314 J/K mol
T = temp in Kelvins
F = faraday constant 96485 J/V mol
ion_o = concentration of ion outside the cell
ion_i = concentration of ion inside the cell
z = valency of ion
genuinely I can’t figure out the fucking answer

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7
Q

Using the Goldman equation explain how the permeability of ions determines membrane potential of cells

A

The Goldman equation shows that the membrane potential is a weighted average of the equilibrium potentials of permeable ions, weighted by how permeable the membrane is to each ion. This allows cells to fine-tune electrical signals by dynamically changing ion channel activity. Best answer I got bruh

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8
Q

Describe the experiments used by Hodgkin and Huxley that revealed how ions flow during an action potential

A

Using the giant axons of squid (because of axon size), they inserted a wire inside the axon and compared it to one outside to measure the voltage. They also used the voltage clamping technique and held the squid giant axon membrane at various voltages, proving that the membrane contains ion channels whose behavior depends on voltage (and proving that voltage-gated channels exist)

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9
Q

Why can axon potentials only propagate unidirectionally down the axon?

A

This is due to the refractory period of voltage-gated sodium channels. Action potentials propagate in one direction only because “upstream” sodium channels, in the direction of the cell body, are in the refractory state. The refractory state means that once Na+ channels have opened and closed, they are less likely to open again for a short period

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10
Q

Why do mammals not have large axons such as the ones found in the giant squid?

A

Large axons arose as adaptations specific to these squid so that rapid signaling could be possible. Other animals, however, instead adapted different cells to wrap around the axons of certain neurons in order to increase the speed of action potential propagation (myelin). Myelination is a more space efficient adaptation for animals (squids can’t move as effectively because of their large axons)

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11
Q

What are the parts of a neuron and how do morphology and function relate in each of those parts?

A

Most neurons have the same three parts: a dendrite, a cell body/soma, and the axon. A dendrite receives electrical signals from the axons of adjacent cells. The soma, which includes the nucleus, integrates the incoming signals and generates an outgoing signal. The axon then sends the signal to the dendrites of other neurons

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12
Q

How and when were neurotransmitters discovered?

A

In the 1920s, Otto Loewi discovered neurotransmitters through an experiment using two frog hearts. Loewi isolated the vagus nerve and heart of a frog, and slowed the heart rate when he stimulated the vagus nerve electrically. Then he took the solution that bathed the first heart and applied it to another frog heart without stimulating the vagus nerve to the heart. The second heart’s rate slowed as well

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13
Q

Describe the sequence of events that take place at the synapse when an action potential arrives

A

Step 1 - an action potential arrives at the end of the axon, near the synaptic cleft
Step 2 - the depolarization created by the action potential opens voltage-gated calcium channels located near the synapse, in the plasma membrane of the presynaptic neuron. The electrochemical gradient for Ca2+ results in an inflow of calcium ions through the open channels
Step 3 - in response to the increased calcium ion concentration inside the axon, synaptic vesicles fuse with the presynaptic membrane and release neurotransmitters into the synaptic cleft. The delivery of neurotransmitters into the cleft is an example of exocytosis
Step 4 - neurotransmitters bind to receptors on the postsynaptic cell. Thus, each neurotransmitter functions as a ligand, a molecule that binds to a specific site on a receptor molecule. Neurotransmitter-receptor binding causes ion channels in the postsynaptic membrane to open, leading to a change in the membrane potential of the cell. The combined effect on membrane potential of many neurotransmitters binding may trigger an action potential in the postsynaptic cell
Step 5 - the response ends when the neurotransmitters unbind from their receptors, causing the ion channels in the postsynaptic membrane to close

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14
Q

What is summation and why is it important?

A

Summation is the additive nature of postsynaptic potentials. It is important because a single synaptic signal is usually too weak to trigger an action potential by itself. Summation allows neurons to integrate information from various inputs. EPSPs (excitatory postsynaptic potentials) and IPSPs (inhibitory postsynaptic potentials) are summed at the axon hillock

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15
Q

How does a neurotoxin that changes the conformation of Na channels so that they stay open affect the transmission of an electrical signal in a neuron?

A

It would disrupt the transmission of electrical signals in a neuron by interfering with the action potential cycle. Na+ will continue to enter the cell and keep the membrane potential elevated (K+ cannot keep up with the amount of Na+). Cell cannot repolarize and the cell will lose its electrical gradient. It can lead to neuromuscular paralysis, as seen with certain toxins like batrachotoxin

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16
Q

What is the patch clamping technique and how did it contribute to the field of neurobiology?

A

Patch clamping is a improved variation of voltage clamping created by Neher and Bert Sakmann. It is used to study individual ion channels, showing that different ion channels behave differently (such as voltage-gated channels, sodium channels, and potassium channels)

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17
Q

Metchromatic leukodystrophy is an inherited disorder characterized by accumulation of fats called sulfatides in the myelin sheath of the cells of the central nervous system. Sulfatides are toxic to neurons. How do you think this affects signal transmission in persons affected with this disorder?

A

The nervous system’s ability to transmit signals effectively is impaired. It damages myelin, such as oligodendrocytes and Schwann cells, resulting in myelin breakdown. Without myelination, neurons conduct impulses much more slowly or not at all. Demyelinated axons are also more vulnerable to damage and may degenerate over time

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18
Q

Which factors modulate the speed of signal transmission in neurons?

A

Factors include axon diameter (larger diameter means less resistance) and myelination (increases the speed of action potential propagation)

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19
Q

What is myelin? Where does it come from? How does myelin increase velocity of signal transmission? Which animals have developed myelination? What happens in multiple sclerosis patients?

A

Myelin is a specialized accessory cell whose membranes wrap around the axons of certain cells. In the central nervous system, these cells are oligodendrocytes. In the peripheral nervous system, they are Schwann cells. Both are glia, nervous system cells that support neurons. When they wrap around an axon, they form a myelin sheath, which acts as a type of electrical insulation. Action potentials “jump” from node to node (called node of Ranvier) down a myelinated axon much more rapidly than they can move down an unmyelinated axon of the same diameter. Myelination is an adaptation that makes rapid transmission of electrical signals possible in axons that have a small diameter. Vertebrates and some invertebrates have myelinated axons. If myelin degenerates, the transmission of action potentials slows considerably. The autoimmune disease multiple sclerosis develops when the immune system targets oligodendrocytes, destroying myelin in the CNS. As damage to myelin increases, electrical signaling becomes more impaired, affecting coordination among neurons and causing muscles to weaken

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20
Q

What are non-spiking neurons and where can they be found?

A

These are neurons (EPSPs and IPSPs) that do not generate action potentials (spikes) and instead communicate through graded potentials. Occur in dendrites and travel along to the cell body (becomes action potential at the axon hillock)

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21
Q

What is a graded potential? Where do they occur in the neuron?

A

A graded potential is a transient (short lasting) localized change (depolarization or hyperpolarization). It’s intensity depends on the intensity of the stimulus and they degrade with time and distance. They only work for short distances and depend on ligand-gated channels. These potentials occur on the dendrites and cell body (soma) of a neuron (once the potential reaches the axon hillock it becomes an action potential)

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22
Q

Give an example of a neurotoxin and its mode of action. Draw how it would change the shape of a conventional action potential

A

Batrachotoxin changes conformation of Na+ gated voltage channels, causing them to remain open (found in beetles)

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23
Q

Draw and describe step by step the molecular events that take place in the synaptic cleft

A

1 - terminal is at rest
2 - action potential arrives; vesicles fuse with terminal membrane, producing exocytosis of transmitter
3 - transmitter binds to postsynaptic receptor proteins; ion channels open
4 - transmitter is removed from cleft; fused membrane is recycled
[draw it!!]

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24
Q

What is the axon hillock and what are its main features?

A

It is the last site in the soma where membrane potentials propagated from synaptic inputs are summated before being transmitted to the axon. Adjacency to axon. High density of voltage-gated sodium channels

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25
What are the main two cell types responsible for photoreception in the human retina? How is light sensed? What are dark currents and how do they happen so that in the dark photoreceptors have a membrane potential of -40mV? What type of potential do photoreceptors have?
Rods and cones. Light is primarily sensed by rods. In darkness, photoreceptor cells are depolarized (~-40 mV membrane potential). "Dark current" = continuous influx of Na⁺ and Ca²⁺ through open cGMP-gated channels in the outer segment. The Na⁺/K⁺ ATPase pump in the inner segment maintains ion gradients by pumping Na⁺ out and K⁺ in. This inward "dark current" keeps the cell depolarized, and glutamate is constantly released at synaptic terminals. They have graded potentials
26
How could you distinguish histologically a cardiac muscle fiber from a skeletal one?
Cardiac muscle is branched while skeletal muscle is not. Cardiac muscle has intercalated discs when skeletal muscle does not. Both have striations but they are less noticeable in cardiac muscle due to branching
27
Draw a muscle fiber and its parts
yep drawing
28
Which are the two main domains of the myosin molecule head?
ATP binding site and acting binding site
29
What is the sliding-filament model? How was it discovered?
The sliding-filament model is a model of muscle contraction in which thin (actin) filaments and thick (myosin) filaments slide past each other, thereby shortening the sarcomere. Shortening all of the sarcomeres in a myofibril results in contraction of the entire myofibril. It was discovered by Hugh Huxley and Jean Hanson observing how the light and dark bands in sarcomeres changed when a muscle contracted
30
How is ATP used during muscle contraction and where?
Step 1 - ATP binds to the myosin head, causing a conformational change that releases the head from the actin in the thin filament Step 2 - ATP is hydrolyzed to ADP and inorganic phosphate. The myosin head then pivots and binds to a new actin subunit farther down the thin filament (toward a Z disc). A myosin head bound to actin forms what is known as a cross-bridge. In this position, the myosin head is "cocked" in its high-energy state, ready for the power stroke Step 3 - when inorganic phosphate is released, the head pivots back to its original conformation. This bending, called the power stroke, moves the entire thin filament relative to the thick filament Step 4 - after ADP is released, the myosin head is ready to bind another molecule of ATP
31
Draw the neuromuscular junction and describe how action potentials trigger muscle contraction
Step 1- when an action potential arrives at the end of the motor neuron, it triggers the release of the neurotransmitter acetylcholine (ACh) into the synaptic cleft between the neuron and the muscle cell Step 2 - ACh diffuses across the synaptic cleft and binds to receptors on the plasma membrane of the muscle cell. Binding of ACh opens a ligand-gated ion channel in the receptor protein, resulting in depolarization of the muscle cell. If enough ACh is released by the motor neuron, the depolarization triggers action potentials in the muscle cell Step 3 - the action potentials propagate along the length of the muscle cell and spread into the interior of the cell via invaginations of the plasma membrane called T tubules (T standing for transverse/"extending across) Step 4 - T tubules intersect with extensive sheets of smooth endoplasmic reticulum called the sarcoplasmic reticulum. When an action potential passes down a T tubule and reaches one of these intersections, it causes nearby calcium channels in the sarcoplasmic reticulum to open. Calcium ions diffuse from the sarcoplasmic reticulum through these channels into the cytoplasm, where the sarcomeres are located Step 5 - calcium ions bind to troponin, causing tropomyosin to move and expose the myosin binding sites on the actin filaments. The muscle fiber can now contract :) [draw the neuromuscular junction too!]
32
Which are the main regulatory proteins in muscle cells and how do they regulate contraction?
Tropomyosin and troponin. Together, they work to block the myosin binding sites on actin. When these sites are blocked, the myosin-actin interaction cannot occur, and thick and thin filaments cannot slide past each other (it is only when calcium ions bind to troponin that the complex moves in a way that exposes the myosin binding sites on actin)
33
What is a T-tubule? How does the shape of the T-tubules present in the membrane of muscle fibers relate to the function of these structures?
A T-tubule is any of the membranous tubes that extend into the interior of a skeletal muscle cell, propagating action potentials throughout the cell and triggering the release of calcium ions from the sarcoplasmic reticulum. They ensure Ca2+ release in a uniform manner for coordinated contraction
34
How is calcium compartmentalized inside muscle cells? How costly is this system for the cell?
Calcium is mainly stored in the sarcoplasmic reticulum and it is very energetically expensive to maintain and regulate Ca2+ (using about 25% of total ATP in muscle)
35
How is it possible that a single action potential triggers multiple cross-bridge cycles of myofibrils?
Calcium ions released into the sarcoplasm remain elevated long enough to allow repeated binding of myosin to actin (also maybe because action potentials are identical in magnitude and duration down the entire axon length)
36
You are trying to separate actin myofibrils from myosin myofibrils in the lab. What molecule should be present in your homogenizing solution and why?
ATP, because it is required to break actin-myosin cross-bridges (remember that actin-myosin fuses together when a person dies because there is no more ATP)
37
Why do low calcium levels (hypoclacemia) result in tingling sensation of fingers and toes?
Low calcium means less membrane stability, therefore easier Na+ influx and increased nerve excitability which leads to tingling or twitching (calcium ions normally bind to and stabilize voltage-gated sodium channels in neurons)
38
The release of more Ca2+ from the sarcoplasmic reticulum occurs primarily by activating ryanodine receptors (RyR2) in the adjacent sarcoplasmic reticulum membrane. Explain how a mutation in the gene that encoded RyR2 could lead to heart failure
Ryanodine receptors are responsible for aiding calcium influx from the SR to trigger muscle contraction in cardiac muscle cells. A mutation could make RyR2 unstable or 'leaky', causing abnormal calcium release which leads to weak contractions. This can subsequently lead to cell damage of cardiac muscle cells and later heart failure
39
How can acetylcholinesterase drugs help Alzheimer's patients?
Acetylcholinesterase inhibitors (AChEIs) help Alzheimer's patients by increasing the levels of acetylcholine (ACh) in the brain, which supports memory and cognitive function (acetylcholinesterase normally breaks down acetylcholine, therefore inhibitors will prevent this breakdown and increase its availability at the synapses)
40
How can a muscle cell maximize the speed of its contraction capacity? Give a list of possible physiological adaptations using hummingbirds as an example
High mitochondrial density, fast-twitch (type II) muscle fibers, and small muscle fiber diameter. Hummingbirds have flight muscles which are up to 35% mitochondria by volume. Their flight muscles are composed almost entirely of oxidative fast-twitch fibers. Their flight muscle fibers are relatively thin, helping to optimize excitation-contraction coupling
41
Give two examples of light detection structures in invertebrates
Simple eyes (small cup shaped eye with single lens) and compound eyes (made up of hundreds of thousands of ommatidia, or light sensing columns)
42
What is the main pigment that is able to sense light (photons)? What is it made of? Where is it located in photoreceptors?
Retinal. Made of the aldehyde form of vitamin A. Found in the opsin (transmembrane protein) of rods and cones
43
How is light absorption transduced to changes in membrane potentials?
-all about cGMP which is constitutively high in photoreceptors -when light reaches rhodopsin (in rods), phosphodiesterase is activated -phosphodiesterase cleaves cGMP -decrease in cGMP levels result in closing of cGMP gated channels -this leads to hyperpolarization of sensory neuron
44
What are the two main photoreceptor cell types in the vertebrate retina?
Rods and cones
45
What is the main secondary messenger that photoreceptors use?
cGMP
46
Draw a hair cell and its main parts
yup drawing of hair cell here
47
Name two pressure sensing organs where you can find hair cells
Lateral line system (in fish and amphibians) and the ears of vertebrates ( the cochlea specifically)
48
What is the name of the neurons found in your nose that sense odorants? Where do these neurons project in the brain?
Olfactory neurons. They project to the olfactory bulb which is where olfactory signals are processed and interpreted
49
Who discovered the olfactory receptor gene family?
Linda Buck and Richard Axel
50
Explain, step by step, the events that occur in the lungs and that result in gas exchange between the blood and the tissues
In the lungs, oxygen partial pressure is high in the inhaled air and low in the blood. Since it is coming from circulating around the body and has been deoxygenated. CO2 concentration is high in the blood and low in the inhaled air/atmosphere. This favors the diffusion of CO2 from the blood to the atmosphere. As this happens, the law of mass action will be reversed compared to what happens in the tissues. This means that protons bound to hemoglobin will be released, interact with bicarbonate and form CO2. Oxygen will diffuse across the thin membrane of the alveoli and enter into the red blood cells. In there, oxygen will bind to hemoglobin displacing the H+ bound to hemoglobin. As H+ concentration increases the law of mass action will be catalyzed "leftwards", releasing CO2 that will diffuse to the atmosphere. Overall, when blood leaves the lungs, it has unloaded CO2 and picked up oxygen
51
A neuron is leakier to
K+ than to Na+
52
If a membrane is impermeable to Cl- and Na+ then
Its membrane potential equals the equilibrium potential of potassium
53
What happens to the action potential when a neurotoxin blocks voltage gated K channels?
The depolarization phase is prolonged
54
Explain, step by step, the events that occur in the TISSUES that result in gas exchange between the blood and the tissues
In the tissues, the partial pressure of CO2 is high and the partial pressure of O2 is low as a result of metabolism. The blood comes highly oxygenated from the pulmonary circulation and bound to hemoglobin inside the red blood cells. First, CO2 will diffuse from the tissues across the cell membrane and the capillary membrane into the blood and reach the inside of the red blood cells where carbonic anhydrase will catalyze the formation of bicarbonate anion and H+. As the concentration of H+ increases (pH decreases), the affinity of hemoglobin for oxygen decreases (Bohr shift) and the O2 will be released from the Hb, cross the red blood cell membrane and diffuse to the tissues following partial pressure gradients. The bicarbonate anion gets transported across the RBC membrane (against chloride) and in the plasma it gets transported as H2CO3
55
What is the main difference between the endocrine and neuroendocrine pathways?
neuroendocrine - signal initiated by neuron. neurosecretory cell releases hormones directly into bloodstream. hormones act on distant target issues endocrine - signal is initiated by endocrine gland. hormones are secreted by endocrine cells in response to other hormones or internal signals. hormones travel through blood to affect target cells
56
When does the negative feedback occur?
Negative feedback regulates endocrine, neuroendocrine, AND neuroendocrine-to-endocrine pathways (important to homeostasis)
57
How do steroid hormones affect target cells?
They affect target cells by altering gene expression through a process that begins at the cell membrane and ends in the nucleus hormone diffuses into target cell -> hormone binds to receptor, induces conformational change -> hormone-receptor complex enters nucleus and binds to DNA, induces start of transcription -> many mRNA transcripts are produced, amplifying the signal -> each transcript is translated many times, further amplifying signal
58
Describe the phenomenon known as signal transduction
For-water soluble messengers such as polypeptide and most amino-acid-derived hormones to affect a cell, they must bind to receptors on the cell surface. Because the messenger never enters the target cell, its message must be transduced -- changed into a form that is active inside the cell (usually involves a specific sequence of molecular events called a signal transduction pathway, which may amplify the signal)
59
Describe the role of TSH in amphibian metamorphosis and consequences on target tissues
T3 is the hormone that triggers many of the changes observed in metamorphosis. In response to a signal from the brain, the pituitary gland secretes thyroid-stimulating hormone (TSH). TSH stimulates the thyroid gland to produce T4 and T4 is then converted to the more active T3 at target tissues
60
What hormones are involved in insect metamorphosis? How do they act?
Two hormones, juvenile hormone (JH) and ecdysone. If JH is present at a high concentration in the larva, surges of the hormones ecdysone induce the growth of the larva via molting. But if the JH level is low, ecdysone triggers a complete remodeling of the body -- metamorphosis -- and the transition to adulthood and sexual maturity
61
What is the role of the Mullerian inhibitory hormone?
It plays a significant role in sexual differentiation. It causes regression of the female reproductive ducts (inhibits development of the female reproductive tract)
62
What stimulates the production of melatonin?
Primarily, it is stimulated by darkness (therefore detection of light by photoreceptors reduces melatonin secretion)
63
What is the main hormone involved in flight-or-fight response? How does it affect blood distribution in tissues?
Epinephrine (adrenaline). It redistributes blood to prioritize organs and tissues that are critical for immediate survival (such as skeletal muscles, the heart, and lungs)
64
When and why do we produce insulin?
Blood glucose levels must be maintained within a narrow range of values. When an animal eats, a rising blood glucose level stimulates the release of insulin from the pancreas. Insulin stimulates effector cells throughout the body to import glucose from the blood for storage or use in metabolism, causing the blood glucose level to drop to normal values
65
Describe the Hypothalamic-Pituitary Axis
It is the functional interaction of the hypothalamus and anterior pituitary gland, which are anatomically distinct but work together to regulate most of the other endocrine glands in the body. They communicate indirectly via blood vessels. Hormones produced by other populations of neurosecretory cells in the hypothalamus travel in the blood to the anterior pituitary, where they control the release of pituitary hormones