Final Exam Flashcards
What are the two types of energy reservoirs?
Short-term and long-term
What is a short-term energy reservoir?
involves the liver and muscles; the small amount of energy that is stored from food consumption in the form of glycogen.
What is a long-term energy reservoir?
- involves adipose tissue
- it is the most efficient form of energy
- it is made up of fats
What is the difference between saturated and unsaturated fats?
saturated fats are usually solid at room temperature and can be good in moderation, whereas unsaturated fats are liquid and the omega 3 varieties are good but not the omega 6s
When we store fat, do the number of fat cells increase or does the size of the fat cells increase?
the size
What are the 3 pathways of energy storage and mobilization?
- hormone release from the pancreas
- insulin is released to store glucose and glucagon is released to mobilize glucose - Adrenal gland activity
- glucocorticoids release glucose from storage when adrenal gland is active - Neuronal activation of fat tissue
- the brain can tell fat cells to release fat tissue or it can also reduce communication with fat cells
What part of the body uses 20% of the body glucose levels?
the brain
If you were in a fasting state, how would your body use glucose?
your body will spare glucose to be used in the brain, your liver, muscles, etc. wouldn’t be able to take in excess glucose without insulin
What are the two phases of metabolism?
Absorptive and Fasting
What happens in the absorptive phase of metabolism?
you eat, the food is separated into glucose, fats, and amino acids. Glucose is distributed throughout the body, fats are stored directly into fat cells, and amino acids are delivered to the muscles and fat cells.
what happens in the fasting phase of metabolism?
liver releases short term energy, but without insulin the energy is transported to the brain. Triglycerides or fat cells release fat tissue. Over prolonged fasting catabolism occurs where muscles break down due the lack of nutrients
what is the difference between ketosis and ketoacidosis?
Ketosis occurs when the body doesn’t have enough glycogen, whereas ketoacidosis occurs in undiagnosed Type 1 diabetics. They will eat and drink a lot, pee a lot but gain no weight. Ketones will be the body’s primary source of energy, but they are highly acidic and it has major side effects.
What are the factors involved in hunger and satiety?
Gastric (stomach) factors, Adipose (fat), Intestinal factors, Liver factors, and Pancreas factors
What are the gastric factors of satiety and hunger?
the stomach conveys satiety by sensing nutrients and the stretching of the stomach.
It conveys hunger by releasing the “hunger hormone” ghrelin
What is the hunger hormone in the stomach?
Ghrelin
What are the Adipose (fat) factors of satiety?
Adipose will release leptin (a satiety hormone) to the brain and other areas to convey satiety.
What is the largest endocrine gland?
Adipose
What is the difference between an Ob and Db mouse?
An Ob mouse has the omission or absence of leptin (no leptin to work with)
A Db mouse has a damaged leptin receptor (has leptin but doesn’t respond to it)
What are the intestinal factors of satiety?
The upper intestine will release the CCK hormone to convey satiety by inhibiting the emptying of the stomach. Peptide YY (PYY) is also released from the small intestine
What would happen if we injected animals with the satiety hormone CCK?
the animal would decrease or stop its eating behavior
What are the liver factors of satiety?
Liver monitors the levels of glucose and lipids, telling the brain to slow down the eating behavior
What are the pancreas factors of satiety and hunger?
The pancreas monitors the insulin and glucagon production to determine if food is needed or not
Is insulin a hunger or satiety hormone?
BOTH!
Why should we be cautious of artificial sweeteners?
sweeteners indicate to the brain that we are taking in glucose, but there is no calories coming in so the body cannot store anything with the insulin it has released
How does the area postrema affect hunger?
it senses toxicity in the blood and activates vomiting or gagging behavior in response to these toxins
What would happen if we lesioned the ventromedial hypothalamus (VMH)?
no “stop” signal would be activated, causing the inability to stop eating and extreme obesity
What would happen if we lesioned or stimulated the lateral hypothalamus (LH)?
if lesioned: no “start” signal would be activated, the animal would experience extreme weight loss because they wouldn’t eat.
if stimulated: the rat would start eating and continue until the stimulus stops
What are the two hormones of the lateral hypothalamus?
Melanin Concentrating Hormone (MCH) and Orexin
Orexin is also involved in wakefulness
If we increased MCH and Orexin would hunger increase or decrease?
increase
what are the two types of orexegins?
MCH and Orexin
What brain areas are involved in hunger and satiety?
Cerebral cortex, thalamus, PAG, RF, and locus coeruleus
What are the two excitatory neurotransmitters in the arcuate nucleus?
NPY (hunger stimulating) and AGRP (agouti related)
What would an orexin agonist do?
stimulate hunger or eating behavior
What do endocannabanoids do?
they facilitate the release of MCH and orexin
What does the PVN do?
it regulates complex metabolic processes
What are the two inhibitory neurotransmitters in the arcuate nucleus?
CART and a-MSH
What is the three pronged approach of leptin?
- it excites CART/a-MSH (the satiety/inhibitory molecules)
- it inhibits NPY/AGRP (hunger molecules/ ravenous eating)
- it inhibits the PVN (which controls complex metabolic processes)
What hormone does adipose tissue release?
leptin
Does leptin stimulate hunger or satiety?
satiety
what is the hormone released from the stomach?
ghrelin
Does ghrelin stimulate hunger or satiety?
hunger
What is the difference between Type I and Type II diabetes?
Type I diabetes is early onset; caused by the lack of insulin production
Type II diabetes starts later in life and is caused by the resistance to insulin and rapid fluctuating glucose levels
How can we treat people with Type II diabetes?
glucose lowering medication or exercising to reset insulin receptors
What is the animal model for anorexia?
Activity based anorexia (ABA) where they offered the animal the ability to exercise on a running wheel. The food was restricted from both the control group and the experiment group. The control group just waited for the food to be administered again, they had a decrease in weight but eventually plateaued. Experiment group exercised, didn’t eat, and lost an extreme amount of weight.
What are the possible explanations for the ABA animal model?
Exercise decreases hunger
Exercise increases rewarding feelings by increasing beta-endorphins in the CNS
Food restriction enhances reinforcing effects
What is Hebb’s rule?
if a synapse repeatedly becomes active at the same time a post synaptic neuron fires, their connection will become stronger
What did the snail video explore?
giant sea snails were given shocks to teach a fear response, and they had a very large neuronal circuit which made them easier to study. We found that you could pair an UCS with the CS to create the same response (similar to classical conditioning)
What are the 3 areas of the hippocampal formation?
hippocampus, dentae gyrus, and subiculum cortex
What is Long-term Potentiation (LTP)?
Picture the weird seahorse diagram:
if A is stimulated B will respond, but over a long period of time the response of B is stronger
If strong stimulus is given between C and D and a weaker stimulus is given to C at the same time, after LTP we should see a strong response between the weak stimulus and D
What receptor is involved in the development of LTP?
AMPA
What are the two requirements for LTP to occur?
1) a weak neuron firing
2) membrane D is already depolarized
What are the two ways that depolarization occurs?
1) Local depolarization (weak stimulus anywhere on the neuron while strong stimulus occurs in the terminal)
2) Dendritic spike (neuron fires and causes weaker synapse’s to fire gun kickback)
What neurotransmitter binds to the AMPA receptor?
ionotropic receptors that allow Na+ into the neuron
What neurotransmitter binds to the NMDA receptor?
ionotropic receptors that allow entry of Na+ and Ca 2+
What is blocking the NMDA receptor?
Magnesium
How is magnesium removed from the NMDA receptor?
Depolarization of the receptor
When the NMDA neurotransmitter is dependent and depolarized, what ions flow into the cell?
Sodium and Calcium
What are the 3 overall categories of changes following protein kinase activation?
Insertion of new AMPA receptors
Thicker dendritic spines
New growth of spines/synapses
What are knockout mice?
mice that are genetically altered by inactivating one gene
What are transgenic mice?
mice that are genetically altered with a new active gene coding
What is the Morris Water Maze?
an animal model that forces rats to swim until they find a clear platform under the water to rest on
What is propranolol?
A beta-blocker originally used to treat high blood pressure, propranolol can be used to target memories and lessen their impact on people with PTSD, etc.
What are the two administration styles of propranolol?
The first was suggested that propranolol be administered immediately following the traumatic event. This was problematic because it wouldn’t be until several hours after the event, and after the adrenaline had dissipated that propranolol would be administered.
The second suggestion would be to administer it after a therapy session that would trigger the memories of the traumatic event. Then the drug would be administered. Pairing it with the memory will allow for the propranolol to target a more specific memory and be more effective.
What is PKMzeta?
an enzyme that activates other proteins by attaching a phosphate group to them
If a fear conditioned rat was given ZIP, what would happen?
It would forget the fear conditioning all together
Why is ZIP not effective in “erasing” human memories?
because it cannot target one specific memory, it just destroys all brain connections
What could we use to enhance/improve memory?
Acetylcholinesterase inhibitors (doesn’t allow the breakdown of ACh, increasing focus and wakefulness)
AMPAkines
Off-label drug use
Altering protein kinases
What are the differences between major depressive disorder and bipolar disorder?
MDD shows persistent sad moods and it has high prevalence (most common disorder)
BD is characterized by its mania and depressive behavior (depressive behavior lasts longer). It is not as common as MDD but it has a much higher suicide rate
What are the current non-drug treatments for depression?
Ventral stimulation (sending electrical pulses to the brain through the vagus nerve) Transcranial Magnetic Stimulation through the PFC (working towards deeper brain stimulation) Light therapy (using different wavelengths of light to increase happiness)
What type of drugs are in the first generation of antidepressants?
Monoamine oxidase inhibitors (MAO inhibitors defined by their activity like ketamine, MAO-A, etc. **restricts diet**) Tricyclic antidepressants (defined by structure, block the reuptake of serotonin, norepinephrine, and dopamine; causes sleepiness and can lead to suicide)
How were MAO inhibitors discovered?
used to treat tuberculosis, patients were claimed to be inappropriately happy, which were the euphoric effects of ketamine (etc)
What are the characteristics of the second generation of antidepressants?
they are atypical antidepressants that are defined by their activity. They were initially found by modifying tricyclic structure. Bupropion or Zyban is an example
What does SSRI stand for?
Selective serotonin reuptake inhibitor
What is the third generation of antidepressants?
SSRIs
What can happen if you administer too many SSRIs?
it can lead to serotonin syndrome (where there is a build up of too many serotonin cells; can lead to flu like symptoms)
Can also lead to serotonin withdrawl (which can cause nausea, dizziness, sleep disturbances, etc.)
What is an “off-label” drug?
not using a drug for its intended purpose
how is esketamine administered?
through a nasal spray (snorted)
Why is serotonin not the answer to “curing” depression?
because antidepressants are desensitizing presynaptic 5HT auto-receptors (which assumes they were already sensitized)
Serotonin can be affected by genetics (short vs long alleles
Complex intracellular effects
What drug is most commonly used to treat bipolar disorder?
Lithium
Why do we use anticonvulsants to treat mania?
because mania is predicted to be caused by brain convulsions
What is St. Johns Wort for? and why is it not the best for treatment?
it is a neurotransmitter re-uptake blocker and it can be effective in treating mild cases of depression
What is DHEA? Why was it not the most effective supplement?
it was promoted for too many issues and we didn’t know its true mechanism; also has undesirable symptoms
What is SAMe? and why is it not the most effective supplement?
it is located in all cells and was originally promoted to elevate mood; it is problematic because when it was tested it was administered intravenously but now its being sold in pill form.
