Essay Questions: Chapter 11, 12, 15 Flashcards Preview

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Flashcards in Essay Questions: Chapter 11, 12, 15 Deck (21)
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Surgically describe HM's procedure. In detail... and why?

Why was it a sucess.

  •  HM had generalized seizures once a week and partial 1-2x a day. Found that seizures occurred from foci in medial portion of Left and Right temporal lobes.
  • A bilateral medial temporal lebectomy was preformed. There was a removal of the medial portions of both temporal lobes including most of the hippocampus, the amgydala and the adjacent cortex.
  • The surgery was a sucess because he was no longer having generalized convulsion and his minor siezures was reduce to one or two per day and his medication was also lowered


Why is HM's Case important to the history of psychology.

  1. Challenged original view that memory was diffusely and equivalently distributed throughout the brain.
  2. . Spawned massive research efforts to clarify the role of medial temporal lobe structures in memory.
  3.  Indicated that Short Term Memory and Long Term Memory have different neuroanatomical substrates.
  4.  Suggests that hippocampus plays a role in memory consolidation.
  5.  First study to distinguish between implicit and explicit memory.



  1. medial temporal lobe amnesia
  2. medial diencephalic amnesia
  3. post traumatic amnesia


  1.  Temporal Lobe amnesia – mnemonic deficits with preserved intellectual functioning and difficulty forming explicit longterm memories while being able to form implicit memories. Is evidence of medial temporal lobe damage (true for all patients)
  2. Medial diencephalic amnesia – Popular in people with Korsakoff syndrome. -This is caused by damage to the Medial Diencephalic. -lesions to this area from consumption of large amounts of alcohol  and thymine deficiency. But it is not because of just damage to one are of the diencephalic.
  3. Post traumatic Amnesia – occurs after traumatic event like a non-penetrating blow to the head leading to a coma. When patient regains consiousness there is a period of confussion.


Temporal lobe amnesia and Medial diencephalic amnesia are perminant damage where as PTA patients once recover they regain their memories



What is:

  1.   Standard Consolidation Theory?
  2. Multi-trace theory?
  3. Reconsolidation theory?


 Standard Consolidation Theory – theory that memories are temporarily stored in the hippocampus until  they can be transferred to a more stable cortical storage system

Multi-trace theory – memories are encoded in a distributed fashion throughout hippocampus and the brain structures for as long as the memories exist, not just during the period after they are learned.

Reconsolidation – once  memory is retrieved from long term storage, it is temporarily held in labile (changeable or unstable) Short Term Memory where it is susceptible to post traumatic amnesia until it is reconsolidated


Describe how the Delayed nonmatching to sample test is conducted.

How has this test been used in monkeys and rats to understand the neural  substrates of object regonition and memory?

Brian reagions that help us form memoeries?




  •  Delayed nonmatching to sample test suggest that when there is a delay participant will take non matching sample not the familiar sample. 
  • There is a sample object with food placed under it. After a delay the sample object is placed infront of the subject along with a new unfamiliar object. The subject must remember the sample object so that he can pick the unfamiliar object.
  • The cortex around the amygdala and the hippocampus are what cause memory loss it was the damage done to the surrounding cortex (rhinal Cortex which is for visual memory)
  • mmonkeys are in a cage rats are in the mummby box
  • the hippocampua alone was damaged and there was not really any deficits they amygdala damage alone showed no deficits. the adjacent cortex alone showed major deficts


Long Term Potentiation:

Why is it imprtant?

How is Glutamate, NMDA receptors, and AMPA receptors are involved in this phenomenon?


  •  A phenomenon that is believe to trigger the formation of new memories. 
  • A word is presented for the first time and seeing it causes the release of glutamate.
  • Some of that glutamate binds to AMPA receptors and slightly depolarizes the cells through the influx of sodium ions.
  • Some of that glutamate binds to NMDA receptors and does nothing because there is a magnesium ion blocking the channel. Then you "learn" the word.
  • You say the word over and over to yourself focusing on the word.
  • By doing this the neurons release large amounts of glutamate, which bind to AMPA receptors and NMDA receptors.
  • Because so much glutamate has been released, the binding to AMPA causes a larger amount of sodium to enter the cell.
  • As the cell becomes more depolarized, the magnesium molecule is dislodged from the NMDA receptor, allowing calcium to enter the cell (because glutamate is already bound to the receptor, but just couldn't activate it because of the magnesium).
  • When calcium enters the cell, it causes a cascade of effects which leads to the generation of new AMPA receptors in the postsynaptic membrane.
  • After learning is all done, once you see the word again and it immediately activates the release of glutamate. However, now there are more AMPA receptors than there were the very first time you saw the word (i.e., before learning).
  • Because there are more AMPA receptors for the glutamate to bind to, the receiving cells become more depolarized.


6 Steps to digestion!

a. Chewing breaks up food and mix with saliva
b. Saliva lubricates food and begins its digestion
c. Swallowing moves food and drink down the esophagus to the stomach
d. Stomach is mainly for storage and all the while, the food is being broken down further by hydrochloric acid.  Pepsin also begins to break down the protein molecules into amino acids.
e. Digestive enzymes in duodenum, many of them from gall badder and pancreas, breaks down protein molecules to amino acids, starch and complex sugars into simple sugars. Simple sugars and amino acids readily pass through the duodenum wall into bloodstream and are carried to liver.
f. Fats are broken down into droplets (emulsified) by bile, which is made in liver and stored in gall bladder until it is released into duodenum.  Emulsified fat cannot pass through duodenum wall and is carried by small ducts in duodenum wall into lymphatic system.
g. Most of remaining water and electrolytes are absorbed from waste in large intestine, and remainder is ejected from anus. 


Three phases of energy metabolism:

what do they do and how do they interact with one another to regulate our metabolic state?

  1.  Cephalic Phase

– Preparatory phase, which is initiated by sight, smell, or expectation of food this phase ends when food starts to absored into the blood stream. 


          2. Absorptive Phase – Nutrients from a meal meeting body’s immediate energy requirements, with the excess being stored

During both phases
---Insulin levels high, Gllcagon levels are low.

-The Insulin-(1)Promotes utilization of blood glucose as a source of energy by the body; (2)conversion of excess glucose to glycogen and fat; (3)conversion of amino acids to proteins; storage of glycogen in liver and muscle, fat in adipose tissue, and protein in muscle

3. Fasting Phase

– Energy being withdrawn from stores to meet body’s immediate needs

-- Glucagon levels high & Insulin levels low

--- Without high levels of insulin glucose can not get into the body. So utilization of glucose is only used for the brain beacuse it doesnt need insulin to get in the brain.

--The conversion of glycogen and protien to glucose

--Free fatty acids are released from adipose tissue to be used as fuel.

--Free fatty acid is converted to ketones


 Compare/Contrast Lipostatic and Leaky Barrel Model


  1.  Lipostatic Theory –Set Point Model; deviation from set point of body fat produces compensatory adjustments in level of eating that return levels of body fat back to set point. 

2. . Leaky Barrel Model – Settling Point Model;
i. amount of water = amount of of avaliable food
ii. water pressure at nozzle = incentive value of available food
iii. amount of water entering barrel = amount of consumed energy
iv. water level in barrel = level of body fat
v. amount of water leaking from barrel = amount of energy being expended
vi. weight of barrel on hose = strength of satiety signal (sense of fullness)

 Compare – both are models for body weight models that attempt to explain the factors that help influence body weight achieve an equilibrium.
Contrast – settling point models are loose explanation for homeostasis regulation and no set point.  Negative Feedback in settling point model merely limits further change in same direction whereas negative feedback in set point model triggers a return to the set point.


 Taste Preference and Taste Aversion


Taste Preference and Taste Aversion – prefer taste that are followed by infusion of calorie and avoid taste that result in illness (daddy and curry chicken). Studies show that rats that are reared together instead of isolation are more likely to learn to eat a healthy diet. (culture affects these two things)

Learning to eat vitamins and minerals – if body is deficient in particular vitamins and minerals like sodium, etc, body will have an immediate preference  for something that has that particular vitamin/mineral in it. 

Rats that have thymine deficiency were giving 2 diets one with thymine and one without it.  Eventually, the rat tailored their diet to the one that contained thymine.  However, when the rats were given 10 diets and only one had thymine, they were less likely to obtain the thymine diet.


Interesting factors that influence why we eat:

Describe four of them

  1.  Satiety Signals – A signal when one is full; depends on volume and nutritive density (calories per unit volume) of the food.
  2. Sham Eating – rat’s esophagus was disconnected from stomach and those rats were fed and the food did not go into stomach BUT eventually the rats did stop eating citing a psychological aspect to eating as well.  Suggest that satiety signals are not need to terminate a meal.
  3. Appetite Effect and Satiety – eating appropriate sized appetizer will make person hungrier because the appetizer activates body to prepare for food.
  4. Social Influence – might eat less if around a group of people ( don’t want to seem fat to others)


   Different long term memories    


Long-term memories

Declative: things you know that you can tell others

-Episodic : remembering your first day of school

- Semantic: knowing the capital of France

Nondeclearative: things you know and can show by doing.

-Skill learning : kowning how to ride a bicycle 

-Priming being more likely to use a word you learned recently

-Conditioning: salivating when you see your favorite food.



Test to examine long-term memory

digit span + 1 test: five digits and then 1 is added after each trial 1 digit is added. Normal subjects can do 25 HM couldnt do 8

Mirrow Drwing Test: Asked to draw a line within the boundries of the star-shaped target, by watching your hand in the mirrow.

Incomplete Picture Test: You are given five fragments og the pictures Set one is terrible and hard to identify and then set five is the complete picture the idea is to see if the subject can guess the picture between every day they should get better.


The historical developement and the state of our current knowledge regarding regarding the neuroanatomy of hunger and satiety.

There was a myth: eating behaviors were thought to be controlled by the different regiond of the hypothalamus. Satiety by the VMH and feeding by the LH . (WRONG!)

 Dual Center Hypothesis – Ventromedial Hypothalamus(VMH)  is considered the satiety center which activates the “full” feeling.  If there is a lesion in the VMH, it results in hyperphagia which is excessive eating and extreme obesity in rats. The obesity in rat began with dynamic phase which is the rapid weight gain.  Once this happens the rat will enter into the static phase in which it maintains the obese bodyweight.  Usually if there is a lesion the Paraventricular Nucleus(PVN) it has been cut with the VMH.  Also, if there is a lesion in JUST the PVN, hyperphagia occurred.
Lateral Hypothalamus is believed to house the Hunger Center which activates the sense of hunger.  A disruptin in the LH can result in no responds of eating and drinking which are Aphagia and Adipsia respectively.  Other areas that are affected are the Amygdala Frontal Cortex and the Substantia Nigra.


Truth is......

Hypothalmus is responsible for regulation of energy metabolism.  the lesion to the VMH caused the animals to overest because they've become over weight not the other way around. They were now over weight because the lesion lead to increase blood insulin levels which increase lipogenesis( the prodcution of body fat)  and a decrease in lipolysis( which is the break down of body fat to use for energy). 


Role of lepin in obesity

The relationship to insulin

he acurate nucleus, nuropeptied Y and the melanocotin system

Fat is released as a peptide hormone call leptin.

Research has shown leptin to be a very important part of obesity. Leptin is released by fat cells and are sent to the hypothalamus where there are leptin receptors. Leptin receptors are mostly found in the arcuate nucleus of the hypothalamus.

Leptin receptor activation suppresses neuropeptide Y, which is associated in initiating hunger and excites the melanocortin system, which plays a role in satiety and is believed to suppress hunger.

Activation of leptin receptors also releases corticotrophin-releasing hormone, which suppresses hunger.

Leptin is believed to be a negative feedback signal regulating body fat by decreasing appetite and increasing fat metabolism.

Insulin is also believed to be a negative feedback signal regulating body fat since receptors are found in the brain, level of insulin in the brain correlates with body fat, and injections of insulin into the brain of lab animals results in weight loss.

Leptin is associated with subcutaneous fat, which is fat beneath the skin. Insulin is associated with visceral fat, which is fat surrounding the organs.

Neuropeptide y= released in the gut and the arcuate nucleus and it is associated with hunger.
Melanocortin system= neurons in the arcuate nucleus that regulate melanocyte-stimulating hormone and in so doing play a role in satiety.


Cross tolerance

Functional tolerance

Metabolic tolerance


how are they important to drug addiction?

Metabloic Tolerance: tolerance that develops because of changes that reduce the amount of durgs getting to the site.

Functional Tolerance: tolerance that reduce the the reactiity of the sites of action to the drug

Cross Torlerance: One drug can produce tolerance to other drug that was not experienced because they act by the same mechanism

*** Impotant because****

Failure to understand this can have tragic consequence to people who believe that because they develop tolerence to a effect of the drug they now believe they are tolerant to the drug


Two ways to demonstrate drug tolerance:

1)Dose of drug curve

2) NO efect!

– state of decreased sensitivity to a drug that develops as a result of exposure to it. Needing more drugs to get same effects; 

Demonstrated in two ways.

1) The dose curve

2) Show that a given drug has less effect now  than it had before exposure



See text for graph


Contigent drug tolerance and conditioned drug tolerance

Contingent Drug Tolerance – demonstration that tolerance develops after a stimulant and not before a stimulant.  Rats were given convulsions before and after administration of alcohol.  Results showed that rats given the convulsion after the injection had almost immune to anticonvulsant effects whereas those that got the injection before were not immune at all.


Conditioned Drug Tolerance – tolerance occurs through a constant, consistent variable that conditions body for drug.  An example: son gave his dad A LOT of painkillers because his father was had been in so much pain over the years and bed ridden.  One day the father begged to go into the living room and was placed there.  The son gave his father the usual dose of pain killers and his father died of OD.  



Neurotransmitter and brain region play role in pleasure and reniforcement


3 evidence to support this

 Neurotransmitter – Dopamine; mescoticolimbic pathway, particularly nucleus accumbens, also hippocamous, prefrontal cortex and amygdala

Animals will self-administer addictive drugs directly into areas of the mesolimbocortical dopamine system but not other brain areas.

Lesions of this system reduce rewarding effects of addictive drugs.

Will see a surplus in dopamine where they self  inject


Drugs Flint spoke about

a. -9-THC (tetrahydrocannibol); Receptor Locations Substantia Nigra, Hippocampus, Cerebellum, Cerebral Cortex.  The Endogenous Ligand is a Anandamide binds to CB1 receptors.  Some of the consequences of Marijuana use are Cognitive Decline, Decline in Respiratory Function, Reduction in Immune Function, and Decrease in Testosterone in Males.

Is Biphasic which means it is a Stimulant/Depressant; Major cause of motor vehicle accidents; Major cause of birth defects; May lead to thiamine deficiency = Korsakoff’s Syndrome Receptors: GABAA Receptor-Coupled Chloride Channels (activates) Dopamine (stimulation at low doses) Increases Binding Cites for Glutamate Opiate Receptors.  Some of the consequences of Alcohol use are cognitive impairments, verbal impairments, motor impairments, hypothermia, korsakoff’s Syndrome, Wernicke’s Encephalopathy, Cirrhosis of liver and Fetal Alcohol Syndrome.

i. Nicotine: Receptors = Nicotinic ACh Receptors; Peripheral Locations of Action: Neuromuscular Junctions and Autonomic Ganglia; Consequences of Smoking: Smoker’s Syndrome, Buerger’s Disease and Second Hand Smoke Accounts for more deaths than the so called “hard” drugs.  Nicotine causes dopamine release in the nucleus accumbens; Reinforcing effects of nicotine appears to be caused by activation of nicotinic receptors in the ventral tegmental area; Insula may be involved in smoking cessation
ii. Cocaine: Potent Dopamine Agonist;
iii. Amphetamine; Potent Dopamine Agonist




 The 5 models of Drug Abuse

a. Moral Model – People that do drugs are morally bad people
b. Disease Model – drug abuse is a life long disease
c. Physical Dependence Theories – Person feels they need the drug
d. Positive Reward Theories – being on the drug makes the person fell really good
e. Incentive-Sensitization Theory – stays on drug so that he/she does not have to deal with the withdrawal side effects