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98 Cards in this Set

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1. What is a zeitgeber? (272, 0) What is the zeitgeber for land dwellers? (272, 0) What happens if the zeitgeber is interrupted or prevented in humans? (lecture)
A zeitgeber is the stimulus that resets the circadian rhythm. Light is the dominant zietgeber for land animals. If a zeitgeber is altered in humans, they do not follow a 24 hour sleep/wake cycle.
2. What happens to normal sleep cycles during jet lag? How can someone adjust to the new cycle with jet lag? What happens to normal sleep cycles when working the midnight shifts? How can someone adjust to working the midnight shift? (page 272; lecture)
Jet lag disrupts the normal sleep cycle (circadian rhythm). If you are traveling west, stay up later and sleep in later (phase delay). If you are traveling east go to bed earlier and wake up earlier (phase advance – harder to do). Third shift people sleep in a dark room during the day and work at night with very bright lights.
3. In the interest of time, we will be skipping most of the section on the stages of sleep.
The only thing I would like you to know is that there are 4 stages of sleep, with the first stage being less sleepy and the fourth stage being a deep sleep. After the fourth stage, REM (rapid eye movement) sleep occurs, during which dreams often occur.
Where is the SCN located and how does this location seem prime for detecting appropriate times to feel tired or awake? (269, 2) How is it controlled? (269, 3) How does this control make it difficult to alter one’s sleep cycle? What gland does the SCN ‘communicate’ with and what hormone is released from this gland? (271, 2; lecture)
The SCN is located just above the optic chiasm. It dictates the circadian rhythms for sleep and temperature; it is genetically controlled – unlearned manner. It is difficult to alter a sleep cycle because the SCN will ultimately regulate the cycle, not the host. The SCN regulates sleeping and waking by controlling the pineal gland which releases melatonin, a hormone that increases sleepiness.
5. What are melatonin pills and at what time of the day should you take them? (271, 3)
Sleeping pills. Take them before bed time. The pineal gland releases melatonin at this time regardless and you will be asleep in 2-3 hours but when the pills are taken during the day - sleep in 2 hours.
6. What does the reticular formation do regarding the cortical arousal? (278, 2)
A cut through the midbrain decreases arousal by damaging the reticular formation, a structure that extends from the medulla into the forebrain. Some neurons in the reticular formation have axons that extend into the brain and some into the spinal cord.
7. What neurotransmitter do locus coeruleus neurons release? How does this impact alertness? (278, 3; lecture)
The locus coeruleus releases norepinephrine. Stimulation to the locus coeruleus strengthens the storage of recent memories and increases wakefulness.
8. What impact does histamine and orexin, when released from neurons in the hypothalamus, on alertness? (278, 5; lecture)
The axons releasing orexin extend widely throughout the forebrain and brainstem, where they stimulate acetylcholine-releasing cells, thereby increasing wakefulness and arousal. Neurons in the hypothalamus also release histamine throughout the brain which sends out excitatory effects.
9. What impact does acetylcholine and GABA have, when released from neurons in the basal forebrain, on alertness? (278, 6; lecture)
Acetylcholine is excitatory and tends to lead to increase arousal, GABA is inhibitory and without it we wouldn’t sleep.
10. What is adenosine and what effect does it have on basal forebrain acetylcholine neurons? (280, 1) What common beverage blocks adenosine receptors? (280, 2)
Adenosine is inhibitory that decreases arousal by inhibiting acetylcholine receptors. Coffee blocks adenosine receptors. Adenosine builds up during the day but has little effect. The accumulated adenosine produces prolonged sleepiness-“sleep debt.”
11. What happens to prostaglandin levels throughout the day and during sleep? What happens to prostaglandin levels during illness? (280, 3)
Prostaglandins are additional chemicals that promote sleep, among other functions. It builds up during the day until it provokes sleep and then decreases once asleep. During an infection the immune system produces more prostaglandins, resulting in the sleepiness that accompanies illness.
• Ambien
Acts like GABA (binds to BZ1 receptor site) in the pons, thalamus, inferior colliculous, substantia nigra and basal ganglia
• Lunesta
Acts at GABA receptors, but company doesn’t disclose precise mechanism
• Rozerem
Agonist at melatonin receptors
13. What is a neuromuscular junction? In skeletal muscles, what neurotransmitter is released from neuromuscular junctions? (232, 7)
A neuromuscular junction is a synapse where a motor neuron axon meets a muscle fiber. In skeletal muscles, every axon releases acetylcholine at the neuromuscular junction and the acetylcholine always excite the muscle to contract.
Primary Motor Cortex
Movement; it has no direct connections to the muscles; its axons extend to the brainstem and spinal cord, which generate the activity patterns that control muscles
Prefrontal Cortex
responds to lights, noises, and other sensory signals that lead to a movement. Damage to this area results in you showering with your clothes on, pouring water on the tube of toothpaste, etcetera.
Premotor Cortex
is active during preparations for a movement and somewhat active during movement itself. It receives information about the target in space, to which the body is directing its movement, as well as information about the current position and posture of the body itself.
Supplementary motor cortex
is important for planning and organizing a rapid sequence of movements, such as pushing, pullin, and then turning a stick in a particular order. Playing sports.
dorsolateral tract
spinal cord is a set of axons from the primary motor cortex, surrounding areas, and the red nucleus, a midbrain area with output mainly to the arm muscles – it controls movements in peripheral areas, such as hands, fingers, and toes
The Ventromedial tract
includes axons from the primary motor cortex, surrounding areas, and also from many other parts of the cortex – this tract controls mainly the muscles of the neck, shoulders, and trunk and therefore such movements as walking, turning, bending, standing up, and sitting down.
What role does the basal ganglia play on these pathways?
The basal ganglia select which movement to make by ceasing to inhibit it – more specifically - the globus pallidus is constantly inhibiting the thalamus, input from the caudate nucleus and putamen tells the globus pallidus which movements to stop inhibiting.
Bradykinesia
Loss of voluntary motor activity.
Rigity
1) even resistance or 2) uneven resistance.
Tremor
Rhythmic involuntary movement of a body part.
What brain region and pathways are damaged in Parkinson’s disease?
Parkinson’s Disease is the gradual death of neurons, especially in the substantia nigra, which sends dopamine-releasing axons to the caudate nucleus and putamen
What is the primary treatment for Parkinson’s disease and what is a serious side effect of this treatment
Levodopa is a drug that is used to treat it but its long term side effect is Dyskinesia-an abnormality in performing voluntary movements
What are the symptoms, pathology, and life expectancy of Huntington’s Disease
Motor sympotoms usually begin with arm jerks and then facial twitches; later, tremors spread to other parts of the body and develop into writhing. Strikes from 30-50 year olds. No treatment is effective at either controlling the symptoms or slowing the disease. Death is certain.
What are the symptoms, pathology, and life expectancy of ALS?
you don't know bitch
19. What are the symptoms and pathology of myasthenia gravis? (234, 2)
Myasthenia gravis is an autoimmune disease, in that the immune system forms antibodies that attack the individuals own body. The immune system attacks the acetylcholine receptors at neuromuscular junctions, causing progressive weakness and rapid fatigue of the skeletal muscles.
20. Note the first sentence of the section called General Principles of Perception.
Each receptor is specialized to absorb one kind of energy and convert it into an electrochemical pattern in the brain.
21. What is the ‘main point’ Kalat discusses
Your brain’s activity does not duplicate the objects that you see; top of visual representation doesn’t have to be at the top of retina or head
23. What is the law of specific nerve energies in modern terms? (152, 7)
Impulses in one neuron indicate light, whereas impulses in another neuron indicate sound. Muller held that whatever excites a particular nerve establishes a special kind of energy unique to that nerve. –Any activity by a particular nerve always conveys the same kind of info to the brain.
What appears to be correct about color detection according to trichomatic
According to the trichomatic theory, we perceive color through the relative rates of response by three kinds of cones, each kind maximally sensitive to a different set of wavelengths.
and opponent-process theory
The opponent process theory is that we perceive color in terms of paired opposites: red vs green, yellow vs. blue, and white vs black.
What do both of these theories fail to account for?
Fail to account for color constancy, which is the ability to recognize the color of an object despite changes in lighting.
What is retinex theory? (161, 7)
The cortex compares info from various parts of the retina to determine the brightness of color for each area.
Parvovellular Neurons
• Smaller cell bodies
• Smaller receptive fields
• Retinal location – in and near fovea
• Color sensitive – yes
• Respond to detailed analysis of stationary objects
Magnocellular Neurons
• Larger cell bodies
• Larger receptive fields
• Retinal location – throughout the retina
• Color sensitive – yes
• Respond to movement and broad outlines of shape
Koniocellular neurons
• Small cell bodies
• Mostly small; variable receptive fields
• Retinal location – throughout the retina
• Color sensitive – some are
• Respond to varied and not yet fully described
After visual input is processed in the primary visual cortex (V1) and then the secondary visual cortex (V2), what are the three pathways that visual input on sent along for even farther processing?
Ventral pathway with mostly parvocellular input – shape detail
Ventral pathway mixed magnocellular/parvocellular path- color and brightness
Mostly magnocellular path- movement and perception
-Simple Cells-Primary Visual cortex (V1)
-Has fixed excitatory and inhibitory zones, like edges or lines-must have specific orientation (horizontal or vertical) and be in fixed position in field.
-Doesn’t move around a lot and in a very small field
-Complex Cells: in areas V1 and V2
-Responds to a pattern of light-must have specific orientation-can be anywhere in field.
-Hyper Complex-book calls end-stop cells
-Similar to complex, but will not be stimulated if pattern moves beyond certain zones within field. LARGEST field.
28. What are sound waves?
Sound waves are periodic compressions of air, water, or other media.
-Human hearing range: 15-20,000 Hz
29. Define amplitude and frequency. What is the perception of amplitude or frequency called?
-Amplitude: Intensity (measured in decibels)
-Loudness: perception of intensity
-Frequency: number of compressions per second (measured in hertz) (Hz)
-Pitch: perception of frequency
30. The three major division of the ear are the outer, middle and inner ear. In the outer ear, what is the pinna and what function does the pinna serve?
Pinna – external auditory canal
Alters reflections of sound waves, allowing us to pinpoint source
 Sounds waves pass through-to ear drum (tympanic membrane)
what are the tiny bones called that the tympanic membrane is attached to
Malleus (hammer)
Incus (anvil)
Stapes (stirrup)
What is the oval window and where is it located?
- Inner ear
-Oval window
-Connected to malleus, incus, stapes
-Vibrations more forceful here
Where is the tympanic membrane(eardrum)?
Middle ear
What is the cochlea and what is it filled with? What are the auditory receptors called? What is the function of the tympanic membrane?
• Cochlea
o Small shaped structure
o Consists of three fluid-filled tunnels
 Scala vestibule
 Scala media
 Scala tympani

When sound waves strike the tympanic membrane (eardrum), they cause it to vibrate the 3 bones which in turn convert the sound waves into stronger vibrations in the fluid filled cochlea- it is necessary to convert sound waves into waves of greater pressure
• Hair cells
o Auditory receptors
o In cochlea
o Between the hard basilar membrane and the more flexible tectorial membrane
o Respond to vibrating fluid between these two membranes
• Frequency theory
the basilar membrane vibrates in synchrony with a sound, causing auditory nerve axons to produce action potentials at the same frequency.
o Rate of action potentials = frequency of sound
o Only true for low-frequencies (up to 100 Hz)
• Place theory
the basilar membrane resembles the strins of a piano in that each area along the membrane is tuned to a specific frequency
o Different areas along the basilar membrane vibrate in response to different frequencies
o True for frequencies between 4-5,000 Hz up to 20,000 Hz
• Volley Mechanism (principle) ) of pitch discrimination
the auditory nerve as a whole can have volleys of impulses up to about 4000 per sec, even though no individual axon approaches that frequency by itself.
o Nerve impulse phase locked with number of waves per second (one impulse may have 4 waves, instead of one impulse per 1 wave)
o The auditory nerve can have “volleys” of impulses up to about 5,000 Hz based on the sum of the nerve impulses
o Used for frequencies below 4000 Hz (common noises, human speech)
34. In what lobe is the primary auditory cortex located?
Superior temporal cortex
Through which colliculus does auditory information travel on the way to the auditory cortex? (Fig. 7.5, page 200).
Inferior colliculus
Note that information then travels through the medial geniculate nucleus of the thalamus.
35. There are three methods (or cues) that we use to determine the location of sounds. What are these methods and how (basically) do they work? (202, 5 – 203, 2)
• Three cues can be used: (consciously or unconsciously)
o Time of arrival - Difference in intensity (loudness) between each ear-(most common)-localize high frequencies
o Sound Shadow- Difference in the time of arrival at each ear (louder at closest ear)
o Phase difference between the ears: see fig. 7.8 pg 203 - reaches ears in different phases of the wave-localize low frequencies
• Conductive Deafness (middle ear)
o Bones of the middle ear do not transmit sound waves properly
o Causes include diseases, infections, tumors, etc.
• Nerve deafness (middle ear)
o Damage to cochlea, hair cells or auditory nerve (use of cochlear implants to “fix”)
o Causes include German measles and other diseases during pregnancy, lack of oxygen at birth, multiple sclerosis, reaction to aspirin (children), and repeated exposes to loud noises
• Tinnitus
o Constant ringing in the ears
o Found with nerve deafness “like phantom limb syndrome”
37. What are mechanical senses?
Mechanical senses respond to pressure, bending, or other distortions of a receptor. They include touch, pain, and other body sensations, as well as vestibular sensation, a system that detects the position and movement of the head. Audition is a mechanical sense also because the hair cells are modified touch receptors; we considered it separately because of its complexity and great importance to humans.
38. What is the vestibular sense and what structure facilitate this sense?
• Vestibular sense
o Detects the direction of tilt and the amount of acceleration of the head (balance)
• Structures include
o The semicircular canals (fluid filled with hair cells)
o Two otolith organs (the saccule and utricle)
39. What is somatosensation?
• Sensations from the body and its movement
o Includes discriminative touch, deep pressure, cold, warmth, pain, tickle and the position and movement of the joints (kinesthetic)
40. What is a dermatome?
A dermatome is the skin area connected to a single sensory spinal nerve
Pain. The receptors for pain are relatively non-specialized (i.e. a bare nerve ending) and is located close to the surface of the skin. Why is pain information carried relatively slowly?
Because the axons carrying pain information have little or no myelin
Does it make a difference in speed if the pain is sharp or dull?
The thicker faster axons convey sharp pain; the thinnest ones convey duller pain (such as postsurgical pain)
Pain in the spinal cord. What neurotransmitters are released in the spinal cord in response to mild or strong pain?
Mild pain releases glutamate
Stronger pain releases both glutamate and substance P
43. Where is the detection of pain processed?
pathway from spinal cord to somatosensory cortex in the parietal lobe
Where is the response to pain processed?
Emotional response: reticular formation of the medulla to several of the central nuclei of the thalamus, the amygdala, hippocampus, prefrontal cortex, and cingulated cortex
44. How are opiates and endorphins similar?
They are both released to inhibit further pain “put the brakes on pain”
Where are these chemical receptors located and how do they decrease pain?
Mostly in the spinal cord and the periaqueductal gray area of the midbrain
Decrease pain by blocking the release of substance P
What is gate theory?
According to the gate theory, spinal neurons that receive messages from pain receptors also receive input from touch receptors and from axons descending from the brain. These other inputs can close the “gates” for the pain messages
45. What is the insula known as?
Primary Taste Cortex, located in the cerebral cortex
A bad taste will be processed in this region and may result in facial response that we call disgust. Interestingly, feelings of disgust (e.g., after watching a violent story on the news) also produce activity in the insula.
Where is the olfactory bulb located relatively to the nasal passage? What is unique about olfactory cell dendrites? (Figure 7.21, page 221) About how many olfactory receptors do humans have? (222, 3)
Receptors in the olfactory epithelium in rear of nasal passages
Receptors replaced every 30 days or so
Several hundred different olfactory receptor proteins (as compared to 3 types of cones)
Only sensory system that doesn’t go thru thalamus first
47. What area(s) of the hypothalamus monitors and regulates body temperature? (300, 1) What are the two ways in which this area monitors body temperature? (300, 2 & 3)
The most critical areas for temperature control are the anterior hypothalamus and the preoptic area, which is just anterior to the anterior hypothalamus.
Two ways this area monitors body temp. 1. by monitoring its own temperature – when an experimenter heats it, the animal gets hot; when he cools it…etc. 2. There are also cells of the area that receive input from temperature sensitive receptors in the skin and spinal cord. The animal will shiver most vigorously when both are chilled. If damaged, can’t be controlled. The animal will just search for comfortable environment.
48. By what mechanism does infection initiate fever? (301, 0)
Once the body has release leukocytes, the leukocytes release small proteins called cytokines that attack the intruders and also communicate with the brain, ultimately sending a signal to the hypothalamus to initiate a fever.
What is vasopresson also known as and what does it do? (303, 3)
Vasopressin is a hormone raising blood pressure by constricting the blood vessels and is also know as antidiuretic hormone (ADH) because it enablesthe kidneys to reabsorb water fro urine and therefore make the urine more concentrated.
50. How are high salt levels detected? (304, 1) What part of the hypothalamus receives this information and what does the hypothalamus do in response to high salt levels in the blood? (304, 2)
The areas important for detecting osmotic pressure and the salt content of the blood include the OVLT (organum vasculosum laminae terminalis) and the subfornical organ (SFO). OVLT, the SFO and stomach relay their information to several parts of the hypothalamus, including the supraoptic nucleus and the paraventricular nucleus (PVN), which controls the rate at which the posterior pituitary releases vasopressin.
51. What is conditioned taste aversion? (308, 5)
If you try something new and then become ill, even hours later, your brain blames the illness on the food, and it won’t taste good to you the next time = the phenomenon know as conditioned taste aversion.
52. It turns out that hunger is a complicated topic. I will focus most on the brain mechanisms of hunger for this course. To begin with, paraphrase/summarize the paragraph about glucose on page 310, paragraph 6. (310, 6)
For the most part, glucose (body fuel) is released into the blood stream thanks to digested food. When the body fuel is high, the liver cells convert some of it into glycogen, and fat cells convert that into fat. When the glucose levels start to fall the process reverses to make more body fuel so the levels stay fairly steady for most people.
53. What are the two important pancreatic hormones that regulate glucose levels and how do they regulate glucose levels? (310, 7 & 8) What happens to glucose in diabetes? (311, 1)
Insulin enables glucose to enter the cells – insulin levels rise as someone is getting ready for a meal, the insulin lets some of the blood glucose enter the cells in preparation for the rush of additional glucose to enter the blood. Glucagon stimulates the liver to convert some of its stored glycogen to glucose to replenish low supplies in the blood. Glucose may be three times the normal level in diabetes. (The insulin level remains constantly low)
What is leptin (312, 2) and how does leptin influence hunger? (312, 3) What are the levels of leptin in people who are overweight? (312, 6) What well-known drug of abuse decreases leptin levels? (lecture)
The body’s fat cells produce leptin (appetite suppressing): the more fat cells, the more leptin. Leptin signals the brain about the body’s fat reserves – a long-term indicator of whether to increase or decrease eating. Researchers soon discovered that almost all overweight people already have high levels of leptin. Low levels of leptin increase hunger, but high levels do not necessarily decrease it, at least not for everyone. Cannabis. (hahaha….he say’s cannabis)
55. What symptoms occur as a result of damage to the lateral hypothalamus? (314, 5) What are the stages of recovery for a damaged lateral hypothalamus? (figure 10.21, page 315) What effect does stimulation of the paraventricular nucleus have on the lateral hypothalamus, and ultimately food intake? (313, 5) What happens as a result of damage to the paraventricular nucleus? (313, 5)
An animal with damage in this area refuses food and water, averting its head as if the food were distasteful. The animal may starve to death unless it is force fed, but if kep alive, it gradually recovers much of its ability to eat.
1. Aphagia and adipsia
rat refuses food and drink, must be force fed
2. Anorexia
rat eats a small amount of palatable foods and drinks sweetened water. It still does not eat enough to stay alive.
3. adipsia
the rat eats enough to stay alive, though at a lower-than-normal body weight. It still refuses plain water.
4. Near recovery
the rat eats enough to stay alive, drinks plain water only to wash down food, if subjected to stressful conditions it will refuse water and food again.
56. What happens if damage selectively occurs to the ventromedial hypothalamus? (315, 2)
A large lesion centered on the ventromedial hypothalamus (VMH) leads to overeating and weight gain.
57. How do steroid hormones exert their effects? (326, 2)
First, they bind to membrane receptors, like neurotransmitters. Second, they enter cells and activate certain kinds of proteins in the cytoplasm. Third, they bind to chromosomes where they activate or inactivate specific genes.
58. What are the two categories of sex hormones and under which categories do testosterone and estradiol fall under? Which categories are considered male and female hormones? (326, 3)
Androgens, a group that includes testosterone and several others, as “male hormones” because men have higher levels. The estrogens, which include estradiol and others are “female hormones” because their levels are higher in women. Progesterone, another predominately female hormone, prepares the uterus for the implantation of a fertilized ovum and promotes the maintenance of pregnancy.
59. Where in the brain do sex hormones act on? Where is the sexually dimorphic nucleus and what is the relative size between males and females? (329, 1)
One area in the anterior hypothalamus, known as the sexually dimorphic nucleus, is larger in the male than in the female and contributes to control of male sexual behavior.
60. List some of the other differences in the brain between males and females that are discussed in 329, 5. What influences this development?
Men tend to have more white matter than women. Women on the average have a greater density of neurons on part of the temporal lobe that is important for language. The language-related areas are larger in the left than right hemisphere for both sexes, but that difference is usually larger in men than women.
rodents
– You can take a rats nuts, but you can’t take away its sex drive.
cats, dogs
– Dogs/Cats
• Males can maintain a decreased level of sexual behavior for several years
• Females cease sexual behavior entirely after removal of ovaries
humans
– Humans are less dependent on current sex hormone levels than other species; Hormonal changes can increase or decrease people’s sexual arousal.
non-human primates
– Nonhuman Primates: less dependent that dogs and cats on sex hormones
63. How does Viagra work? (332, 2)
Viagra increases male sexual ability by prolonging the effects of nitric oxide (nitric oxide facilitates the hypothalamic neurons important for sexual behavior and increases blood flow to the penis.
64. What may happen if testosterone levels are too low in males or too high in females?
A genetic male who has low testosterone may develop a female or intermediate appearance. A genetic female who is exposed to more testosterone than the average female can be partly masculinized.
65. What is the condition known as ‘androgen insensitivity’? (343, 2)
Individuals with an XY chromosome pattern have the genital appearance of a female…this condition is known as androgen insensitivity, or testicular feminization. Although such individuals poroduce normal amounts of androgens (including testosterone), they lack the androgen receptor that enables it to activate genes in a cell’s nucleus.