Psych 202 #3

145 flashcardsby Maya
Study these flashcardsFree · spaced repetition · iPhone, Android, Mac & web

All cards

1
Explain Otto Loewi's experiment
His experiment discovered the first neurotransmitter, he electrically stimulated a frog's vagus nerve to slow its heart rate and, by collecting the fluid around the heart and applying it to another frog's heart, realized that the cause of the heart rate slowing down had been chemical rather than electrical.
2
These ligands come from within the body
Endogenous
3
These ligands come from outside the body (eg drugs)
Exogenous
4
This is when a neuron can make or release more than 1 type of transmitter.
Co-localization of transmitter
5
This neurotransmitter is the most common, and the most important excitatory neurotransmitter, it is especially important for learning and memory and is sent to/from everywhere. Oversupply of this neurotransmitter may lead to migraines or seizures.
Glutamate
6
This is the major inhibitory neurotransmitter, it is sent to/from everywhere. Undersupply of this neurotransmitter is linked to seizures, tremors, and insomnia.
GABA
7
This neurotransmitter is sent from the basal forebrain and is crucial for learning, memory, motor control, and parasympathetic activity. When the neurons producing this transmitter deteriorate, it can lead to Alzheimer's.
Acetylcholine
8
This neurotransmitter is sent from the midbrain (ventral tegmental area and substantia nigra). It influences reward, learning, attention, movement, and emotion. Oversupply of this is linked to schizoprenia, while undersupply is linked to Parkinson's.
Dopamine
9
This neurotransmitter is sent from the raphe nuclei in the midbrain. It participates in mood, vision, hunger, anxiety, sexual behavior, sleep, and arousal. Undersupply of this is linked to depression.
Serotonin
10
This neurotransmitter is sent from the locus coeruleus and lateral tegmental area. It controls alertness, mood, and sexual behavior. Undersupply can lead to a depressed mood.
Norepinephrine
11
This neurotransmitter is sent from everywhere, and influences perception of pain, thrill, sexual behavior, hunger, and maternal care. Oversupply via opiate drugs can suppress critical functions like heart rate and breathing.
Opioid peptides/endorphins
12
Specialized proteins that help with reuptake by binding to a neurotransmitter and bringing them back to the presynaptic terminal to be recycled.
Transporters
13
When enzymes break down neurotransmitters to deactivate them.
Degradation
14
Receptors that open or close an ion channel when bound to a neurotransmitter (ligand-gated)
Ionotropic receptors
15
Receptors that provide a link to G-proteins in the postsynaptic neuron, which changes the postsynaptic cell due to second messengers activated by the G-proteins.
Metabotropic receptors
16
Criteria for classical neurotransmitters
They can be synthesized by presynaptic neurons and stored in axon transmitters, released when action potentials reach terminals, recognized by specific receptors in the postsynaptic membrane, and blocking its release can interfere with the presynaptic cell's ability to impact the postsynaptic cell.
17
Transmitters that can diffuse across the synapse back to the presynaptic neuron, causing changes in the presynaptic neuron.
Retrograde transmitters
18
Exogenous substances that compete with endogenous ligands for the same binding sites.
Competitive substances
19
Exogenous substances that bind to a different site as the endogenous ligands.
Noncompetitive substances
20
An exogenous substance that can weakly activate a receptor.
Partial agonist
21
Any substance that binds to a receptor
Ligand
22
The amount of drug in the body that is free to act on the target tissue, as opposed to being used elsewhere or in the process of being eliminated.
Bioavailability
23
When the metabolites of drugs themselves are active, the drug itself can be biologically modified into a different substance.
Biotransformation
24
Drugs usually bind strongly to certain receptor types and weakly to others, what is this called?
Binding affinity
25
The extent to which a drug molecule affects a receptor it is bound to.
Efficacy
26
This curve is used to describe how dangerous a drug is. It typically includes two sigmoidal shapes, one representing how much dose is required to get the maximal effect, and another representing what percentage of test subjects die at certain doses.
Dose-response curve
27
On a dose response curve, the difference between the dose where 50% of test subjects die and the dose where 50% of the maximal effect is achieved.
Therapeutic index
28
This system in the brain makes designing drugs difficult, as it requires drug molecules be small to get in the brain.
Blood-brain barrier
29
This route of drug administration is typically slow to moderate, and the drug is affected by gut absorption and digestive factors.
Ingestion
30
This route of drug administration is typically moderate to fast, taking advantage of nose/lungs vascularization to bring drugs directly to the bloodstream. It involves techniques such as smoking or snorting.
Inhalation
31
This route of drug administration is typically moderate to fast, as the drug is injected directly into the body.
Peripheral injection
32
This route of drug administration is typically the fastest, as it circumvents the blood-brain barrier, rules out peripheral effects, and directly affects a discrete brain location.
Central injection
33
When the body/metabolic organs become more effective at removing a certain drug from the bloodstream.
Metabolic tolerance
34
When the target tissue changes its sensitivity to the drug through postsynaptic neurons up/downregulating their receptors.
Functional tolerance
35
When tolerance to a drug generalizes to tolerance to other drugs of the same chemical class.
Cross-tolerance
36
Stages of transmitter production that can be affected by drugs
Inhibiting the enzyme required to synthesize a transmitter, blocking axonal transport of materials to make a transmitter, or preventing the storage of a transmitter.
37
Stages of transmitter release that can be affected by drugs
Blocking action potentials, shutting down synaptic transmission, blocking calcium channels, modifying systems used to regulate transmitter release,
38
Stages of transmitter clearance that can be affected by drugs
Inhibiting reuptake, blocking enzymes that cause degradation
39
These are drugs that block dopamine receptors.
Neuroleptics/antipsychotics
40
These drugs block reuptake of serotonin, they are used to treat depression.
SSRIs/selective serotonin reuptake inhibitors
41
These drugs block reuptake of both serotonin and norepinephrine, they are used as antidepressants.
SNRIs, tricyclics
42
An enzyme that breaks down monoamine transmitters (serotonin, norepinephrine, dopamine, epinephrine).
Monoamine oxidase
43
Antidepressants that block monoamine oxidase.
MAOIs (monoamine oxidase inhibitors)
44
A class of drugs that inhibits neural activity using GABA receptors.
Depressants
45
An depressant that can be used to help treat narcolepsy, but also has high potential for abuse. It is a direct GABA_B receptor agonist.
GHB
46
Depressants that are noncompetitive GABA_A receptor agonists.
Barbiturates
47
Depressant drugs that can be used to treat anxiety.
Anxiolytics
48
This class of anxiolytic is used to treat anxiety and can also help with REM behavior disorder, seizures, relaxation and sleep, it is a noncompetitive GABA_A receptor agonist. Some examples of this are Xanax and Ativam.
Benzodiazepines
49
The most commonly used depressant drug, this is a direct GABA_B receptor agonist.
Alcohol
50
These drugs reduce pain sensations, especially in the periaqueductal gray, these can be fatal if one gets addicted, examples are OxyContin and fentanyl.
Opioids
51
Painkilling drugs.
Analgesics
52
An active ingredient in cannabis that is responsible for producing a high.
THC
53
An active ingredient in cannabis that has anxiolytic effects and other medicinal actions.
CBD
54
Effects of cannabis/endocannabinoids
Elevated mood, pain relief, lowered blood pressure, relief from nausea, improvements in the eye disease glaucoma
55
A stimulant that activates Ach receptors, it increases heart rate, blood pressure, digestive action, and alertness, can hurt the physiology/cognitive development of babies if used by pregnant women, can enhance some aspects of cognitive performance, but is addictive. It is most commonly consumed in cigarettes.
Nicotine
56
A stimulant that boosts the effects of monoamine transmitters like dopamine and norepinephrine by blocking their reuptakes. Overuse of this drug may lead to stroke, psychosis, loss of gray matter in the frontal lobe, severe mood disturbances, and can change the structure and function of brain parts to make quitting even harder. It was originally found in the coca plant from Bolivia.
Cocaine
57
A stimulant that acts within axon terminals so an especially large amount of dopamine/norepinephrine is released into synapses. It also blocks reuptake and metabolic breakdown of these transmitters. In the short term it can lead to increased vigor, stamina, wakefulness, euphoria, and decreased appetite. Addiction to it can lead to sleeplessness, severe weight loss, deterioration of mental/physical condition, and schizoprenia-like symptoms. This can be used to treat ADHD symptoms.
Amphetamines
58
Stronger, more addictive drug that is similar to amphetamines.
Methamphetamine
59
A stimulant that blocks presynaptic adenosine receptors that monitor transmitter release, leading to extra transmitter being released.
Caffeine
60
Other word for psychedelic drugs, especially if used for spiritualeligious purposes.
Entheogens
61
A psychedelic drug with a mostly visual effect, it activates 5-HT_2A receptors in the visual cortex, microdoses can boost cognition and mood.
LSD (lysergic acid diethylamide)
62
A psychedelic amphetamine derivative that is associated with prosocial feelings and behavior such as empathy alongside euphoria and visual effects. It is being investigated to help treat PTSD, but long-term use can cause cognitive performance and mood problems and lasting changes in patterns of brain activation.
MDMA/Ecstasy
63
This psychedelic is often referred to as "magic mushrooms", it alters brain activity in the prefrontal cortex, amygdala, and anterior cingulate cortex. Users report spiritual experiences, feelings of transcendence, and visual and time distortions. It can be used to treat OCD symptoms, cluster headaches, depression, anxiety, and anguish.
Psilocybin
64
This psychedelic blocks NMDA receptors and stimulates opioid/Ach receptors. It creates a detached, trancelike state and psychedelic perceptual alterations. It can be used as an anesthetic or an antidepressant in low doses.
Ketamine (Special K)
65
Weakness of character and lack of self control is the reason people get addicted to drugs. This model is fairly outdated.
Moral model of substance use disorder
66
Substance abusers need medical treatment. The main criticism of this model is that there are no physical abnormalities for drug addiction (except a bit genetic susceptibility).
Disease model of substance use disorder
67
Drug abusers keep taking drugs to avoid withdrawal symptoms. The main criticism of this model is that it doesn't explain why people start substance abuse before they face withdrawal symptoms, or get addicted to drugs with no withdrawal symptoms.
Physical dependence model of substance use disorder
68
Drugs provide powerful reinforcement that can make people addicted.
Positive reward model of substance use disorder
69
Many addictive drugs cause dopamine release in the _______ _______, making the user associate them with pleasure.
Nucleus accumbens
70
This part of the brain plays a role in addiction, cravings, and pleasure. For example, stimulation here via rTMS can reduce nicotine cravings.
Insula
71
The process of shifting a circadian rhythm/synchronizing it with one's environment.
Entrainment
72
A cue one can use to synchronize their circadian rhythm with their environment, like light.
Zeitgeber
73
What kinds of brain waves do EEGs show in awake individuals?
Beta waves
74
What kinds of brain waves do EEGs show in individuals who are relaxed or in stage 1 sleep?
Alpha, theta waves, vertex spikes
75
What kinds of brain waves do EEGs show in individuals in stage 2 sleep?
Theta waves with sleep spindles and K-complexes
76
What kinds of brain waves do EEGs show in stage 3 sleep?
Delta waves
77
What kinds of brain waves do EEGs show in REM sleep?
Beta-ish waves similar to waking
78
What activity is in the muscles, eyes, and brain during REM sleep?
Increased brain temperature and cerebral blood flow, atonia, increased twitches, suppressed knee-jerk reflex, rapid eye movement, increased cerebral cortex activity, variable heart rate
79
What activity is in the muscles, eyes, and brain during non-REM sleep?
Slow heart rate, low postural tension and twitches, infrequent eye movement, less cerebral cortex activity, high growth hormone secretion in SWS
80
Which stage tends to happen more at the beginning of the night, and which tends to happen more at the end of the night?
SWS, REM
81
What do sleep spindles do? What do K-complexes do?
Sleep spindles aid in memory consolidation. K-complexes help keep us asleep in the presence of distractions such as noises.
82
These waves often occur during REM sleep, they are associated with rapid eye movement, thought to trigger visual imagery in dreams, and help with memory consolidation.
PGO waves
83
These rhythms last longer than 1 day.
Infradian rhythms
84
These rhythms last less than 1 day.
Ultradian rhythms
85
This part of the brain is in the hypothalamus above the optic chiasm, it is responsible for circadian rhythms.
Suprachiasmatic nucleus
86
A circadian rhythm that isn't influenced by zeitgebers, it is typically a bit over 24 hours, sometimes around 25 hours, in humans.
Free-running rhythm
87
The resetting of one's circadian rhythm, with zeitgebers such as light and dark cues.
Phase shift
88
How do human sleep patterns change across our lifespans?
We sleep less as have less REM sleep as we get older.
89
What four neural systems underlie sleep?
The forebrain system generates SWS, brainstem system activates the sleeping forebrain into wakefulness, pontine system triggers REM sleep, hypothalamic system coordinates the other brain regions.
90
This part of the brain recieves signals from the SCN and secretes melatonin, which signals darkness to the brain.
Pineal gland
91
Photopigment in the eye that communicates with the SCN about light and dark cues.
Melanopsin
92
The axonal pathway used to send light cues from the eyes to the SCN in the hypothalamus.
Retinohypothalamic pathway
93
A diffuse group of cells with axons and dendrites in many directions, going from the medulla to the hypothalamus. Electrical stimulation here activates the forebrain, so it is responsible for waking the forebrain up from SWS.
Reticular formation
94
This part of the brainstem is responsible for triggering REM sleep.
Pons
95
This part of the forebrain produces slow-wave sleep.
Basal forebrain
96
This part of the forebrain contains the SCN, it produces orexin and uses it to switch between wakefulness, non-REM sleep, and REM sleep.
Hypothalamus
97
What are 4 theories about why we sleep?
Energy conservation, niche adaptation, physical restoration, memory consolidation
98
What was found out about rats' memory consolidation when they sleep during the rat maze experiment?
Rats' neurons were firing in the same way that they had been firing earlier during the day when they were asleep. They were consolidating memories of the maze.
99
The theory that dreams have no meaning, and they are just an explanation synthesized by the cortex for random brainstem activity.
Activation-synthesis model
100
Effects of sleep deprivation
Irritability, difficulty concentrating, disorientation, microsleeps, prolonged sleep deprivation affects motor and cognitive performance, creativity, is related to dementia, compromises the immune system, can lead to death.
101
An effect of medium-term sleep deprivation where one sleeps for a few seconds at a time while awake.
Microsleeps
102
When one has trouble falling asleep. This can be caused by shift work, time zone changes, and daily routine changes.
Sleep-onset insomnia
103
When one has trouble staying asleep. This can be caused by drugs and other factors.
Sleep-maintenance insomnia
104
When one feels excessively sleepy during the day, even while getting a normal amount of sleep.
Hypersomnia
105
A disorder where one gets frequent sleep attacks due to degenerating orexin neurons. They typically last 5-30 minutes and happen multiple times a day, such as every 90 minutes, and typically involve REM sleep early on in the attack.
Narcolepsy
106
A sudden loss of muscle tone, leading to collapse of the body without loss of consciousness. This can happen to people with narcolepsy.
Cataplexy
107
A complete absense of muscle tone, typically associated with REM sleep.
Atonia
108
A sleep disorder where breathing becomes unreliable during sleep, often due to relaxation of chest/throat muscles or changes in the pacemaker respiratory neurons of the brainstem. This is common in obese people and often is accompanied by loud snoring.
Sleep apnea
109
A neuropeptide/hormone used by the hypothalamus to switch between wakefulness and REM/non-REM sleep. In narcoleptic people, neurons that use this substance start degenerating between the ages of 15-25 when symptoms start, and continue to degenerate throughout life.
Orexin
110
These 3 sleep disorders are most common in kids and happen during Stage 3 sleep.
Sleepwalking/somnambulism, night terrors, sleep eurenesis
111
Temporary paralysis either just before or after waking, typically after waking from a REM episode, it feels similar to cataplexy.
Sleep paralysis
112
A sleep disorder most common in older people and men, where one acts out their dreams. Getting this disease often precedes symptoms of Parkinson's and Dementia, so this is often the beginning of widespread neurodegeneration.
REM behavior disorder
113
What was found by the 2013 mouse sleep study?
CSF flow increases during sleep, so sleep is important for clearing out metabolic waste in the brain.
114
Memories here stay in your memory for about 30 seconds or as long as you keep rehearsing the info. They can either be consolidated into long-term memory, or gone for good if you get distracted. These memories are stored in different parts of the prefrontal cortex.
Working, short-term memory
115
This type of memory represents things that have happened in one's life, it is declarative and stored in the medial temporal lobe and neocortex.
Episodic memory
116
This type of memory represents facts that can be declared/explained to others, it is stored in the medial temporal lobe and neocortex.
Semantic memory
117
This type of memory represents skills that can be learned and demonstrated, it is stored in the striatum, motor cortex, and cerebellum.
Procedural memory
118
This type of memory is the reason why words we have recently seen come to mind more easily, it is stored in the neocortex.
Priming
119
This type of memory happens when we associate a certain stimuli with something that would lead us to elicit a response, and thus respond to the stimuli a certain way. It is stored in the amygdala and cerebellum.
Classical conditioning
120
This type of memory happens when a certain action is associated with a reward/consequence, and this affects if the action will be done again or not.
Operant conditioning
121
This type of memory is not associative, and includes concepts such as habituation. It is stored in reflex pathways.
Nonassociative learning
122
This type of memory has to do with navigation, and is stored in the hippocampus and the cortex.
Spatial memory
123
Classical conditioning of emotional reactions, stored in the amygdala.
Emotional conditioned responses
124
Classical conditioning of motor responses, stored in the cerebellum.
Motor conditioned responses
125
This patient had mild retrograde amnesia and severe anterograde amnesia after a surgery where his hippocampus was removed. His declarative memory was impaired, although his nondeclarative memory was fine.
Henry Molaison (HM)
126
This patient had damage to his left frontoparietal and right parieto-occipital cerebral cortex, and severe shrinkage of both left and right hippocampus and nearby cortex, after a motorcycle accident. He lost his ability to remember his past or create new episodic memories, although his semantic memory was fine.
Kent Cochrane (KC)
127
This patient was a famous orchestra conductor who suffered from herpes encephalitis. He lost almost all his declarative memories, remembering only some semantic stuff and his wife. He could no longer form new declarative memories and had a short-term memory span of 7-30 seconds. He frequently felt like he had just woke up from a coma.
Clive Wearing
128
Loss of memories that happened before an event
Retrograde amnesia
129
Loss of the ability to form new memories
Anterograde amnesia
130
Thanks to HM, we know that this part of the brain is necessary for episodic memory.
Medial temporal lobe
131
Which brain region is necessary for spatial learning?
Hippocampus
132
These neurons in the hippocampus selectively encode specific locations.
Place cells
133
These neurons in the entorhinal cortex can act like grids to help with spatial navigation.
Grid cells
134
This is a task used to test for monkeys' declarative memory through object recognition where a monkey must pick the object it hasn't seen before.
Delayed non-matching to sample task
135
This part of the brain is important for declarative memories, it is damaged in the brains of those with Korsakoff's Syndrome. It likely connects the medial temporal lobes to the thalamus.
Mammillary bodies
136
Damage to these two brain parts impairs skill learning.
Basal ganglia, striatum
137
A process in which neural connections and brain structure are changed, necessary for learning.
Synaptic plasticity
138
What is the Hebbian learning rule?
Neurons that fire together wire together
139
Which change in brain structure can be seen in those with highly superior autobiographical memories?
The medial temporal lobe and caudate are larger
140
A process in Hebbian synapses where a tetanus applied to the presynaptic neuron leads it to produce many action potentials and cause the postsynaptic neuron to fire repeatedly, making this synapse stronger and more effective.
Long-term potentiation (LTP)
141
A brief high frequency burst of stimuli that causes long-term potentiation.
Tetanus
142
The neurotransmitter that is most studied when it comes to Hebbian synapses and LTPs.
Glutamate
143
Before LTP, these ions block NMDA receptors' calcium channels in the postsynaptic cell, preventing them from responding to glutamate. These ions are ejected from the receptor channels if large amounts of glutamate are released due to depolarization.
Magnesium
144
During LTP, calcium ions are free to enter NMDA receptors. What effects do they have on the cell?
They allow NMDA receptors to respond to glutamate and release enzymes causing nearby AMPA receptors to move to the active synapse, modifying AMPA receptors to be more efficient, and causing more AMPA receptors to be created on the postsynaptic membrane.
145
The opposite of LTP, where a synapse gets weaker due to lack of use.
Long-term depression (LTD)
Study all 145 cards for free