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Behavioral Neuroscience > Exam 2: Chapters 2-6 > Flashcards

Exam 2: Chapters 2-6 Flashcards

1
Q

Psychopharmacology

A

The study of the effects of drugs on the nervous system and on behavior

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2
Q

Drug effects

A

The changes we can observe in an animal’s physiological processes and behavior

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3
Q

Sites of action

A

The points at which molecules of drugs interact with molecules located on or in cells of the body

  • causes an effect on some biochemical processes of these cells
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4
Q

What contributions have psychopharmacology studies made to science?

A
  • development of psychotherapeutic drugs

- tools to study functions of the cells of the nervous system/ behaviors controlled

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5
Q

What do molecules of drugs have to do to be effective?

A

Reach its sites of action

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6
Q

How do drug molecules reach their sites of action?

A
  1. Enter the body
  2. Enter the bloodstream
  3. Be carried to the organ/s they act on
  4. Leave the bloodstream to come into contact with molecules with which they interact
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7
Q

What happens to molecules of drugs that enter the body?

A

They are metabolized > broken down by enzymes

OR

Excreted in urine

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8
Q

What is the process by which drugs are absorbed, distributed within the body, metabolized, and excreted?

A

Pharmacokinetics

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9
Q

What is the most common route of administration in laboratory animals?

A

Injection

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10
Q

Fastest route of injection

A

Intravenous (IV) injection - injection into a vein

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11
Q

Disadvantages of IV injections

A
  1. Increased care and skill to complete

2. Entire dose reaches the bloodstream at once > if sensitive, there is little to do to counteract the effects

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12
Q

What is an intraperitoneal (IP) injection?

A

Drug is injected through the abdominal wall > into the peritoneal cavity

  • most common route for small animals
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13
Q

What is an intramuscular (IM) injection?

A

An injection made directly into a large muscle, such as in the upper arm, thigh, or buttocks.

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14
Q

How are IM injections absorbed into the bloodstream?

A

The drug is absorbed through the capillaries that supply the muscle with blood

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15
Q

What is a subcutaneous (SC) injection?

A

An injection made into the space beneath the skin

> useful for small amounts of a drug
can be modified for slow administration through use of dry pellet

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16
Q

What is the most common form of administration of medicinal drugs to humans?

A

Oral administration

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17
Q

Sublingual administration

A

Accomplished by placing them beneath the tongue

> is absorbed by by capillaries that supply the mucous membrane that lines the mouth
ex: nitroglycerine (causes blood vessels to dilate)

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18
Q

How are suppositories administered?

A

Through intrarectal administration

> most commonly used to administer drugs that might upset a person’s stomach
not common for animals

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19
Q

Forms of inhalation drugs + benefits of inhalation

A

Vapor, fine mist, gases

> route from lungs to brain is very short, drugs have rapid effects

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20
Q

How can drugs be absorbed directly through the skin?

A

Through topical administration

> creams, ointments, patches, snorted cocaine is actually topical as well

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21
Q

What makes the sniffing of cocaine a topical administration?

A

It comes into contact with the nasal mucosa which is a rapid route for topical administration to the brain.

> is called insufflation NOT inhalation

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22
Q

What are the (2) ways that drugs can be administered directly into the brain?

A
  1. Intracerebral administration

2. Intracerebroventricular (ICV) administration

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23
Q

Intracerebral administration

A

A very small amount of drug is injected directly into the brain

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24
Q

Intracerebroventricular administration

A

Way of getting a widespread distribution of a drug in the brain > is conducted via injection into the cerebral ventricles

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25
Q

What is the most important factor that determines the rate at which drugs can be introduced into the body?

A

Lipid solubility of the drug

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26
Q

The blood-brain barrier is a barrier only for ______- soluble molecules.

A

Water

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27
Q

Inactivation and Excretion main points

A
  1. Drugs do not remain in the body indefinitely
  2. Many are deactivated by enzymes in the liver, blood, and brain
  3. All are eventually excreted, primarily but the kidneys
  4. Some enzymes transform drug molecules into even more active molecules
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28
Q

What is the best way to measure the effectiveness of a drug?

A

to plot a dose-response curve

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29
Q

How to plot a dose-response curve

A

Subjects are given various doses of a drug per body weight of the individual and effects are plotted

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30
Q

Heavier subjects require a _______ quantity of a drug to achieve the same concentration of a small subject.

A

Larger

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31
Q

Increasingly stronger doses of a drug cause increasingly _______ effects.

A

Larger

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32
Q

What is the point at which increasing the dose of a drug does not produce any more effect?

A

Point of maximum effect

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33
Q

What is the margin of safety?

A

Reflected by the difference between the dose-response curve for its’ therapeutic effects and that for its’ adverse side effects

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34
Q

How to calculate therapeutic index

A

The ratio of the dose that produces desired effects and the dose that produces toxic effects.

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35
Q

The _________ the therapeutic index, the more care must be taken in prescribing the drug.

A

Lower

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36
Q

Why do drugs vary in their effectiveness?

A
  1. Different drugs (even with the same effects) may have different sites of action.
  2. The drug’s affinity with its site of action.
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37
Q

What is affinity?

A

The readiness with which the two molecules join together

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38
Q

A drug with a high affinity will produce effects at a relatively _____ concentration.

A

Low

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39
Q

What is the most desirable drug?

A

High affinity for sites of action that produce therapeutic effects and low affinity for sites of action that produce toxic side effects.

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40
Q

Tolerance

A

When a drug is administered repeatedly, it’s effects will diminish

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41
Q

Sensitization

A

A drug becomes more and more effective

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42
Q

Withdrawal symptoms

A

If an individual stops taking the drug that they have become tolerant to, they will experience the opposite effects of the drug itself

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43
Q

What is tolerance the result of?

A

the body’s attempt to compensate for the effects of the drug

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44
Q

What are the types of compensatory mechanisms?

A
  1. Decrease in effectiveness of binding
    - either the receptor’s affinity for the drug decreases OR there are less receptors
    - prolonged stimulation of receptors causes one or more steps in the coupling process to become less effective
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45
Q

What is sensitization?

A

Repeated doses of a drug produce larger and larger effects (less likely)

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46
Q

What is a placebo?

A

An innocuous substance that has no specific physiological effect

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47
Q

What do placebos have the potentiality to do?

A

To create the mind-body self-healing process

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48
Q

When do we use placebos?

A

When experimenters want to investigate the behavioral effects of drugs in humans they must use placebos so they can be sure that the behavioral effects they observe are caused by specific effects of the drug

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49
Q

Antagonists

A

Drugs that block or inhibit the postsynaptic effects

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50
Q

Agonists

A

Drugs that facilitate postsynaptic effects

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51
Q

Sequence of synaptic activity (1-5)

A
  1. Neurotransmitters are synthesized and stored in synaptic vesicles
  2. Synaptic vesicles travel to the presynaptic membrane
  3. Axon fires
  4. Voltage-dependent calcium channels open & allow calcium ions in
  5. Calcium ions interact with proteins in the synaptic vesicles and cause the release of neurotransmitter
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52
Q

Sequence of synaptic activity (6-8)

after release of neurotransmitter

A
  1. Molecules of the neurotransmitter bind with post-synaptic receptors & cause particular ion channels to open
  2. Opening of ion channels influences an excitatory or inhibitory postsynaptic potentials
  3. Neurotransmitters experience re-uptake or destruction by enzymes
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53
Q

Effects on production of neurotransmitters (+)

A

The rate of synthesis/release of a neurotransmitter is increased with the administration of a precursor

  • the precursor serves as an agonist
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54
Q

What is a precursor?

A

Molecules readily available in the diet that only require a small amount of biosynthetic steps to be converted into neurotransmitters

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55
Q

Effects of production of neurotransmitters (-)

A

A drug my inactivate an enzyme needed to synthesize the neurotransmitter. Therefore the NT cannot be produced.

> drug is an antagonist

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56
Q

Effects on the storage of NT

A

Drug molecules may bind with a particular site on the transporter and inactivate it. Since the transporters are responsible for pumping NT across the vesicle membrane, there will be no NT in the vesicle when it eventually ruptures against the presynaptic membrane

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57
Q

Effects on the release of NT (-)

A

Drugs deactivate the proteins that cause synaptic vesicles to fuse with the presynaptic membrane and release their contents into the synaptic cleft

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58
Q

Effects of the release of NT (+)

A

Some drugs act as agonists and bind with proteins that cause synaptic vesicles to fuse with the membrane to directly trigger release of the NT

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59
Q

Explain how a drug can affect postsynaptic receptors

A

The drug can bind with a receptor, instead of the NT binding to it, and serve as either an agonist or antagonist

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60
Q

What is a direct agonist?

A

A drug that mimics the effects of a NT

> the drug attaches to the binding site where the NT usually attaches and opens ion channels

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61
Q

What is a direct antagonist?

A

A drug that binds with the receptors & do not open the ion channel. They occupy the binding site so that NT cannot bind

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62
Q

Non-competitive binding

A

Binding of a drug to a site on a receptor but does not interfere with the binding site for the principle NT

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63
Q

Indirect antagonist

A

A drug that attaches to a binding site on a receptor and interferes with the action of the receptor; does not interfere with the binding site for principle NT

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64
Q

Indirect agonist

A

A drug that attaches to a binding site on a receptor and facilitates the action of the receptor; does not interfere with the binding site of principle NT

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65
Q

Explain autoreceptors

  • How can they be affected?
A

Autoreceptors regulate the amount of NT that is released

  • They can be activated > less NT released
  • They can be blocked > more NT released
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66
Q

Effects on reuptake of NT

A

Drugs can bind with transporter molecules responsible for reuptake and inactivate them > drugs stay in the synapse longer and create the effects of the drug for an extended period of time

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67
Q

Effects on the destruction of NT

A

The drug binds with the enzyme that normally destroys the NT

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68
Q

Effects on reuptake and destruction of NT are both _____.

A

Agonists

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69
Q

What are the two general effects of neurotransmitters?

A
  1. Depolarization (EPSP)

2. Hyperpolarization (IPSP)

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70
Q

Is glutamate excitatory or inhibitory?

A

Excitatory

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71
Q

Is GABA inhibitory or excitatory?

A

Inhibitory

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72
Q

All sensory organs transmit information to the brain through axons whose terminals release _______.

A

Glutamate

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73
Q

What is the difference between other neurotransmitters and glutamate/GABA?

A

These other neurotransmitters tend to activate or inhibit entire circuits of neurons involved in particular brain functions

  • they are more of modulators than information-transmitters
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74
Q

Example of the modulator vs information-transmitter effect of glutamate/GABA and other NT

A

AcH activates the cerebral cortex and facilitates learning > the information learned/remembered is transmitted by neurons secreting GABA/glutamate

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75
Q

Where and by who is ACh secreted?

A

Secreted by efferent axons in the CNS

> found in the CNS, ganglia of the ANS, and the target organs of the parasympathetic branch of the ANS

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76
Q

What does ACh do?

A

All muscular movement is controlled by the release of ACh

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77
Q

What are synapses of ACh called?

A

Acetylcholinergic

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78
Q

Other functions of ACh

A

Dorsolateral pons - REM sleep
Basal forebrain - activating cerebral cortex/facilitating learning
Medial septum- electrical rhythms of hippocampus > formation of memories

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79
Q

What is acetylcholine made of?

A
  1. Choline

2. Acetate

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80
Q

How are choline and acetate joined to become ACh?

A

The acetyl group of acetyl-CoA is transferred to the choline molecule by the enzyme choline acetyltransferase (ChAT).

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81
Q

What are the products of the biosynthesis of acetylcholine?

A
  1. Acetylcholine

2. Coenzyme A (CoA)

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82
Q

What two drugs affect the release of AcH?

A
  1. Botulinum toxin

2. Black widow spider venom

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83
Q

Botulinum toxin big points

A
  1. Prevents the release of AcH (antagonist)

2. VERY toxic…one teaspoon of pure substance can kill entire human population

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84
Q

Black widow spider venom important points

A
  1. Stimulates the release of AcH (agonist)

2. Can be fatal but is much less toxic than botulinum toxin

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85
Q

A drug that affect acetylcholinesterase (AChE)

A
  1. Neostigmine
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86
Q

What does neostigmine do?

A

A drug that inhibits the activity of acetylcholinesterase

> used for patients with myasthenia gravis

87
Q

What two types of ACh receptors are there?

A
  1. Ionotropic

2. Metabotropic

88
Q

Which drug positively affects the ACh ionotropic receptors?

A

Nicotine

89
Q

Which drug positively affects the metabotropic ACh receptors?

A

Muscarine

90
Q

Nicotinic receptor

A

An ionotropic acetylcholine receptor that is stimulated by nicotine and blocked by curare

91
Q

Muscarinic receptor

A

A metabotropic acetylcholine receptor that is stimulated by muscarine and blocked by atropine

92
Q

What is more prevalent? Muscarinic or nicotinic receptors?

A

Muscarinic receptors

93
Q

Which is faster? Metabotropic or ionotropic receptors?

A

Ionotropic

94
Q

What drug negatively affects acetylcholine muscarinic receptors?

A

Atropine

95
Q

What drug negatively affects the nicotinic receptors of acetylcholine?

A

Curare

96
Q

Atropine

A

A drug that blocks the muscarinic acetylcholine receptors

Example: the eye drops that block ACh activity on the pupil to make females more attractive

97
Q

Curare

A

A drug that blocks nicotinic acetylcholine receptors

> these receptors are found on muscles therefore cause paralysis

98
Q

What is curare used for?

A

To paralyze patients who are to undergo surgery so that their muscles will relax completely and not contract when cut with a scalpel

99
Q

Four major monoamines

A
  1. Dopamine
  2. Norepinephrine
  3. Epinephrine
  4. Serotonin
100
Q

What are the 3 major catecholamines?

A
  1. Dopamine
  2. Norepinephrine
  3. Epinephrine
101
Q

Dopamine (DA)

A
  1. One of the catecholamines

2. Produces excitatory and inhibitory postsynaptic potentials

102
Q

Dopamine affects what functions

A

Movement, attention, learning

103
Q

Precursor for dopamine/norepinephrine

A

Tyrosine- an amino acid

104
Q

Converting enzyme for tyrosine

A

L-DOPA

105
Q

Process of dopamine creation

A
  1. Precursor (tyrosine) is obtained from our diet
  2. An enzyme converts it into L-DOPA

IF a dopaminergic neuron:
3. Another enzyme converts L-DOPA into dopamine

IF a noradrenergic neuron:
4. Dopamine is converted into norepinephrine

106
Q

Where do the most important dopaminergic neurons originate?

A

In the midbrain

107
Q

Nigrostriatal system

A

A system of neurons originating in the substantial Nigeria and terminating in the neostriatum

108
Q

Mesolimbic system

A

A system of dopaminergic neurons originating in the ventral tegmental area and terminating in the nucleus accumbens, amygdala and hippocampus

109
Q

What does the nucleus accumbens play an important role in?

A

The reinforcing/rewarding effects of certain categories of stimuli

110
Q

Where are the cell bodies of the mesocortical system located?

A

The ventral tegmental area…their axons project to the prefrontal cortex

111
Q

What behavioral effects is mesocortical system responsible for?

A

Short-term memories, planning, strategies for problem-solving

112
Q

What is Parkinson’s disease?

A

A neurological disease characterized by tremors, rigidity of the limbs, poor balance, and difficulty in initiating movements; caused by degeneration of the nigrostriatal system

113
Q

Where do the cell bodies of the neurons involved in Parkinson’s disease located?

A

In the substantial nigra

114
Q

What is the substantia nigra generally stained with?

A

Melanin

115
Q

How are the symptoms of patients with Parkinson’s disease alleviated?

A

Administration of the dopamine precursor, L-DOPA, so that it can interact with dominergic neurons and be converted into dopamine. This causes a chain reaction for more dopamine to be secreted by the few surviving dopaminergic neurons.

116
Q

What is AMPT?

A

A drug that blocks the activity of tyrosine hydroxylase which then interferes with the synthesis of the catecholamines

117
Q

Explain the process of creation of dopamine

A

Tyrosine > (enzyme - tyrosine hydroxylase) > L-DOPA > (enzyme) > dopamine

118
Q

What is reserpine?

A

A drug that interferes with the storage of monoamines in the synaptic vesicles (antagonist)

119
Q

What are the two most common dopamine receptors?

A
  1. D1 dopamine receptors
    - solely postsynaptic
  2. D2 dopamine receptors
    - presynaptic
    - postsynaptic (in brain)
120
Q

What drugs inhibit the reuptake of dopamine?

A
  1. Amphetamine
  2. Cocaine
  3. Methylphenidate
121
Q

How is cocaine used in medicine?

A

It blocks voltage-dependent sodium channels so it is used as a topical anesthetic in the form of eye drops for eye surgery

122
Q

What enzyme is needed to regulate the production of catecholamines?

A

Monoamines oxidase (MAO)

123
Q

What drug destroys MAO? Because of this, what kind of drug is it

A

Deprenyl (dopamine agonist)

124
Q

What neurotransmitter do we suspect is involved in schizophrenia?

A

Dopamine

125
Q

What does chlorpromazine do?

A

It blocks D2 receptors and alleviates schizophrenic symptoms

126
Q

Therefore what is the overarching suspicion of the cause of schizophrenia

A

An overactivity of dopaminergic neurons

127
Q

What is norepinephrine and where is it found?

A

One of the catecholamines; a neurotransmitter found in the brain and in the sympathetic division of the ANS

128
Q

What is epinephrine and where is it found?

A

One of the catecholamines; a hormone secreted by the adrenal medulla; serves also as a neurotransmitter in the brain

129
Q

How is norepinephrine produced?

A

It is essentially dopamine converted by an enzyme into norepinephrine

130
Q

What is fusaric acid?

A

A drug that inhibits the activity of the enzyme dopamine-beta-hydroxylase and thus blocks the production of norepinephrine

131
Q

What is the locus coeruleus?

A

A dark-colored group of noradrenergic cell bodies located in the pons near the rostral end of the floor of the 4th ventricle

132
Q

What types of noradrenergic receptors are there?

A
  1. Beta 1
  2. Beta 2
  3. Alpha 1
  4. Alpha 2
133
Q

What does the drug idazoxan do?

A

It blocks the alpha 2 autoreceptors for norepinephrine and acts as an agonist

134
Q

What does serotonin play a role in?

A

Eating, sleep, arousal, dreaming, and in the regulation of pain

135
Q

What is the precursor for serotonin?

A

Tryptophan

136
Q

Process of serotonin production

A

Tryptophan > 5-hydroxytrytophan (5-HTP) > serotonin (5-HT)

137
Q

How many different types of serotonin receptors have been found?

A

Nine

138
Q

What does fluoxetine do? (Prozac)

A

It inhibits the reuptake of serotonin and helps with depression, anxiety disorders, and OCD

139
Q

What does fenfluramine do?

A

It causes the release of serotonin as well as inhibits the reuptake. It used to treat obesity by means of appetite repression.

140
Q

What does lysergic acid diethylamide (LSD) do?

A

It produces distortions of visual perceptions by acting as a direct agonist for postsynaptic serotonin alpha 2 receptors in the forebrain

141
Q

What is MDMA responsible for?

A

It is both a noradrenergic and serotonergic agonist that has both excitatory and hallucinogenic effects.

142
Q

What does MDMA (ecstasy) do to serotonergic transporters?

A

It causes them to run backwards and is responsible for the hallucinogenic effects. But it can damage serotonergic neurons and cause cognitive deficits as well.

143
Q

What is histamine?

A

A neurotransmitter that plays an important role in stimulating wakefulness

144
Q

What are the three most common neurotransmitters in the CNS?

A

Glutamate, gamma-aminobutyric acid (GABA), and glycine

145
Q

What is glutamate?

A

An amino acid, the most important excitatory neurotransmitter in the brain

146
Q

How is glutamate produced?

A

It is produced in abundance by the cells’ metabolic processes

> therefore there is no effective way to prevent its’ synthesis without disruption of other activities of the cell

147
Q

How many glutamate receptors have been found?

A

Four major types

148
Q

List the 3 glutamate ionotropic receptors

A
  1. NMDA receptor
  2. AMPA receptor
  3. Kainate receptor
149
Q

What is the one metabotropic receptor for glutamate?

A

Metabotropic glutamate receptor

150
Q

What does the AMPA receptor do?

A

It is the most common glutamate receptor and controls a sodium channel. When glutamate attaches to the binding site, it produces EPSPs.

151
Q

What two substances are the NMDA receptors of glutamate sensitive to?

A
  1. Alcohol

2. PCP

152
Q

What is GABA?

A

An amino acid, teh most important inhibitory neurotransmitter in the brain

153
Q

What drug prevents the synthesis of GABA?

A

Allyglycine

154
Q

How many GABA receptors have been discovered?

A

Two

  1. GABA a (ionotropic) - controls a chloride channel
  2. GABA b (metabotropic) - controls a potassium channel
155
Q

How are seizures prevalent in the human body?

A

As neurons fire and excite other neurons around them, the inhibitory mechanisms usually provided by GABA are not there and thus cannot stop the uncontrollable firing.

156
Q

What are a few drugs that affect GABA binding?

A
  1. Muscimol
  2. Benzodiazepines
  3. Bicuculline
157
Q

Barbiturates are drugs known for ________ the activity of the GABA receptor.

A

Promoting

158
Q

What effects to barbiturates have if they are GABA agonists?

A

They are effective anxiolytics or “anxiety-dissolving” drugs.

  • effective sleep medications and sometime seizure control
159
Q

What is glycine?

A

An amino acid; an important inhibitory neurotransmitter in the lower brain stem and spinal cord

160
Q

What are peptides?

A

They consist of two or more amino acids linked together by peptide bonds

161
Q

What are the precursors for peptides?

A

Large polypeptides

> they are broken into pieces by special enzymes

162
Q

Where does the synthesis of peptides take place?

A

In the soma…must be delivered to the terminals

163
Q

Are peptides recycled?

A

No, they are only destroyed by enzymes

164
Q

What are endogenous opioids?

A

A class of peptides secreted by the brain that act as opiates

165
Q

What do opiates do?

A

They reduce pain because they have direct effects on the brain

166
Q

What are enkephalins?

A

One of the endogenous opioids

167
Q

What are some effects of opiate receptor stimulation?

A

Analgesics, inhibition of species-typical defensive responses (fleeing/hiding), and reinforcement/reward neurons

168
Q

What is naloxone?

A

An opiate receptor blocker that is used clinically to reverse opiate intoxication

169
Q

What are the three types of opiate receptors?

A
  1. Mu
  2. Delta
  3. Kappa
170
Q

How can peptides have different effects in the brain vs the body?

A

The blood-brain barrier keeps most peptide hormones from the extra cellular fluid in the brain

171
Q

What are endocannabinoids?

A

A lipid; an endogenous ligand for receptors that bind with THC, the active ingredient of marijuana

172
Q

How many cannabinoid receptors have been discovered? What type are they?

A
  1. CB1
  2. CB2

Both are metabotropic

173
Q

What is anandamide?

A

The first cannabinoid to be discovered and most likely the most important one

174
Q

Where are cannabinoid receptors found? Where are they seldom found?

A

In the brain…specifically the frontal cortex, anterior cingulate cortex, basal ganglia, cerebellum, hypothalamus, and hippocampus.

They are found in much lower levels in the brain stem…i.e the low toxicity of THC.

175
Q

What drug blocks CB1 receptors?

A

Rimonabant

176
Q

What are the positive effects of THC?

A
  1. Analgesia
  2. Sedation
  3. Stimulation of appetite
  4. Reduces nauseas from cancer drugs
  5. Decreases pressure in eyes for glaucoma patients
  6. Reduces symptoms of some motor disorders
177
Q

What are the negative effects of THC?

A
  1. Interferes with concentration/memory
  2. Alters visual/auditory perception
  3. Distorts perceptions of passage of time
178
Q

What is a nucleoside?

A

A compound that consists of a sugar molecule bound with a purine or pyramidine

179
Q

What is adenosine?

A

A nucleoside; a combination of ribose and adenine; serves as a neuromodulator

180
Q

What does adenosine do?

A
  1. Activates receptors on blood vessels to cause them to dilate
  2. Acts as a neuromodulator
  3. Opens potassium channels through G proteins to produce IPSPs
  4. Its’ receptors play an important role in the control of sleep
181
Q

What does caffeine do?

A

It blocks adenosine receptors and produces excitatory effects

182
Q

What is nitric oxide? (NO)

A

A gas produced by cells in the nervous system, used as a means of communication between cells

183
Q

What does nitric oxide do?

A
  1. Used as a messenger in many parts of the body

2. Involved in the control of muscles in the wall of the intestines

184
Q

How is nitric oxide produced?

A

Arginine > nitric oxide synthase > nitric oxide

185
Q

What drugs have an effect on nitric oxide?

A
  1. L-NAME (production)

2. Sildenafil–aka Viagra (destruction)

186
Q

MPTP story

A

Young people who were using heroin came in with Parkinson’s Disease-like symptoms. They were given L-DOPA which alleviated symptoms but did not get rid of them. It was found that the heroin had a new chemical, MPTP, which is highly toxic to the same neurons lost in Parkinson’s Disease. Because of this, researchers found a new drug that is now used to treat symptoms of Parkinson’s.

187
Q

Sensation

A

Detection of physical energy (light, sound waves) by specialized neurons (sensory receptors) which then convert or transducer the energy into a neural signal (a receptor potential)

188
Q

Perception

A

The organization and interpretation of incoming sensory information

189
Q

Parvocellular (P) cells

A

Smaller, low convergence from cones, sensitive to color and detail

190
Q

Magnocellular (M) cells

A

Larger, high convergence from rods, sensitive to dim light and movement

191
Q

What is the pathway for the parvocellular cells?

A

One cone to one bipolar cell to one retinal ganglion cell

192
Q

What is the pathway for magnocellular cells?

A

Several rods to one bipolar cell to one retinal ganglion cell

193
Q

What is the primary retino-geniculo-cortical pathway?

A

It is responsible for conscious visual perception

194
Q

Describe the primary retino-geniculo-cortical pathway steps

A
  1. Optic nerves receive information from the retina of each eye
  2. Crosses through the optic chiasm
  3. Goes to the lateral geniculate nucleus of the thalamus
  4. The LGN then sends axons ipsilaterally along the optic tracts to the primary visual cortex
  5. The primary visual cortex “sees” the opposite half of the visual field yet still receives information from both the left/right eyes
195
Q

What is the Trichromatic Theory?

A

We have 3 types of cones that are sensitive to 3 primary colors of light (red, green, blue)

> the 3 primary colors of light that are coded by the cones can then be combined to create any color … this is called additive color mixing

196
Q

What is protanopia?

A

A version of red-green color blindness where red cones are filled with green opsin

197
Q

What is deuteranopia?

A

A form of red-green color blindness where green cones are filled with red opsin

198
Q

What is tritanopia?

A

A form of blue-yellow color blindness where there is a missing of blue cones

199
Q

What are the shortcomings of the Trichromatic theory?

A
  1. It doesn’t explain color blindness

2. It does not explain negative after-images

200
Q

How do we perceive color or hue?

A

it is determined by the wavelength of the light waves

201
Q

How do we perceive brightness?

A

it is determined by the light wave, amplitude and intensity

202
Q

How is saturation perceived?

A

It is determined by the purity of the wavelength

203
Q

Characteristics of cones

A

(About 6 million of them) they are responsible for our day-time vision, providing us with information about small features in the environment and are the source of vision for the highest acuity. Also responsible for color vision

204
Q

Characteristics of rods

A

(120 million) they are more sensitive to light and help us see in dim light. They lack color differentiation and provide poor acuity

205
Q

What are bipolar cells?

A

They are neurons whose two arms connect the shallowest and deepest layers of the retina

206
Q

What are ganglion cells?

A

A neuron located in the retina that receives visual information from bipolar cells; its axons give rise to the optic nerve

207
Q

What are photoreceptor?

A

The rods and cones

208
Q

What is the dorsal stream responsible for?

A

It is a system of interconnected regions of the visual cortex involved in the perception of spatial location. Begins with the striate cortex and ends with the posterior parietal cortex

209
Q

What does the dorsal stream recognize?

A

Where objects are located, if they are moving, their speed, and their direction of movement. It provides visual information that guides navigation and skilled movements directed toward objects.

210
Q

What is the ventral stream?

A

It is a system of interconnected regions of the visual cortex that is involved in the perception of form. Begins with the striate cortex and ends with the inferior temporal cortex

211
Q

What does the ventral stream do?

A

It recognizes what an object is and what color it is. It provides visual information about the size, shape, color, and texture of objects.

212
Q

What are cytochrome oxidase (CO) blobs?

A

The central region of a module of the striate cortex that contains wavelength-sensitive neurons. It is part of the parvocellular system and receives information only from ‘red’ and ‘green’ cones

213
Q

How does anatomy affect how images are projected?

A

Because axons from the nasal halves of the retinas cross to the other side of the brain, each hemisphere receives information from the contralateral half of the visual scene.

Behavioral Neuroscience (2 decks)

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