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Y3R3 - Behavior ⚛️ > L1: Genetics, Neurosnatomy & Biochemistry of Behavior > Flashcards

L1: Genetics, Neurosnatomy & Biochemistry of Behavior Flashcards

1
Q

Studies for Examining The Genetics of Behaviour

A
  • Family Risk Studies
  • Twin Studies
  • Molecular Studies
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2
Q

Family Risk studies

A
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3
Q

Def of Twin Studies

A

Adoption studies using monozygotic twins or dizygotic twins and reared in the same or in different homes.

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4
Q

Importance of Twin Studies

A

used to differentiate the effects of genetic factors from environmental factors in the occurrence of psychiatric disorders.

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5
Q

Outcome of Twin Studies

A

If there is a genetic component to the etiology, a disorder may be expected to have a higher concordance rate in monozygotic twins than in dizygotic twins.

(i.e. if concordant, the disorder occurs in both twins).

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6
Q

Molecular Studies

A
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6
Q

Is Intelligence Genetic or Environmental?

A
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7
Q

Divisions of Brain

A
  • Anatomically
  • Functionally
  • By arrangement of neuron layers or cytoarchitecture.
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8
Q

Functional Divisions of Brain

A
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8
Q

Anatomical Divisions of Brain

A
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9
Q

Connections between the two hemispheres

A
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10
Q

functions of the hemispheres are lateralized, how?

A
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11
Q

Sex differences in cerebral lateralization

A
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12
Q

What does a lesion in Frontal lobe cause?

A

Mood changes:

  • dominant hemisphere lesions → depression
  • non-dominant hemisphere lesions → mood elevation
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13
Q

What does a lesion in Dorsolateral area of Frontal lobe cause?

A

Difficulties with motivation, concentration, attention,
orientation and problem solving

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14
Q

What does a lesion in Orbitofrontal area of Frontal lobe cause?

A
  • Difficulties with judgment, inhibitions, emotions.
  • Personality changes
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15
Q

What does a lesion in Broca’s area of Frontal lobe cause?

A
  • Inability to speak fluently
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15
Q

What does a lesion in Temporal lobe cause?

A
  • Impaired memory
  • Psychomotor seizures
  • Changes in aggressive behavior
  • dominant lesions —-> Inability to understand language (i.e. Wernicke’s aphasia)
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15
Q

What does a lesion in Parietal lobe cause?

A
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16
Q

What does a lesion in Occipital lobe cause?

A
  • Visual hallucinations and illusions.
  • Inability to identify camouflaged objects.
  • Blindness.
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17
Q

What does a lesion in Limbic lobe cause?

A
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17
Q

What does a lesion in Hypothalamus cause?

A
  • Ventromedial nucleus damage > incresed appetite leading to obesity
  • Lateral nucleus damage → decreased appetite leading to weight Loss
  • Effects on sexual activity and body temperature regulation.
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18
Q

What does a lesion in Reticular system cause?

A
  • Changes in sleep-wake mechanisms (e.g., / REM sleep)
  • Loss of consciousness
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19
Q

What does a lesion in Basal Ganglia cause?

A
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20
Q

What does a lesion in Substantia nigra cause?

A

Parkinson disease

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21
Q

What does a lesion in Caudte & Putamen cause?

A

Huntington disease

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22
Q

What does a lesion in Caudate cause?

A

Tourette syndrome

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23
Q

Devisions of ANS

A

sympathetic & parasympathetic

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24
Q

Functions of ANS (Related to Psychology)

A
  • Innervates the internal organs to coordinate emotions with visceral responses such as heart rate, blood pressure, and peptic acid secretion.
  • Visceral responses to a psychological stress are involved in the development and exacerbation of some physical illnesses
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24
Q

what are types of memory systems?

A
  • Declarative (explicit or conscious) involves the knowledge of acts
  • Non-declarative (implicit or unconscious) how to perform an act
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25
Q

Types of Declarative memory (explicit or conscious)

A
  • Episodic
  • Semantic
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26
Q

Anatomy associated to Episodic memory

A
  • Temporal lobes (medial)
  • anterior thalamic nuclei
  • fornix
  • hippocampus
  • mammillary bodies
  • prefrontal cortex
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27
Q

Length of recall of Episodic memory

A

Long term

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28
Q

Episodic Memory used to remember ….

A

Personally experienced events

e.g., what you ate yesterday

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29
Q

Anatomy associated with Semantic memory

A

Inferolateral temporal lobes

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30
Q

Length of Recall in Semantic memory

A

Long term

31
Q

Semantic memory used to remember …..

A

General knowledge about the world

e.g.. the capital of New Jersey

32
Q

Types of Non-declarative (implicit or unconscious) memory

A
  • Procedural
  • Working
33
Q

Anatomy assoiated with Procedural Memory

A
  • Cerebellum
  • basal ganglia
  • supplementary motor area
34
Q

length of recall in Procedural Memory

A

Long term

35
Q

Procedural Memory used to remember …….

A

Things you do automafically

e.g., how to tie your shoes

35
Q

Anatomy associated with Working memory

A
  • Prefrontal cortex
  • Language and visual-association areas
36
Q

Length of recall in Working memory

A

Short term

37
Q

Working memory used to remember …….

A

Recent information

E.g: the phone number just obtained from a new acquaintance

38
Q

Def of Neuronal plasticity

A

The changeability of number or affinity of receptors or specific neurotransmitters

38
Q

Steps of Transmission of neuronal information

A
39
Q

Importance of Neuronal plasticity

A

can regulate the responsiveness of neurons

40
Q

Def of Presynaptic and postsynaptic receptors

A

proteins present in the membrane of the neuron

41
Q

Function of Presynaptic and postsynaptic receptors

A

can recognize specific neurotransmitters

41
Q

Effect of Neuritransmitter on Presynaptic and postsynaptic receptors

A
42
Q

classification of neurotransmitters

A
43
Q

Regulation of neurotransmitter activity

A
44
Q

Psychiatric Conditions and Associated Neurotransmitter Activity

A
45
Q

Synthesis of Dopamine

A
46
Q

Receptor of Dopamine

A

At lease five dopamine receptor subtypes (D1 -D5) have been identified

47
Q

Site of action for antipsychotic agents

A
  • traditional antipsychotic agents → D2 (major site of action).
  • newer “atypical” antipsychotic agents → D1 and D4 as well as D2.
48
Q

what are Dopaminergic tracts?

A
  • nigrostriatal tract
  • mesolimbic-mesocortical tract
  • tuberoinfundibular tract
49
Q

nigrostriatal tract

A
50
Q

mesolimbic-mesocortical tract

A
51
Q

tuberoinfundibular tract

A
52
Q

Synthesis of Serotonin

A
53
Q

Levels of serotonin and assossiated behavioral changes

A
54
Q

site of serotonergic cell bodies

A
55
Q

Antidepressants and serotonin

A
56
Q

Significance of Norepinephrine

A
  • As a catecholamine, it plays a role in mood anxiety, arousal learning, and memory.
57
Q

Synthesis of Norepinephrine

A
58
Q

Site of Noradrenergic Neurons

A

Most of them (Approximately 10000 per hemisphere) are located in the locus cerelus in brainstem.

59
Q

Serotonin & associated Psychopathology

A
60
Q

NE & associated Psychopathology

A
61
Q

Dopamine & associated Psychopathology

A
62
Q

Characters of Histamine

A
  • It’s an ethylamine
  • affected by psychoactive drugs.
63
Q

Significance of Histamine

A

Histamine receptor blockade with drugs such as antipsychotics and tricyclic antidepressants is associated with common side effects of these drugs such as:

  • sedation
  • Increases appetite leading to weight gain.
64
Q

Characters of acetylcholine

A
  • quaternary amine
  • it’s the transmitter used by nerve-skeleton-muscle junctions
65
Q

Synthesis & Degradation of acetylcholine

A
66
Q

Degeneration of cholinergic neurons is associated with ……….

A

Alzheimer disease, Down’s syndrome, and movement and sleep disorders (e.g., decreased REM sleep)

67
Q

Blocking the action of AchE with drugs such as …….. may ………..

A
  • donepezil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl)
  • delay the progression of Alzheimer disease but cannot reverse the function already lost.
68
Q

Blockade of muscarinic Ach receptors with drugs such as antipsychotics and Tricyclic antidepressants results in:

A
  • the classic “anticholinergic” adverse effects seen with the use of these drugs, including dry mouth, blurred vision, urinary hesitancy, and constipation.
  • central anticholinergic effects such as confusion and memory problems.
69
Q

Anticholinergic agents are commonly used to treat the ……… caused by antipsychotic agents.

A

Parkinson-like symptoms caused by

70
Q

Significance of Glutamate

A
  • It’s an excitatory neurotransmitter
  • It contributes to the pathophysiology of neurodegenerative illnesses such as Alzheimer’s disease and schizophrenia.
71
Q

Role of Glutamate in AD

A

The mechanism of this association involves:

  1. activation of the glutamate receptor N-methyl-d-aspartate (NMDA) by sustained elevation o glutamate.
  2. Such activation results in calcium ions entering neurons leading to nerve cell degeneration and death through excitotoxicity.
72
Q

How to treat AD using Memantine?

A

Memantine (Namenda), an NMDA receptor antagonist:

  • ultimately blocks this influx of calcium.
  • indicated for patients with moderate to severe Alzheimer’s disease.
73
Q

Synthesis of GABA

A
  • It is synthesized from glutamate by the enzyme glutamic acid decarboxylase, which needs vitamin B6 (pyridoxine) as a cofactor.
74
Q

…….. is the principal inhibitory neurotransmitter in the CNS.

A

GABA

75
Q

GABA is closely involved in the action of ……….. agents such as benzodiazepines (e.g., diazepam [Valium]) and barbiturates (e.g., secobarbital [Seconal])

A

antianxiety

76
Q

GABA is closely involved in the action of antianxiety agents such as benzodiazepines (e.g., diazepam [Valium]) and barbiturates (e.g., secobarbital [Seconal]) how?

A
77
Q

Endogenous opiods

A
  • Endogenous opioids such as enkephalins, endorphins, dynorphins, and endomorphins are produced by the brain itself.
  • They act to pain and anxiety and have a role in addiction and mood.
78
Q

Placebo effects & Neuropeptides

A
  • Placebo effects may be mediated by the endogenous opioid system. For example, prior treatment with an opioid receptor blocker such as naloxone can block placebo effects.
79
Q

Done

A

✅

Y3R3 - Behavior ⚛️ (7 decks)

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