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PSY 2120 > Neuroanatomy and Antidepressants > Flashcards

Neuroanatomy and Antidepressants Flashcards

1
Q

Effects of MAOIs

A 
tremors
weight gain
blurred vision
dry mouth
low blood pressure
postural hypotension
first were non-selective and irreversible; this has changed
the "Cheese Effect:
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2
Q

Serotonin Syndrome

A

can be brought on by any antidepressant (AD)
consequence of too much 5-HT
Clinical triad of symptoms
1. Cognitive: headaches, agitation, hypomania, hallucinations, coma
2. Autonomic: sweating, hyperthermia, tachycardia, vasoconstriction, nausea
3. Somatic: myoclonus, hyperreflexia, tremors
can be life-threatening

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3
Q

Effects of TCAs

A

increase ANS function (via anticholinergic effects)
- inhibit the PNS, resulting in dry mouth, constipation, blurred vision, tremors, and sweating
Adrenergic receptor function impaired, resulting in dizziness
Histamine receptor impairment results in a sweet-tooth

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4
Q

Effects of 3rd Generation ADs (SNRIs and Atypicals)

A

antagonism of ACh and histamine receptor activity
enhancement of 5-HT2-3 receptor activity

increase appetite
weight gain
increased BP (blood pressure)
dizziness
dry mouth 
GI problems
etc.
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5
Q

Major Affective Disorders

A

aka mood disorders
characterized by: disordered feelings and disturbances in mood/emotion

2 types:
MDD: depression without mania
Bipolar Disorder: alternating mania and depression

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6
Q

DSM-5 diagnosis of MDD

A

symptoms must be present for at least two weeks, for a substantial portion of the day, every day
there must be a change from previous function
there must be one of either depressed mood or loss of interest
change in appetite and/or weight
sleep and/or psychomotor disturbances
tired/devoid of energy
worthlessness and unwarranted guilt
trouble focussing/thinking clearly/making decisions
thought and/or plans of suicide

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7
Q

Monoamine Theory of Depression

A

mood related to the functioning of monoamine systems, especially 5-HT, NE and DA
increased monoamine levels through cocaine and amphetamine make people feel good, the decrease results in depressive symptoms
Parkinson’s occurs alongside low monoamine levels, and depression rates are abnormally high in that population
the drug Reserpine blocks VMAT (monoamine transporter), and people who were treated with Reserpine developed severe MDD

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8
Q

Glucocorticoid Theory of Depression

A

clinical depression as a consequence of disregulated HPA axis
patients with MDD often have hypercortisolemia
- cortisol normally serves as a negative feedback,
inhibiting the release of CRH and ACTH by acting on
the hypothalamus, pituitary, hippocampus, amygdala,
and cortex
receptors are dynamic, so if cortisol is always present in excess, the receptor population may change, leading to neuronal and structural (and functional) neuroanatomic changes
can work with other theory: chronic stress altering neuroanatomy and monoamine production

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9
Q

Neurophysiology of MAOIs

A

inhibit the activity of MAO
- prevents molecules of DA, NE, and 5-HT from being
destroyed in the cytoplasm when they leak from
vesicles
effect is not limited to the CNS (can have side effects)

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10
Q

Neurophysiology of SSRIs

A

block reuptake of 5-HT without many effects on other monoamine or NT systems

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11
Q

Neurophysiology of SNRIs

A

block reuptake of 5-HT and NE
sometimes can block DA reuptake as well
minimal effects on other NT systems

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12
Q

Neurophysiology of Atypical ADs

A

mechanism of action varies depending on the drug

e.g. can antagonize 5-HT autoreceptors

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13
Q

Antidepressant Absorption

A

first pass metabolism destroys a significant portion of the dose of most ADs
- physicians account for this because most ADs are
taken orally
- this effect is inhibited by alcohol, and is part of the
reason it is dangerous to drink, especially on first and
second gen. ADs

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14
Q

Cheese Effect

A

can occur in MAOI users
MAO is required for the breakdown of the AA tyramine
tyramine found in aged food (e.g. cheese)
excess tyramine causes symptoms mimicking an overactive SNS: sweating, nausea, increased BP, internal bleeding, stroke, death

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15
Q

Effects of SSRIs

A 
far fewer side effects than previous ADs
nausea
GI problems
headache
dizziness
sweating
nervousness
agitation

tolerance develops quickly through effects on 5-HT2 receptors

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16
Q

Serotonin Discontinuation Syndrome

A

to avoid, when coming off ADs, decrease dose gradually
lasts on average 1-4 weeks, but can be sever/extended with certain drugs
must be on an AD for at least 4 weeks for this to occur

flu-like symptoms
sleep disturbances
sensorimotor disturbances
mood disturbances
cognitive disturbances
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17
Q

Skull and Vertebral Column

A

bone protecting the CNS

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18
Q

Inferior

A

below (ventral to) something

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19
Q

Rostral

A

toward the beak (anterior)

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20
Q

Caudal

A

towards the tail (posterior)

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21
Q

Coronal Section

A

frontal view into the brain

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22
Q

Horizontal Section

A

dorsal view (top down into brain)

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23
Q

Sagittal Section

A

medial view (side view central into brain)

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24
Q

White Matter

A

collections of myelinated axons

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25
Q

Grey Matter

A

collections of cell bodies and dendrites

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26
Q

Contralateral

A

2 distinct structures on opposite sides

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27
Q

Ipsilateral

A

2 structures on the same side

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28
Q

Medial

A

toward the midline of the brain

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29
Q

Lateral

A

away from the midline, outside

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30
Q

Afferent

A

moving toward the point of reference (usually the CNS in neuroscience)

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31
Q

Efferent

A

moving away from the point of reference (usually the CNS in neuroscience)

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32
Q

Nucleus

A

collection of cell bodies in CNS

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33
Q

Ganglion

A

collection of cell bodies in PNS

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34
Q

Tract

A

collection of axons in CNS

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35
Q

Nerve

A

collection of axons in PNS

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36
Q

Cortex

A

4 lobes

Frontal, parietal, temporal, occipital

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37
Q

Motor Cortex

A

behind frontal lobe, on precentral gyrus

responsible for movement

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38
Q

Sensory Cortex

A

responsible for sensations

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39
Q

Occipital Lobe

A

responsible for vision

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40
Q

Temporal Lobe

A

responsible for memory, understanding language

41
Q

Corpus Callosum

A

band of axons that connects corresponding parts of the association cortex of left and right hemispheres
matching cortices connect

42
Q

Primary Cortices

A

main location of a type of signal, subserve one particular function
e.g. primary motor cortex- touch and grab
primary auditory cortex- sounds
primary visual cortex- sight signals

43
Q

Amygdala

A

almond-shaped group of nuclei at the end of the hippocampus

responsible for emotions (especially fear and anger), emotional behaviour, and motivation

44
Q

Infundibulum/Pituitary Stalk

A

connects the hypothalamus to the pituitary glad

45
Q

HPA Axis

A

1) Stressful situation
2) Hypothalamus: CRH
3) Anterior Pituitary: ACTH
4) Adrenal Cortex: Corticosteroid (e.g. cortisol)
- creates a negative feedback loop

46
Q

Cerebellum

A

receives sensory info, spinal cord and brain info
regulates voluntary motor movements (e.g. posture, balance, coordination, speech)
Mild damage = jerky movement
Severe damage = loss of balance/posture

47
Q

Reticular Activating System

A

Ascending reticular formation
filter/prioritizes sensory information
habituation (ignoring repetitive/meaningless stimuli)
- disregulation contributes to psychosis
behavioural arousal
consciousness

48
Q

Medulla Oblongata

A

most caudal portion of the brain stem
borders rostral end of spinal cord
contains nuclei that act as control centres for ANS
- vital functions: breathing, heart rate, temperature
control, etc.
damage usually results in rapid death

49
Q

Spinal Cord

A

responsible for exchange between CNS and PNS
distributes motor fibres to effector organs
collects somatosensory info for the brain
has some autonomy from the brain (e.g. reflexive circuits)

50
Q

Somatic Nervous System

A

controls voluntary motor outputs
comprised of sensory neurons (conveys information from 5 senses)
motor neurons (impulses from CNS to skeletal muscles)

51
Q

Autonomic Nervous System

A

sensory neurons in visceral organs
motor neurons to smooth muscle, cardiac muscle, glands

2 functional divisions

 - sympathetic: fight or flight
 - parasympathetic: rest and digest

CNS- Preganglionic neuron- Autonomic ganglion- Postganglionic neuron- Target tissue

52
Q

Structural/Functional Abnormalities in Depressed Brains

A

hyperactive amygdala

reduced pre-frontal cortex, hippocampus, and nucleus accumbens

53
Q

Types of Antidepressants

A

most work by increasing activity in 1+ monoamine system(s)
classified by principle mechanism of action

  1. MAOIs and TCAs
  2. SSRIs
  3. SNRIs and Atypicals
54
Q

Neurophysiology of TCAs

A

block reuptake (main form of daectivation) of 5-HT and NE
also affects other NT systems
e.g. antagonises muscarinic, histamine and A-1
adrenergic receptors
non-specific = many unwanted side effects

55
Q

Pharmacokinetics of MAOIs

A

Absorption: widely varied time
Distribution: readily cross BBB
Metabolism: mostly in liver
Elimination: Half-life of 2-4 hours

56
Q

Pharmacokinetics of TCAs

A

Absorption: 1-3 hours
Distribution: high bioavailabilit; readily cross BBB
Metabolism: in liver
Elimination: Half-life of 24 hours

57
Q

Pharmacokinetics of 2nd and 3rd Generation ADs

A

Absorption: 4-8 hours
Distribution: high bioavailability
Metabolism: in liver
Elimination: Half-life of less than 24 hours

58
Q

Parasympathetic Nervous System (PNS) Pathway

A
  1. Craniosacral division (nerves at top & bottom of spine)
  2. Pre-ganglionic axon terminals release ACh (long axon)
  3. Post ganglionic neuron releases ACh or NO (short axon)
59
Q

Functions of the NS

A

relay info (sensory system [afferent])
- sensory neurons
interpret/make decisions (association system)
- interneurons
carry out some action (motor system [efferent])
- motor neurons

60
Q

Dura Mater

A

tough outer layer of meninges

made of fibrous tissue

61
Q

Arachnoid Layer

A

like a spider web
thin sheet of delicate connective tissue
between dura and pia mater

62
Q

Pia Mater

A

moderately tough inner layer of meninges

clings directly to brain’s surface

63
Q

Ventricular System

A

hollow, interconnected chambers in brain
made up of 2 lateral ventricles, 3rd ventricle, 4th ventricle, interventricular foramen, cerebral aqueduct and the central canal
the Choroid Plexis produces CSF
filled with CSF

64
Q

Interventricular Foramen

A

connects lateral and third ventricles

65
Q

Flow of CSF

A

3 openings above the 4th ventricle allow CSF to flow outside and recirculate
- Foramen of Magendie
- 2 Lateral foramina of Luschka
Ends up being absorbed by bloodstream

66
Q

Frontal Lobe

A 
front of brain
motor cortex
responsible for executive functions (thinking, planning, organising, etc.)
emotional and behavioural control
personality
67
Q

Parietal Lobe

A

Responsible for…
perception, making sense of the world
arithmetic
spelling

68
Q

Central Sulcus

A

Major valley in centre of brain

Separates frontal and parietal lobes

69
Q

Lateral Fissure

A

predominant sulcus in brain

front bottom up diagonally

70
Q

Precentral Gyrus

A

primary motor cortex

71
Q

Postcentral Gyrus

A

somatosensory cortex

72
Q

Longitudinal Fissure

A

Separates left and right brain hemispheres

73
Q

Sensory Association Cortices

A

receives information from adjacent primary sensory area
analyzes info received
e.g. the visual association cortex analyzes shape, size, orientation, colour, etc

74
Q

Multimodal Association Cortex

A

analyzes and interprets sensory experiences
provides perceptions, memory, reasoning, verbalization, judgement, and emotions
integrates senses
directs information to appropriate area for response

75
Q

Forebrain

A

Lateral

 - Cerebral Cortex
 - Basal Ganglia
 - Limbic System

Third Ventricle

 - Thalamus
 - Hypothalamus
76
Q

Basal Ganglia

A

3 components

 1. Caudate Nucleus
 2. Putamen
 3. Globus Pallidus

Striatum (combo of 1 &2) is the major input centre
main function is motor control
also responsible for motor learning, executive function/behaviour and emotions
Parkinson’s disease occurs when messenger neurons for Basal Ganglia are damaged

77
Q

Limbic System

A

hippocampus and amygdala

responsible for emotion and memory

78
Q

Hippocampus

A

beneath the cortex of the temporal lobe

mainly responsible for memory

79
Q

Thalamus

A 
2 distinct lobes
     - 1 per hemisphere (contralateral)
     - connected by massa intermedia
primary sensory cortex
     - relays sensory info from receptors to proper brain 
     area    
sleep, consciousness, alertness
80
Q

Hypothalamus

A

control over 4 Fs: fight, flee, feed, mate
controls ANS
controls endocrine system

81
Q

Anterior Pituitary Gland

A

hypothalamus creates hormone directly delivered to anterior pituitary via local blood circuits
anterior pituitary produces hormones and releases them into the bloodstream
- e.g. HPA axis
secretion of these hormones is regulated by hypothalamus

82
Q

Tegmentum

A

includes many structures…
reticular formation (rostral): consciousness
nuclei: eye movements
periaqueductal grey matter: pain modulation
red nucleus: motor coordination
substantia nigra: DA system (to striatum), reward & movement
ventral tegmental area: point of origin for mesolimbic and mesocortical dopaminergic pathways

83
Q

Posterior Pituitary

A

neural tissue; an extension of the hypothalamus
hypothalamus produces posterior pituitary hormones and directly controls their secretion
oxytocin: milk, contractions (birth)
vasopressin (ADH): urine output
neurosecretory cells’ axon terminals are in the posterior pituitary and secrete peptide hormones
- these are picked up by capillaries and go into general
circulation

84
Q

Midbrain

A

surrounding cerebral aqueduct

tectum: dorsal to cerebral aqueduct
tegmentum: ventral to cerebral aqueduct

mesencephalon

85
Q

Brainstem

A

part of the midbrain and part of hindbrain but not all

collectively

 - tegmentum
 - pons
 - medulla
86
Q

Hindbrain

A

fourth ventricle region
Cerebellum
Pons
Medulla Oblongata

87
Q

Pons

A 
bulge in brain stem
contains portion of reticular formation
functionally connects cerebellum and cortex
Influences ANS functions
heart rate
blood pressure
respiration
88
Q

Reticulospinal Tracts

A 
Descending reticular formation
Affects ANS activity (breathing, BP, etc)
Reflexes (e.g. coughing)
Posture
Balance
Motor Control
89
Q

Components of the Spinal Cord

A 
Vertebral column: bony cage
Central canal: filled with CSF
White matter: myelinated axons
Grey matter: unmyelinated axons and soma
Motoneuron: ventral
Sensory neuron: dorsal
31 pairs of mixed spinal nerves
90
Q

Peripheral Nervous System

A

means through which the brain and spinal cord communicate with the rest of the body (cranial and spinal nerves)
conveys sensory info to CNS
conveys motor info from CNS to effectors

91
Q

Sympathetic Nervous System Pathway

A
  1. Nerves leave/enter CNS in thoracicolumbar region (centre of spine)
  2. Pre-ganglionic neurons release ACh (short)
  3. Post-ganglionic neuron (long) releases NE
92
Q

Tectum

A

Superior (top) Colliculi: visual system

Inferior (bottom) Colliculi: auditory system

93
Q

Tolerance to ADs

A

therapeutic effectiveness may show some tolerance after a few months
- extent and clinical significance unclear
tolerance to many side effects occurs within several weeks
- except tiredness with SSRIs

94
Q

Withdrawal from TCAs

A 
DO NOT ABRUPTLY DISCONTINUE
restlessness
anxiety
chills
akathesia (compulsion to move)
muscle aches
95
Q

Withdrawal from SSRIs

A 
DO NOT ABRUPTLY DISCONTINUE
dizziness
lightheadedness
insomnia
fatigue
anxiety
nausea
headache
sensory disturbances
96
Q

Withdrawal from SNRIs

A

DO NOT ABRUPTLY DISCONTINUE
heart palpitations
nausea
delusions

97
Q

Problem with Monoamine Theory of Depression

A

lag time between the start of antidepressant treatment and any alleviation of depressive symptoms (4-6 weeks, up to 12)

98
Q

Effectiveness in Treating Depression

A

efficacy roughly similar for all classes of ADs
significant individual differences and different types of depression respond differently
60-70% of individuals with MDD get relief from some symptoms
30-50% show full remission

99
Q

Limitations in AD Effectiveness and Development

A

All ADs have lengthy response time
- clinically significant effects occur after 2 weeks of
treatment
- full effects after 4 weeks (time for downstream
neuroadaptive effects to occur)
Treatment-resistant depression
- successive failed attempts at significant sympton
reduction
- 29-46% of patients

PSY 2120 (4 decks)

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