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Psych MCQs > Neuroanatomy + Neurochemistry > Flashcards

Neuroanatomy + Neurochemistry Flashcards

1
Q

Pupillary light reflex

A

Some light travels directly to pretectal area (not LGN), to Edinger-Westphal nuclei, which controls pupillary constriction via CN III.

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2
Q

Visual pathway

A

Optic nerve -> optic chiasm -> optic tract -> lateral geniculate nucleus (thalamus) -> visual cortex (posterior occipital lobe)

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3
Q

Basal ganglia - Components

A

= group of subcortical nuclei situated at base of forebrain and top of midbrain.

Components:
- Caudate + putamen (dorsal striatum)
- Nucleus accumbens + olfactory tubercle (ventral striatum)
- Globus pallidus
- Substantia nigra
- Subthalamic nucleus

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4
Q

Basal ganglia - Function

A

Associated with a number of functions including voluntary motor control, procedural learning, habit learning, conditional learning, eye movement, cognition, emotion.

The basal ganglia are inhibitory. They work with the cerebellum, which is excitatory, to allow smooth coordinated movement.

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5
Q

Basal ganglia - Neurotransmitters

A

Predominantly GABA-ergic efferent fibres, modulatory cholinergic fibres, and significant dopamine (in VTA and substantia nigra).

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6
Q

Nucleus accumbens

A

Component of the basal ganglia.
Involved in addiction.
Part of the reward pathway.

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7
Q

Hypothalamus - Function

A

Homeostasis

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8
Q

Hypothalamus - Inputs

A
  1. Nucleus of solitary tract (visceral sensation)
  2. Reticular formation (from spinal cord)
  3. Retina (from optic nerve)
  4. Circumventricular organs (monitor substances in blood)
  5. Limbic and olfactory systems
  6. Intrinsic receptors
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9
Q

Hypothalamus - Neural outputs

A

The lateral hypothalamus projects to lateral medulla, which contains cells involved in autonomic control. In this way, the hypothalamus can control HR, vasoconstriction, digestion, etc.

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10
Q

Hypothalamus - Endocrine outputs

A
  • Large hypothalamic cells send axons directly to posterior pituitary, where they can release oxytocin and vasopressin directly.
  • Smaller cells send axons to base of pituitary and release releasing factors into capillaries of anterior pituitary, which secretes hormones in response, such as TSH, ACTH, etc.
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11
Q

Orexin

A

Also called hypocretin.
Produced by lateral hypothalamus, but not during sleep.
Deficient in narcolepsy.

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12
Q

Medial preoptic nucleus

A

Part of hypothalamus.
Contains sexually dimorphic GnRH nucleus which releases gonadotrophic releasing hormone.

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13
Q

Supraoptic nucleus

A

Part of hypothalamus.
Releases oxytocin and vasopressin.

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14
Q

Paraventricular nucleus

A

Part of hypothalamus.
Releases oxytocin, vasopressin, and corticotrophin releasing hormone.

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15
Q

Anterior hypothalamic nucleus

A

Part of hypothalamus.
Involved in thermoregulation.

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16
Q

Suprachiasmatic nucleus.

A

Part of hypothalamus.
Involved in circadian rhythm (some fibres from optic nerve project here).
Releases vasopressin.

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17
Q

Ventromedial nucleus

A

Part of hypothalamus.
Involved in satiety, sexual behaviour.

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18
Q

Arcuate nucleus

A

Part of hypothalamus.
Involved in feeding.
Releases dopamine.

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19
Q

Lateral nucleus

A

Part of hypothalamus.
Involved in hunger, thirst.

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20
Q

Dorsomedial hypothalamic nucleus

A

Part of hypothalamus.
Involved in BP and HR.

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21
Q

Mammillary nuclei

A

Part of hypothalamus.
Act as a relay for impulses coming from the amygdala and hippocampus, via the mamillothalamic tract to the thalamus.
Therefore involved in memory.

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22
Q

Thalamus - Function

A

Regulation of sleep/wake
Processing/relaying of sensory information
Arousal/consciousness

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23
Q

Thalamus - Connections

A
  • to the hippocampus via mammillothalamic tract (mammillary bodies and fornix)
  • to cerebral cortex via thalamocortical tract
  • from spinal cord via lateral and anterior spinothalamic tracts
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24
Q

Thalamic syndome

A

Contralateral hemi-anaesthesia + mood swings

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25
Q

Frontal lobe - Function

A

“Action cortex”
Involved in actions such as skeletal and ocular movement, speech control, expression of emotions.
The prefrontal cortex is involved in reasoning.

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26
Q

Orbitofrontal syndrome

A

Impulsivity, disinhibition.
Also called pseudo-psychopathy, Witzelsucht.

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27
Q

Mediofrontal syndrome

A

Apathy, akinetic mutism

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28
Q

Dorsolateral frontal syndrome

A

Impaired executive function

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29
Q

Tests of frontal lobe function

A
  • finger tapping
  • design or verbal fluency
  • Wisconsin card sorting test
  • tests of language, numeracy or decision making
  • Stroop test
  • Tower of London
  • trail-kaing
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30
Q

Anterior cingulate

A

Part of frontal lobe
Involved in detection of errors, anticipation and preparation for tasks, emotion regulation.
Involved in mood disorders.

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31
Q

Broca’s area

A

Dominant inferior frontal cortex
Involved in generation of speech

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32
Q

Non-dominant dorsolateral/orbitofrontal cortex & insula

A

Depersonalisation

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33
Q

Temporal lobe - Function

A

Involved in processing sensory information.
- Visual memories (communicates to hippocampus, mediated by amygdala)
- Processing auditory (primary auditory cortex and superior temporal gyrus) and visual (ventral temporal cortex) input
- Language recognition
- New memories (hippocampi in medial temporal lobe)

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34
Q

Fusiform gyrus

A

Recognition of faces (prosopagnosia).
In temporal lobe.

35
Q

Parahippocampal gyrus

A

Recognition of scenes
In temporal lobe

36
Q

Wernicke’s area

A

In dominant temporal lobe
Brodmann area 22
Language comprehension

37
Q

Mediobasal temporal lobe

A

Deja vu/jamais vu

38
Q

Uncus

A

Olfactory hallucinations originate from here.
Common origin of temporal lobe epilepsy.
Lies next to the parahippocampal gyrus, which contains primary olfactory cortex.

39
Q

Parietal lobe - Function

A

Integrates sensory information from various modalities (spatial sense, proprioception) and involved in language processing.
Functions include two-point discrimination, graphaesthesia, touch localisation.

40
Q

Unilateral parietal lobe lesion

A

Contralateral hemianaesthesia
Agraphaesthesia
Contralateral homonymous hemianopia
Contralateral extinction phenomenon (unable to perceive one of two simultaneously presented stimuli in same sensory modality)
Sensory seizures

41
Q

Lesion of dominant parietal lobe

A

Dysphasia/aphasia
Dyslexia
Apraxia
Gerstmann syndrome (agraphia, acalculia, left-right disorientation, finger agnosia)

42
Q

Lesion of non-dominant parietal lobe

A

Spatial disorientation
Constructional apraxia
Dressing apraxia
Anosognosia (lack of insight)

43
Q

Lesions of bilateral parietal lobes

A

Balint’s syndrome = simultanagnosia, optic ataxia, oculomotor ataxia

44
Q

Lesion of unilateral occipital lobe

A

Homonymous hemianopia

45
Q

Parieto-temporal-occipital association area

A

Lesion leads to colour agnosia, movement agnosia, agraphia.

46
Q

Cerebellum - Function

A

Motor control, particularly coordination, precision, accurate timing.

47
Q

Inferior olivary nucleus

A

In medulla
Coordinates signals from cerebellum to regulate coordination and learning
Receives inhibitory signals via GABA

48
Q

Cerebellum - Tests

A

Gait (ataxia)
Finger-pointing
Dysdiadachokinesia

49
Q

Subthalamic nucleus

A

Located at junction of midbrain and diencephlon
Functions as part of basal ganglia
Contains glutaminergic neurons which project to globus pallidus
Lesion leads to contralateral hemiballismus

50
Q

Brainstem - Components

A
  1. Midbrain - includes substantia nigra, reticular formation (contains locus coeruleus), ventral tegmental area
  2. Pons
  3. Medulla
51
Q

Ventral tegmental area

A

Located in midbrain
Projects throughout brain (mesocortical and mesolimbic pathways)
Part of reward pathway
Contains dopaminergic, GABAergic and glutamatergic neurons

52
Q

Locus coeruleus

A

Located in reticular formation in midbrain
Involved in intensive alertness and autonomic reflexes
Contains noradrenergic neurons

53
Q

Mesolimbic pathway

A

= the reward pathway.
Dopaminergic.
Connects the VTA (midbrain) to ventral striatum (basal ganglia).
Regulates incentive salience, facilitates reinforcement and reward-related motor function learning.

54
Q

Clinical significance of Mesolimbic pathway

A
  • Addiction
  • Schizophrenia (increased dopamine in this pathway is linked to positive symptoms)
  • Also implicated in depression and Parkinson’s
55
Q

Mesocortical pathway

A

Dopaminergic pathway.
Connects VTA to prefrontal cortex:
- Ventromedial prefrontal cortex (mood)
- Dorsolateral prefrontal cortex (executive function and cognition)
Involved in cognitive control, motivation, emotional response.

56
Q

Nigrostriatal pathway

A

Bilateral dopaminergic pathway.
Connects substantia nigra (midbrain) to dorsal striatum (caudate + putamen, in basal ganglia).
Part of the basal ganglia motor loop involved in production of movement.

57
Q

Clinical significance of Nigrostriatal pathway

A
  • Parkinson’s (degeneration of dopaminergic neurons in substantia nigra reduces dopamine function, with resulting motor deficits)
  • Schizophrenia (presynaptic dopamine metabolism altered, antipsychotics can cause EPSE/parkinsonism)
58
Q

Tuberoinfundibular pathway

A

Dopaminergic pathway.
Connects the arcuate nucleus (hypothalamus) to median eminence.
Dopamine released inhibits prolactin secretion, so antipsychotics which block this pathway will cause increased PL.

59
Q

Neurotransmitters

A

Signaling molecules secreted by a neuron to affect another cell. Generally synthesised in neurons from precursor molecules. Released in response to action potential from synaptic vesicles into synaptic cleft, where they can interact with receptors on target cell.

60
Q

Metabotropic receptor

A

G-protein-coupled receptor
Initiates a number of metabolic steps to modulate cell activity
Indirectly linked with ion channels through signal transduction molecules (such as G proteins)

61
Q

Ionotropic receptor

A

Ligand-gated ion channels
Allow ions to pass through in response to neurotransmitter binding

62
Q

Neuromediator

A

Also called second messenger.
Postsynaptic compound that participates in generation of postsynaptic responses.
For example; cGMP cAMP

63
Q

Neurotrophin

A

Released by postsynaptic structures to maintain the presynaptic neuronal structure

64
Q

Neuromodulator

A

Originate from non-synaptic sites
Influence neuronal activity
For example; steroid hormones

65
Q

Neurohormone

A

Peptide secreted directly into bloodstream, that acts on other neurons
For example; pituitary hormones

66
Q

Glutamate

A
  • Most prevalent neurotransmitter
  • Excitatory
  • Amino acid
  • Excessive glutamate release can cause overstimulation and excitotoxicity
  • Metabotropic receptors: metabotropic glutamate receptors
  • Ionotropic receptors: NMDA, kainate, AMPARs
67
Q

GABA

A
  • Second most prevalent neurotransmitter
  • Inhibitory
  • Amino acid
  • Metabotropic receptors: GABA-B
  • Ionotropic receptors: GABA-A, GABA-A-p
68
Q

Acetylcholine

A
  • Activates skeletal muscle, either excites or inhibits viscera in autonomic system, acts centrally in brain
  • Metabotropic receptors: muscarinic ACh
  • Ionotropic receptors: nicotinic ACh
  • Primary source is nucleus basalis of Meynert (NBM)
69
Q

Dopamine

A
  • Monoamine
  • Involved in regulation of motor behaviour, motivation/reward, emotional arousal
  • Low in Parkinson’s, high in schizophrenia
  • Metabotropic receptors: dopamine receptor, TAARI
70
Q

Serotonin

A
  • Monoamine
  • 90% found in intestine in enterochromaffin cells, with remainder in CNS
  • Involved in appetite, sleep, learning/memory, mood, behaviour
  • Metabotropic receptors: 5-HT1, 2, 4, 5, 6, 7
  • Ionotropic receptors: 5-HT3
71
Q

Noradrenaline

A
  • Monoamine
  • Synthesised from tyrosine in CNS and sympathetic nerves
  • Primary source is locus coeruleus
  • Modulates autonomic nervous system, sleep patterns, alertness
  • Metabotropic receptors: adrenergic receptors
72
Q

Adrenaline

A
  • Monoamine
  • Synthesised from tyrosine, released in adrenal glands and brainstem
  • Involved in sleep, alertness, fight-or-flight
  • Metabotropic receptors: adrenergic receptors
73
Q

Ghrelin

A

Neuropeptide
Produced in stomach
Promotes hunger

74
Q

Leptin

A

Neuropeptide
Produced by adipose
Reduces hunger

75
Q

BDNF

A

Neurotrophin
Helps support neuron survival and differentiation of new neurons/synapses
Decreased by stress
Increased by exercise, SSRIs

76
Q

Neurotransmitter metabolism

A

First step usually hydroxylation.
This is followed by decarboxylation.
Feedback mechanisms to balance excitation and inhibition.

77
Q

Dopamine metabolism

A

L-phenylalanine converted by phenylalanine hydroxylase to L-tyrosine, which is converted by tyrosine hydroxylase to L-dopa (rate limiting step), which is converted by dopa decarboxylase to dopamine.

78
Q

Dopamine breakdown

A

Dopamine is converted to inactive metabolites by, MAO-A, MAO-B (inhibited by seligline) and COMT (note diGeorge syndrome). These are further broken down to metanephrines and normetanephrines by aldehyde dehyroxylase.

Dopamine is also converted by dopamine beta-hydroxylase to noradrenaline, which is converted by PNMT, with SAMe as co-factor, to adrenaline.

79
Q

Glycine metabolism

A

Serine is converted to glycine (excitatory), by serine transhydroxymethylase, with pyridoxal phosphate as co-factor.

80
Q

Glutamate/GABA metabolism

A

Glutamate is converted by glutamate decarboxylase to GABA, with pyridoxal phosphate as co-factor.

GABA is converted back to glutamate via GABA shunt pathway.

81
Q

Serotonin metabolism

A

Ingestion of tryptophan is the rate-limited step. Tryptophan is converted by tryptophan hydroxylase to 5-HTP, which is converted by 5-HTP decarboxylase to serotonin. Serotonin is then converted by MAO-A to 5-HIAA.

[Note low MAO-A levels associated with conduct issues. Low 5-HIAA levels associated with aggression, eating disorders, suicide attempts.]

82
Q

Basal ganglia pathology

A
  • Huntington’s chorea (caudate nucleus)
  • Wilson’s disease (copper deposition in putamen + globus pallidus (lenticular))
  • Parkinson’s disease (substantia nigra)
  • Hemiballism (subthalamic nucleus)
83
Q

Caudate - blood supply

A

Anterior and middle cerebral arteries.

The symptoms and signs from caudate infarctions vary but behavioural symptoms, especially abulia and agitation, loss of executive abilities, and motor weakness are most common.

Psych MCQs (10 decks)

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