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PHRM 100 – APPP > APPP Quiz – Neuro > Flashcards

APPP Quiz – Neuro Flashcards

1
Q

What are the major cell types of the CNS? (3)

A
  • neurons
  • glial cells
  • cells of the blood-brain barrier (BBB)
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2
Q

What does myelination result in? (2)

A
  • increase in speed of nerve conduction (due to insulation)
  • accumulation of voltage-gated Na+ channels at nodes of Ranvier (gaps on axon in between myelin sheaths)
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3
Q

What is multiple sclerosis (MS)?

  • Symptoms
  • Treatment
A

immune-mediated destruction of myelin that results in interrupted electrical nerve signals

  • most common demyelinating disease of CNS
  • symptoms: numbness, weakness, cognitive difficulties
  • treatment: aim to slow disease progression and improve quality of life / high-dose corticosteroids are used to dampen inflammation
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4
Q

How do metabotropic receptors act?

A
  • respond to neurotransmitters
  • indirectly opens ion channels
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5
Q

Describe the membrane potential at resting state and the channels and transporters at work.

A
  • RMP = -70 mV
  • all voltage-gated Na+ channels and most voltage-gated K+ channels closed
  • Na+/K+ transporter actively pumps K+ ions into cell and Na+ ions out to maintain resting levels
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6
Q

Describe voltage-gated Na+ channels.

A
  • open at -55 mV
  • inactivated at +40 mV
  • Na+ flows in when open
  • cause depolarization
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7
Q

Describe voltage-gated K+ channels.

A
  • slow to open
  • K+ flows out when open
  • cause hyperpolarization
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8
Q

How does synaptic transmission occur?

A

generation of AP

  1. ligands bind receptors on post-synaptic neuron (ligand-gated ion channel or metabotropic receptor)
  2. ion channels open, which changes ion concentration and therefore membrane potential (from resting -70 mV)
  3. when net charge increases to -55 mV, voltage-gated Na+ channels open
  4. concentration of Na+ channels at axon hillock initiates AP
  5. depolarization spreads down axon, and repolarization follows
  6. depolarization of pre-synaptic terminal opens Ca2+ channels
  7. Ca2+ binds to SNARE proteins, which triggers the complete fusion of the vesicle with the target membrane
  8. neurotransmitters in vesicles at the terminal bouton are released into the synaptic cleft, which causes activation or inhibition
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9
Q

How does vesicle loading occur?

A
  • carrier vesicles containing membrane transporter proteins are moved along microtubules
  • small molecules (ie. acetylcholine) produced in the cell are taken into vesicles
  • loaded vesicles are stored at pre-synaptic membrane
  • depolarization leads to docking of vesicles and exocytosis into synapse
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10
Q

What are the neurotransmitters in the CNS? (9)

A
  • dopamine
  • norepinephrine
  • serotonin
  • acetylcholine
  • GABA
  • glutamate
  • glycine
  • histamine
  • orexin
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11
Q

Dopamine

  • Mechanism (Inhibitory or Excitatory)
  • Type (Monoamine, Amino Acid, or Neuropeptide)
A
  • inhibitory or excitatory
  • monoamine
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12
Q

Norepinephrine

  • Mechanism (Inhibitory or Excitatory)
  • Type (Monoamine, Amino Acid, or Neuropeptide)
A
  • inhibitory or excitatory
  • monoamine
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13
Q

Serotonin

  • Mechanism (Inhibitory or Excitatory)
  • Type (Monoamine, Amino Acid, or Neuropeptide)
A
  • inhibitory or excitatory
  • monoamine
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14
Q

Acetylcholine

  • Mechanism (Inhibitory or Excitatory)
  • Type (Monoamine, Amino Acid, or Neuropeptide)
A
  • inhibitory or excitatory
  • amino acid
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15
Q

GABA

  • Mechanism (Inhibitory or Excitatory)
  • Type (Monoamine, Amino Acid, or Neuropeptide)
A
  • inhibitory
  • amino acid
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16
Q

Glutamate

  • Mechanism (Inhibitory or Excitatory)
  • Type (Monoamine, Amino Acid, or Neuropeptide)
A
  • excitatory
  • amino acid
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17
Q

Glycine

  • Mechanism (Inhibitory or Excitatory)
  • Type (Monoamine, Amino Acid, or Neuropeptide)
A
  • inhibitory
  • amino acid
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18
Q

Histamine

  • Mechanism (Inhibitory or Excitatory)
  • Type (Monoamine, Amino Acid, or Neuropeptide)
A
  • inhibitory or excitatory
  • monoamine
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19
Q

Orexin

  • Mechanism (Inhibitory or Excitatory)
  • Type (Monoamine, Amino Acid, or Neuropeptide)
A
  • excitatory
  • neuropeptide
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20
Q

What forms the bulk of the brain?

A

cerebrum

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21
Q

What is the cerebral cortex made of?

A

grey matter

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22
Q

What are the 4 lobes of the cerebrum and their functions?

A

frontal:

  • contains motor areas
  • controls intellectual activities – ability to organize
  • personality, behaviour, and emotional control

parietal:

  • contains somatosensory areas
  • controls ability to read, write, and understand spatial relationships

temporal:

  • contains auditory areas
  • controls memory, speech, and comprehension

occipital:

  • contains visual areas
  • controls sight
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23
Q

What are the functions of the cerebrum? (5)

A
  • perception
  • higher motor functions
  • cognition
  • memory
  • emotion
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24
Q

What is the corpus callosum?

A

thick bundle of axons (nerve fibres) that ensures both sides of the brain (left and right cerebral hemispheres) can communicate and send signals to each other

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25
Q

What is the function of the limbic system and what are its 3 components?

A

involved in behavioural and emotional responses

  • hippocampus
  • amygdala
  • thalamas – and portion of hypothalamus (mammillary body)
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26
Q

What is the amygdala and what is its function?

A

region of the brain comprised of a group of nuclei (or cluster of neurons) that is primarily associated with emotional processes

  • involved in fear and other emotions related to aversive (unpleasant) stimuli, and fight or flight
  • now known to be involved in positive emotions elicited by appetitive (rewarding) stimuli
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27
Q

What is are the functions of the hippocampus?

A
  • processing of long-term memory, spatial navigation, regulation of hypothalamic function, and emotional responses
  • memory of the location of objects or people
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28
Q

What are the functions of the thalamus?

A

acts as a relay between a variety of subcortical areas and cerebral cortex

  • processing sensory and motor signals to relay to cerebral cortex
  • regulating consciousness, sleep, and alertness
  • every system (except olfactory) has a thalamic nucleus that receives sensory signals and sends them to the associated primary cortical area
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29
Q

What is the function of the hypothalamus?

A

coordinates hormonal and behavioural circadian rhythms, complex patterns of neuroendocrine outputs, and homeostatic mechanisms

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30
Q

Where is the brainstem?

A

connects the brain to the spinal cord and the rest of the body

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31
Q

What are the 3 parts of the brainstem and what are their functinos?

A

midbrain:

  • auditory and visual signals
  • arousal and human consciousness

pons:

  • carries signals that control basic functions (ie. sleep)

medulla:

  • controls involuntary functions (ie. breathing, heart rate)
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32
Q

How does the amygdala form associations (ie. good vs. bad)?

A

uses interconnections with limbic and sensory cortex – then triggers appropriate responses

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33
Q

What are the two different key nuclei of the amygdala and what are their functions?

A
  • lateral nucleus (LA): sensory interface of the amygdala – key site of plasticity
  • central nucleus (CE): viewed as the output region
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34
Q

What is the normal physiological state of the amygdala and how is it regulated?

A
  • balance between glutamate and GABA maintains emotional responses at the level appropriate to external stimuli
  • regulated by activation of either glutamatergic neurons or GABAergic neurons
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35
Q

What pathways associated with the amygdala can lead to fear memory formation?

A

auditory thalamic and prefrontal input pathways on the lateral nucleus (LA)

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36
Q

What can happen with amygdala dysfunction? (3)

A
  • anxiety disorders – generalized anxiety disorder, phobias, panic attacks, PTSD, etc.
  • seizures
  • pain conditions – ie. neuropathic pain
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37
Q

What are the treatments for amygdala dysfunction? (3)

A
  • benzodiazepines / anti-anxiety drugs (valium): enhances GABA-mediated synaptic inhibition, and increases inhibitory signals to balance activation
  • serotonin levels are low in patients with emotional disorders – enhanced glutamatergic activity in lateral nucleus (LA) of amygdala and potentiated fear behaviours
  • SSRIs: decreases amygdala response to fear and other aversive stimuli
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38
Q

What is the entorhinal cortex (EC) and what are the different parts?

A

the major input and output structure of the hippocampal formation

  • spatial information (WHERE) relays through medial entorhinal complex (MEC) – to parietal cortex
  • non-spatial information (WHAT) relays through lateral entorhinal cortex (LEC) – to temporal cortex
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39
Q

What type of neurons does the medial entorhinal complex (MEC) and lateral entorhinal cortex (LEC) contain?

A

cholinergic neurons (acetylcholine)

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40
Q

What neurotransmitter do hippocampal neurons mainly release?

A

glutamate or GABA

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41
Q

What are the 4 sections/sub-structures of the hippocampus?

A
  • MEC and LEC project into the hippocampus dentate gyrus (DG) region
  • project into CA3 region (cornu ammonis)
  • CA3 projects to CA2 and CA1
  • CA1 projects back to entorhinal cortex
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42
Q

What is Alzheimer’s disease?

A

progressive neurodegenerative disease most often associated with memory deficits and cognitive decline

  • damage and progressive loss of cholinergic neurons
  • LEC and MEC (hippocampus) contain cholinergic neurons
  • progressive memory impairment and cognitive dysfunction
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43
Q

What causes the damage to cholinergic neurons in Alzheimer’s disease?

A
  • Aβ plaques (generated from amyloid precursor protein cleavage)
  • Tau protein aggregates
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44
Q

What is the treatment for Alzheimer’s disease?

A

cholinesterase inhibitors – agents that block the breakdown of acetylcholine

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45
Q

Which 2 structures of the brain play an essential role in sleep-wake regulation and arousal?

A

thalamus and brainstem

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46
Q

The hypothalamus is important for communicating with what gland?

A

pituitary gland

  • one of the most important functions of the hypothalamus is linking the nervous system to the endocrine system via the pituitary gland
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47
Q

What can hypothalamus dysfunction cause?

A

appetite, temperature, and sleep disorders

  • hypothalamic obesity – can develop from major hypothalamic injury/damage affecting the centres of appetite regulation and energy balance
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48
Q

How does the reflex arc occur?

A
  • incoming sensory signals from the body (afferent sensory nerve fibres) synapse at posterior/dorsal horn with interneurons found in the intermediate grey
  • interneurons signal to efferent motor nerve fibres in anterior horn to stimulate muscle movement
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49
Q

Branches that Feed Into the brain

A
  1. AP travels through dorsal root ganglion (DRG) nerve fibre
  2. synapse at posterior/dorsal horn (PH)
  3. action on afferent nerves leading to actions at specific sites in the brain
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50
Q

Relay Signals from the Brain

A

efferent nerves from the cortex signal to anterior horn to stimulate motor movements

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51
Q

What system does the spinal cord link to?

A

autonomic system

  • intermediate grey matter contains autonomic neurons with axons that leave through ventral roots
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52
Q

How many bones does the skull have and what are the major ones?

A
  • 22 bones
  • cranial bones enclose and protect the brain – frontal, temporal, occipital, parietal, sphenoid, ethmoid
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53
Q

What is the function of the meninges?

A
  • form a major part of the mechanical suspension
  • necessary to keep CNS from self-destructing
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54
Q

What is the dura mater and what is its function?

A

thick connective tissue (abundant collagen) membrane

  • provides mechanical strength
  • connects skull to arachnoid cell layer
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55
Q

What is the arachnoid and what is its function?

A

thinner collagenous membrane

  • connects to pia mater cell layer by delicate strands of connective tissue (arachnoid trabeculae)
  • suspends CNS in its bath of CSF
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56
Q

What is the pia mater?

A

thinner collagenous membrane

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57
Q

What stabilizes the CNS during head movement?

A

partial flotation of CNS in subarachnoid CSF, in combination with mechanical suspension

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58
Q

How is CSF formed? Where does it enter circulation?

A
  • formed by filtration of blood
  • enters venous circulation through arachnoid villi
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59
Q

What are arachnoid villi and what are their function?

A

outpouchings that poke through holes in the walls of the venous system

  • act like valves
  • when CSF pressure is greater than venous pressure, CSF moves into venous system
  • when CSF pressure is less than venous pressure, villi snap shut and venous fluid does not enter subarachnoid space
  • imbalance can lead to intracranial pressure
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60
Q

What is an epidural hematoma?

A

bleeding between dura mater and skull

  • result of epidural bleeding due to skull fracture causing a blood vessel rupture
  • can lead to increased pressure on, and damage to, brain tissues
  • presents as severe headache, nausea and vomiting, slurred speech
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61
Q

What is a stroke?

A

lack of blood flow to the brain

  • result of subarachnoid bleeding due to spontaneous rupture of blood vessel
  • build-up of blood can cause pressure on the brain
  • symptoms are similar to epidural hematoma
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62
Q

What is the blood brain barrier (BBB) and what are its functions?

A

protective functional separation of the circulating blood from the CNS

  • limits the penetration of substances – keeps toxins and pathogens (and drugs) out, and facilitates select transport of molecules
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63
Q

What are the 4 layers of the BBB?

A
  • endothelial cell layer
  • pericyte layer
  • protecting basement membrane
  • glial barrier formed by astrocyte endfeet
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64
Q

What is the pericyte layer of the BBB and what is its function?

A

lines 80% of the capillary layer

  • stabilizes endothelial layer
  • regulates BBB permeability
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65
Q

What is the glial barrier of the BBB and what is its function?

A

formed by astrocyte endfeet

  • astrocytes interact with blood vessels with their endfeet and regulate dilation and constriction of microvessels to control blood flow
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66
Q

What do both the pericyte cell layer and glial barrier of the BBB contribute to?

A

maintenance and regulation of endothelial cell tight junctions (length, wide, and complexity)

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67
Q

What are the transport systems to cross the BBB? (3)

A

endothelial cell layer has specific transport systems that permit the supply of nutrients, ions, and bioactive molecules

  • diffusion of CO2 and O2 and lipid-soluble (small nonpolar) molecules (transcellular) or small water soluble (paracellular)
  • active transport – ie. glucose
  • receptor-mediated (ie. insulin) and adsorptive transcytosis (albumin)
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68
Q

What is key to proper BBB function?

A

maintenance and regulatino of endothelial cell tight junctions

69
Q

What does transport of drugs into the BBB often require?

A

requires the drug to engage specific transport mechanisms

  • ie. L-DOPA (precursor of dopamine) uses an amino acid transporter
70
Q

How can we reduce drug uptake in the brain?

A

if drugs are not desired in the brain, creating more polar compounds reduces uptake

  • ie. 2nd generation antihistamines cause less drowsiness
71
Q

What are the 3 support cells of CNS protection?

A
  • astrocyte
  • oligodendrocyte
  • microglia
72
Q

What are the functions of astrocytes?

A
  • role in BBB
  • provide nutrients to nerve cells
  • control chemical composition of fluids around nerve cells, enabling them to thrive
  • support or protection in stroke or trauma
  • blood flow, K+ housekeeper
73
Q

What are the functions of microglia?

A
  • help protect the brain against infection and help remove debris from dead cells
  • activation has been implicated in inflammatory alterations observed in severe neurodegenerative disease (Alzheimer’s, Parkinson’s, Huntington’s, MS, ALS) – these disorders share several pathological characteristics such as abnormal protein aggregation, failure in protein degradation pathways, and impaired axonal transport
74
Q

What are the 5 major structures of the basal ganglia (and their sub-structures)?

A
  • caudate nucleus (striatum)
  • putamen (striatum)
  • globus pallidus (GP) – GPe and GPi
  • subthalamic nucleus (STN)
  • substantia nigra (SN) – SNpc (contains dopaminergic neurons) and SNpr (considered a displaced piece of GPi)
75
Q

What are the functions of the basal ganglia?

A
  • work primarily by integrating signals from cerebral cortex and outputting to the thalamus
  • have a role in initiation of movements, thoughts, and motivations
76
Q

What are the main neurotransmitters involved with the basal ganglia? (4)

A
  • glutamate
  • acetylcholine
  • dopamine
  • GABA
77
Q

Direct Pathway (D1) of the Basal Ganglia

A

excitatory – motor initiation

  • striatum releases GABA at GPi/SNpr
  • GABA inhibits GPi/SNpr
  • GPi/SNpr does NOT release GABA at thalamus
  • thalamus is NOT inhibited
  • thalamus releases Glu at cerebral cortex
  • cerebral cortex is activated
  • cerebral cortex releases Glu to (1) spinal cord and brainstem, (2) SNpc, and (3) striatum
78
Q

Indirect Pathway (D2) of the Basal Ganglia

A

inhibitory – movement termination

  • striatum releases GABA at GPe
  • GPe is inhibited
  • GPe does NOT release GABA at STN
  • STN is activated
  • STN releases Glu at GPi/SNpr
  • GPi/SNpr GABAergic neurons are activated
  • GPi/SNpr releases GABA at thalamus
  • thalamus is inhibited
  • thalamus does NOT release Glu at cerebral cortex
  • cerebral cortex is not activated and does NOT release Glu at (1) spinal cord and brainstem, (2) SNpc, and (3) striatum
79
Q

What inputs does the striatum of the basal ganglia receive? (2)

A
  • excitatory glutamatergic input from cerebral cortex
  • dopaminergic input from SNpc
80
Q

How are the D1 (excitatory) or D2 (inhibitory) pathways activated?

A

Glu released from cerebral cortex to striatum stimulates interneurons, which use ACh as a neurotransmitter on the direct and indirect pathways

  • interneurons in striatum and neurons from SNpc connect with neurons in striatum
  • striatal neurons in direct pathway express excitatory D1 DA receptor and inhibitory M4 ACh receptor
  • striatal neurons in indirect pathway express inhibitory D2 DA receptor and excitatory M1 ACh receptor
81
Q

What is the function of dopamine on the basal ganglia?

A

SNpc provides dopaminergic innervation to striatal neurons and modulates the relative activity of the two pathways

  • increases activity of direct pathway – GABA release from striatum inhibits GPi/SNpr and no GABA is released at thalamus
  • decreases activity of indirect pathway – less Glu release from STN to GPi/SNpr results in less GABA release at thalamus
82
Q

What is Parkinson’s disease?

A

loss of dopaminergic neurons projecting from SNpc to striatum

  • direct pathway is less active
  • indirect pathway is more active
83
Q

What are the 4 characteristic signs of Parkinson’s disease that result from neuron loss?

A
  • bradykinesia – slowed movement
  • rigidity – increased resistance
  • tremor – rhythmic oscillatory movement around joints
  • gait/balance problems
84
Q

What are the treatments for Parkinson’s disease? (3)

A
  • levodopa – forms a dopamine that can cross BBB
  • early management with exercise and lifestyle
  • anticholinergics for mild symptoms

(most progress and levodopa is eventually required)

85
Q

What is Huntington’s disease?

A

loss of GABA neurons in striatum

  • region of striatum containing D2 neurons that project to GPe (indirect pathway) are affected earlier in disease progression
  • leads to loss of inhibition on GPe, therefore GABA is released at STN and there is less glutamatergic output to GPi (and less inhibitory release of GABA to thalamus, which releases excitatory Glu to cortex)
  • interneurons are largely unaffected
86
Q

What is the cause of Huntington’s disease?

A

autosomal dominant inherited disorder – mutation in Huntington gene (excessive CAG repeats)

  • results in abnormal protein, and therefore neuronal damage (cell death of striatal neurons)
87
Q

What are the signs and symptoms of Huntington’s disease? (8)

A
  • gradual onset of motor incoordination
  • movement disorder (jerk-like movements) – involuntary and irregular
  • progressive motor dysfunction
  • chorea – rapid, involuntary movements,
  • asthetosis – slow, writhing movement
  • ballism – flailing movements of limbs
  • cognitive decline – loss of spatial awareness
  • psychiatric disturbances – depression anxiety
88
Q

What is the treatment for Huntington’s disease?

A
  • tetrabenazine (inhibitors of VMAT2) – depletes dopamine and reduces severity of chorea

(nothing slows disease progression)

89
Q

Most of the information required for complex movements is generated by what?

A

basal ganglia and cerebellum, in coordination with motor cortex

90
Q

What is the function of the cerebellum? (4)

A
  • receives information from cerebral cortex and basal ganglia about body position
  • modifies motor commands of descending pathways to make movements more adaptive, smooth, and accurate by constantly adjusting muscle tone and posture (does NOT initiate commands)
  • interacts with vestibular nuclei (brainstem) that are connected with organs of the inner ear to provide a sense of balance
  • enables highly coordinated movements
91
Q

What are the 5 cell types of the cerebellum?

A
  • Purkinje cell
  • granualar cell
  • basket cell
  • stellate cell
  • Golgi cells
92
Q

What are Purkinje cells and what are their functions?

A

GABAergic neurons

  • form inhibitory synaptic connections on neurons in deep cerebellar nuclei
  • the sole output neurons – receive two distinct excitatory inputs (parallel fibres and climbing fibres)
93
Q

What are climbing fibres thought to do?

A

convey error signals – mismatch between motor command and actual movement

94
Q

How does the main output from the cerebellum occur?

A
  • excitatory input from granule cell is integrated in Purkinje cell with inhibitory input from basket and stellate cells, and excitatory climbing fibre input from inferior olive
  • Purkinje cell axons make inhibitory synaptic contact with neurons in cerebellar nuclei
  • provides connections to a wide range of other CNS structures to control movement and influence many other functions
95
Q

What are the 3 layers of the cerebellar cortex?

A
  • molecular layer
  • Purkinje layer
  • granular layer
96
Q

What is cerebellar ataxia?

A

lack of muscle control or coordination of voluntary movements

  • persistent ataxia can be an indicator of damage to cerebellum
97
Q

What are the 2 types of waking?

A
  • active waking (aW)
  • quiet waking (qW)
98
Q

What are the 2 types of sleep?

A
  • slow wave sleep (SWS) or non-REM sleep (NREM)
  • paradoxical sleep or rapid eye movement sleep (REM)
99
Q

What do electromyograms (EMG) measure?

A

muscle tension

100
Q

What do electroencephalograms (EEG) measure?

A

brain activity – mostly from cortex

101
Q

What are the 5 named human brainwaves and what do they tell us?

A
  • gamma – problem-solving
  • beta – active thinking, arousal
  • alpha – calm
  • theta – deep meditation, REM
  • delta – deep dreamless sleep
102
Q

What waves are associated with waking?

A
  • measurable EMG readings
  • gamma waves on EEG
103
Q

What waves are associated with active waking (aW)?

A
  • gamma
  • beta
104
Q

What waves are associated with quiet waking (qW)?

A
  • alpha
  • theta
105
Q

What is slow wave sleep (non-REM) and what are some characteristics?

A

staged from light sleep to deep sleep (4 stages) by pattern of rhythmic slow waves, indicating marked synchronization of neuronal firing

  • decreased motor tone
  • loss of awareness to surroundings
106
Q

What is REM sleep and what are some characteristics?

A
  • associated with dreaming
  • complete motor atonia – tone in antigravity muscles disappears, preventing movement during dreaming
  • rapid eye movement (REM) in phasic periods, but not tonic periods
  • behavioural sleep (quiescence)
  • cortical activity typical of waking
107
Q

What are the 4 stages of slow wave sleep and what are their characteristics?

A

stage 1: light sleep

  • eye movement slow
  • loss of awareness
  • easily awakened

stage 2: light sleep

  • heart rate slows
  • occasional high amplitude slow waves (delta)

stage 3: deep sleep

  • breathing slows, muscles relax
  • more delta waves

stage 4: very deep sleep

  • very deep, dreamless sleep
  • mostly delta waves

(sleepwalking occurs in slow wave sleep)

108
Q

What is idiopathic rapid eye movement sleep behaviour disorder?

A
  • nocturnal dream enactment behaviour that occurs every night in REM – punching, kicking, falling out of bed, talking, screaming
  • some medications may promote this (antidepressants, beta blockers)
  • caused by loss of motor atonia – dysfunction in lower brainstem nuclei that control REM sleep
  • patients develop motor and cognitive dysfunction over time
  • associated with development of Parkinson’s disease, dementia, and some forms of narcolepsy
109
Q

What are some treatment options for idiopathic REM sleep behaviour disorder? (2)

A
  • melatonin
  • benzodiazepine – enhances GABA activity
110
Q

Describe how sleep changes with age.

A
  • infants spend most time in REM – can transition rapidly from wake to REM
  • slow wave sleep is maximal in young children, and declines with age (we spend less time sleeping)
  • arousal from sleep is difficult in young children in slow wave sleep or REM, but considerably easier in elderly
111
Q

What is the arousal system and what does it do?

A

includes a set of interconnected nuclei that are located throughout the brainstem

  • stimulates frontal/cortical activation, maintaining wakefulness
112
Q

What is Major Pathway 1 of the arousal system?

A

arousal is promoted by ACh-producing cell groups in two brainstem nuclei – pednuculepontine (PPT) and laterodorsal tegmental (LDT)

  • cholinergic neurons stimulate thalamocortical relay neurons (sensory information to cortex)
  • neurons in PPT/LDT fire most rapidly during wakefulness and rapid eye movement (REM) sleep
113
Q

What is Major Pathway 2 of the arousal system?

A

neurons in upper brainstem and caudal hypothalamus

  • locus ceruleus (LC) – norepinephrine system that innervates prefrontal cortex and exerts a potent modulatory influence on executive functions
  • tuberomammillary nucleus (TMN) – contains histamine
  • raphe nuclei – release histamine and serotonin, and increases excitability of cortical neurons

nuclei fire fastest during wakefulness, slows down during SWS/NREM sleep, and stops during REM sleep

114
Q

How is Major Pathway 2 augmented? (2)

A
  • basal forebrain (BF) projections to forebrain are largely cholinergic (ACh), with some GABAergic neurons, and are active during both wake and REM sleep
  • lateral hypothalamic (LH) neurons release melanin-concentrating hormone (MCH) that are active during REM sleep, or orexin that are most active during wakefulness
115
Q

How does orexin contribute to arousal?

A
  • located in thalamus, sends excitatory projections to entire CNS
  • innervates LC, raphe, LDT, and PPT
116
Q

What is the ventrolateral preoptic nucleus (VLPO) and what is its function?

A

mainly GABAergic neurons

  • sends inhibitory signals to ascending, arousal-promoting regions
  • triggers sleep via active inhibition
117
Q

What is the flip-flop switch theory?

A

nuclei of Major Pathway 2 (LC, raphe, TMN) and VLPO inhibit each other to achieve sleep or waking

  • circadian control: ie. superchiasmatic nucleus receives information from retina and signals to pineal gland to control secretion of melatonin, which promotes sleep – this contributes to the change in the flip-flop switch by increasing activity of VLPO
  • homeostatic control: as energy carrier ATP breaks down, adenosine builds up and triggers neuron activity in VLPO
118
Q

What is narcolepsy?

A

loss of orexin neurons – possibly autoimmune

  • caused by intrusions of REM sleep while awake
  • genetic predisposition suggested
119
Q

Cranial Neve I

A

olfactory nerve

  • smell
120
Q

Cranial Neve II

A

optic nerve

  • vision
121
Q

Cranial Neve III

A

oculomotor nerve

  • eye movement
  • pupil constriction
122
Q

Cranial Neve IV

A

trochlear nerve

  • eye movement
  • moves eyeball down and out
123
Q

Cranial Neve V

A

trigeminal nerve

  • touch
  • pain
  • muscles for chewing
124
Q

Cranial Neve VI

A

abducens nerve

  • eye movement
  • directs pupil laterally
125
Q

Cranial Neve VII

A

facial nerve

  • taste (anterior 2/3 of tongue)
  • sound
  • facial expression
126
Q

Cranial Neve VIII

A

vestibulocochlear nerve

  • hearing
  • balance/equilibrium
127
Q

Cranial Neve IX

A

glossopharyngeal nerve

  • taste (posterior 1/3 of tongue)
  • gag reflex
  • swallowing
128
Q

Cranial Neve X

A

vagus nerve

  • extensive distribution in body
  • supplies parasympathetic innervation (digestion, breathing, heart rate, secretion)
129
Q

Cranial Neve XI

A

spinal accessory nerve

  • head movement
  • turning
130
Q

Cranial Neve XII

A

hypoglossal nerve

  • tongue movement
131
Q

Which spinal nerves are involved in the sympathetic nervous system?

A
  • thoracic
  • lumbar
132
Q

Which cranial nerves are involved in the parasympathetic nervous system?

A
  • oculomotor (III)
  • facial (VII)
  • glossopharyngeal (IX)
  • vagus (X)
133
Q

Describe the 2-neuron system of the autonomic nervous system?

A
  • cell of origin in CNS
  • synapse occurs in autonomic ganglia outside CNS
  • preganglionic fibre utilizes neurotransmitter to signal postganglionic fibre, and postganglionic fibre uses neurotransmitter to signal effector organ (transmistters may be different)
134
Q

Where are parasympathetic ganglia located and what is the major neurotransmitter?

A
  • in or near organs innervated by them
  • acetylcholine
135
Q

Where are sympathetic ganglia located and what is the major neurotransmitter?

A
  • in proximal ganglion
  • acetylcholine and norepinephrine
136
Q

What are the 2 neurotransmitters of the ANS?

A

acetylcholine and norepinephrine

  • both can be excitatory or inhibitory
137
Q

What are the 3 types of receptors of the ANS?

A
  • nicotinic receptors (sympathetic or parasympathetic)
  • muscarinic receptors (parasympathetic)
  • adrenoreceptors (sympathetic)
138
Q

What are nicotinic receptors?

A

ligand-gated ion channels responsive to ACh

  • activation causes rapid increase in cellular permeability to Na+ and Ca2+
  • depolarization and excitation
139
Q

What are muscarinic receptors?

A

metabotropic receptors that can inhibit or excite postsynaptic neurons depending on their coupling to G-protein alpha-subunits

  • 5 distinct types, each produced by different genes, with distinct anatomic locations in periphery and CNS, and differing chemical specificities
140
Q

Gs Protein Family

A

activation

141
Q

Gi Protein Family

A

inhibition

142
Q

Gq Protein Family

A

activation

143
Q

G12 Protein Family

A

activation

144
Q

M1 Muscarinic Receptor

  • Location
  • Post-receptor Mechanism
A
  • nerves
  • IP3, DAG cascade
145
Q

M2 Muscarinic Receptor

  • Location
  • Post-receptor Mechanism
A
  • heart, nerves, smooth muscle
  • inhibition of cAMP production, activation of K+ channels
146
Q

M3 Muscarinic Receptor

  • Location
  • Post-receptor Mechanism
A
  • glands, smooth muscle, endothelium
  • IP3, DAG cascade
147
Q

M4 Muscarinic Receptor

  • Location
  • Post-receptor Mechanism
A
  • CNS
  • IP3, DAG cascade
148
Q

M5 Muscarinic Receptor

  • Location
  • Post-receptor Mechanism
A
  • CNS
  • IP3, DAG cascade
149
Q

M1, M3, and M5 Muscarinic Receptors

A
  • phosphotidyl inositol
  • IP3, DAG
  • excitation
150
Q

M2 and M4 Muscarinic Receptors

A
  • adenylyl cyclase
  • cAMP
  • inhibition
151
Q

What does acetylcholine act on?

A

released at both the target organs of primarily the parasympathetic, but also the sympathetic

  • acts on muscarinic receptors
152
Q

What does epinephrine/norepinephrine act on?

A

released at most sympathetic post-ganglionic neuroeffector sites

  • acts via alpha receptors (a1 and a2)
  • acts via beta receptors (b1, b2, and b3)
153
Q

What happens when epinephrine/norepinephrine binds to a1 receptors?

A
  • increase IP3, DAG
  • IP3 promotes release of Ca2+ from intracellular stores
  • DAG activates protein kinase C
  • excitation
154
Q

What happens when epinephrine/norepinephrine binds to a2 receptors?

A
  • inhibit adenylyl cyclase
  • inhibition
155
Q

What happens when epinephrine/norepinephrine binds to b1 receptors?

A

increase cAMP

ie. heart

156
Q

What happens when epinephrine/norepinephrine binds to b2 receptors?

A

increase cAMP

ie. bronchial smooth muscle

157
Q

What happens when epinephrine/norepinephrine binds to b3 receptors?

A

increase cAMP

ie. adipose tissue, bladder

158
Q

What happens when epinephrine/norepinephrine binds to beta receptors?

A

increase in Ca2+ influx across cell membrane and sequestration inside cell – increases force of contraction

159
Q

Sympathetic vs. Parasympathetic System

Cell of Origin (Pre-ganglionic)

A
  • sympathetic: thoracic and upper lumbar spinal cord
  • parasympathetic: brainstem (cranial nerves) and sacral spinal cord
160
Q

Sympathetic vs. Parasympathetic System

Number of Nerve Fibres

A
  • sympathetic: many
  • parasympathetic: few – vagus (X) nerve is the major nerve of this division
161
Q

Sympathetic vs. Parasympathetic System

Length of Cell of Origin

A
  • sympathetic: short axon
  • parasympathetic: long axon
162
Q

Sympathetic vs. Parasympathetic System

Ganglion Location

A
  • sympathetic: near spinal cord
  • parasympathetic: near organ
163
Q

Sympathetic vs. Parasympathetic System

Length of Ganglion Neuron

A
  • sympathetic: long axon
  • parasympathetic: short axon
164
Q

Sympathetic vs. Parasympathetic System

Major Neurotransmitter

A
  • sympathetic: acetylcholine and norepinephrine
  • parasympathetic: acetylcholine
165
Q

What nerve affects lung function and how?

A

vagus nerve modulates airway tone

  • in airways, ACh is released from efferent endings of the vagus nerve fibre
  • ACh acts on M3 receptors and stimulates muscles to contract
  • muscarinic antagonists block this effect
166
Q

How does syncope occur?

A

caused by a temporary drop in blood pressure or heart rate, and therefore temporary drop in amount of blood flow to brain

  • vagus nerve overstimulation, excess ACh release
  • heart rate slows and blood vessels dilate, making it harder for blood to be pumped to brain
167
Q

What is dopamine β hydroxylase deficiency?

A

rare genetic syndrome characterized by the complete absence of norepinephrine in PNS and CNS

  • deficiency in enzyme that converts dopamine to norepinephrine
  • results in progressive sympathetic denervation, but normal cholinergic innervation
168
Q

Describe the neuron system in the SNS.

A
  • cell bodies located in either brainstem or spinal cord
  • extremely long course, as they do not synapse after they leave CNS until they are at their termination in skeletal muscle
169
Q

What neurotransmitter acts in the SNS and how?

A
  • ACh binds to nicotinic receptors
  • influx of Na+ changes membrane potential
  • Ca2+ channels at SR open and leads to increase in cytoplasmic Ca2+
  • Ca2+ binds troponin, actin active site is exposed, myosin binds and pull actin filaments

PHRM 100 – APPP (23 decks)

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