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Year 2 Semester 2 > CNS > Flashcards

CNS Flashcards

0
Q

What are the 4 parts of the hypothalamus?

A 
Caudal region (mammillary group)
Intermediate region (tuberal group)
Rostral region (chiasmatic group): supraoptic and preoptic regions
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1
Q

What is the difference between ionotropic and metabotropic neurotransmitter receptors?

A

Ionotropic: fast, ligand-gated, receptor is present on ion channel
Metabotropic: slower, G-protein coupled, receptor is separate from ion channel, sends G-protein or second messenger to different receptor on ion channel to make it open

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2
Q

What is the function of the caudal region of the hypothalamus?

A

Relay station for reflexes related to sense of smell

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3
Q

What is the definition of learning?

A

The acquisition of abilities or knowledge, a change in behaviour which occurs as a consequence of experience, instruction or both.

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4
Q

What is the definition of memory?

A

The storage of acquired knowledge or abilities for later recall

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5
Q

What are the 2 types of memory?

A

Declarative: specific facts, events and places often resulting from a single experience
Procedural: skilled motor movements gained through repetitive training/ how to do things

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6
Q

Where are short-term memories formed?

A

Hippocampus

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7
Q

Where are short-term memories consolidated to long-term memory?

A

Hippocampus

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8
Q

Where are long-term memories stored permanently?

A

Cerebral cortex

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9
Q

Where is accessing and manipulating of long-term memories carried out (through working memory)?

A

Prefrontal cortex of forebrain

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10
Q

Where are ‘how to’ procedural memories stored?

A

Cerebellum and relevant cortical regions

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11
Q

How long does short-term memory last?

A

Seconds to hours

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12
Q

How long does long-term memory last?

A

Days to years

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13
Q

What is the definition of a synapse?

A

Junction between neurones and other neurones, or between neurones and their effector cells

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14
Q

What is the definition of a neurotransmitter?

A

A chemical released by a synapse that diffuses from the pre-synaptic membrane to the post-synaptic membrane
Packed in vesicles

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15
Q

What are the 3 main types of neurotransmitter?

A

L-type : slow release, high threshold
T-type : transient (fast) release, low threshold
N-type : neither fast nor slow release

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16
Q

What is summation?

A

Many subthreshold synaptic inputs arriving simultaneously at a synapse to evoke a postsynaptic action potential

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17
Q

What are local anaesthetics used for?
Which fibres do they target?
Give some examples

A

Analgesia
Target pain fibres
Examples: Procaine, Lidocaine, Bupivacaine, Mepivacaine

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18
Q

What are opioids used for?

Give some examples

A

Analgesia and sedation

Morphine, codeine, butorphanol

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19
Q

What is a neuroleptanalgesic?
What is it comprised of?
What are its 3 uses?

A

A drug which causes sedation and profound analgesia
Neuroleptic and opioid
Pre-med, minor surgical procedures, restraint (large animals)

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20
Q

Why should you always wear gloves and use a rifle when administering etorphine as restraint?

A

Absorption through cuts or self-injection is fatal

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21
Q

What is the Lewis Triple Response?

A

A cutaneous response that occurs from firm stroking of the skin which produces an initial red line, followed by a flare around that line, then a wheal.

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22
Q

The Lewis Triple Response occurs due to the release of what chemical?

A

Histamine

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23
Q

What are polymodal receptors?

A

Receptors which pick up different types of pain

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24
Q

Where does decussation occur for:
Motor and touch
Pain

A

Motor and touch: at midbrain

Pain: around the spinal cord segment

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25
Q

Nociception only becomes pain when it reaches what?

A

Thalamus

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26
Q

Which are the fastest nerve fibres? What speeds do they operate at?
Which are the slowest (and what are their speeds)?

A

Fastest: A-alpha (72-120 m/s)
Slowest: C-fibres (0.4-2 m/s)

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27
Q

First order neurons synapse in which part of the grey matter of the spinal cord?

A

Substantia gelatinosa (lamina II)

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28
Q

What is meant by an antidromal impulse?

A

One in which conduction is opposite to that of the normal (orthodromic) direction

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29
Q

Where is the chemoreceptor trigger zone located?

A

4th ventricle of brain

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30
Q

When is benzodiazepine use contra-indicated?

A

Liver disease

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31
Q

Discuss diazepam’s mechanism, absorption, distribution, metabolism and elimination

A

Mechanism: GABA-A agonist
Absorption: IV
Distribution Binds to plasma proteins, also crosses BBB. Half-life=2hrs in dog, longer in cats and horses
Metabolism: First pass metabolism by cytochrome P450. Metabolites include oxazepam
Elimination: Dog=60% kidney

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32
Q

What is a side effect of using benzodiazepines as a sedative?

A

Respiratory depression

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33
Q

What is the definition of general anaesthesia?

A

The controlled, reversible loss of consciousness with reduced perception of external stimuli, and motor response to such stimuli (eg loss of consciousness with loss of pain)

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34
Q

Give some examples of inhalation anaesthetics

A

Nitrous oxide
Isoflurane
Halothane
Di-ethyl ether

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35
Q

Give some examples of intravenous anaesthetics

A

Barbiturates (not commonly used anymore)
Propofol
Alphaxolone
Ketamine

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36
Q

What 3 agents are included in a pre med?

A

Parasympathetic
Sedative
Analgesic

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37
Q

The speed of anaesthesia (rate at which concentration of anaesthetic in the brain rises) depends on what 2 things?

A

The solubility of the agent in the blood

Anaesthetic concentration in the inspired mixture

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38
Q

Which kinds of anaesthetics take longer to work: ones that are more or less blood soluble?

A

More blood soluble.

Therefore ones that are less blood soluble are more desirable (hit neurones and enter the brain more quickly)

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39
Q

Which is the quickest injectable route for anaesthesia?

Which is the slowest?

A

Quickest: Intravenous
Slowest: Subcutaneous

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40
Q

Give 4 treatment options for cognitive dysfunction (Alzheimers) in dogs

A

1) Acetylcholine agonists and anticholinesterases
2) Choline precursors
3) Dietary: antioxidants
4) Selegiline: a MAO-B inhibitor (therefore increases dopamine availability)

41
Q

What is cognitive dysfunction (Alzheimers) in dogs thought to be caused by?

A

ACh deficiency

42
Q

What effects does stress have on the body? Explain

A

Increased heart rate-due to increased sympathetic nerve supply to the sinus node, and to circulating epinephrine released from the adrenal medulla
Increased bloodflow-due to circulating epinephrine stimulating vasodilating B2-adrenergic receptors in the skeletal muscle vessels
Increased blood pressure-due to increased cardiac output

43
Q

What are the two theories behind the mechanism of stereotypies?

A

1) Related to obsessive compulsive disorder in humans (involves basal ganglia)
2) Related to schizophrenia in humans (too much dopamine in substantia nigra)

44
Q

What kind of drugs can we use to reduce aggression?

A

Want to increase serotonin levels, therefore use a SSRI (specific serotonin reuptake inhibitor)

45
Q

Why is the orbit not fully enclosed by bone in carnivores and pigs?

A

To enable wider opening of the jaw

46
Q

In the dog, which bones is the orbit made up of?

A

Frontal, lacrimal, zygomatic, sphenoid, palatine

47
Q

Where does the orbital ligament extend to and from?

A

Extends from the frontal process of the zygomatic bone, to the zygomatic process of the frontal bone

48
Q

Birds and snakes lack which ocular muscle?

A

Retractor bulbi

77
Q

Where does the hypothalamus lie?

A

Inferior to (underneath) the thalamus, in the diencephalon of the brain

78
Q

What does the hypothalamus develop from?

A

The prosencephalon of the neural tube

79
Q

What is the function of the mammillary bodies?

A

Two small, rounded projections that serve as a relay station for reflexes related to sense of smell

80
Q

Stimulation of which parts of the hypothalamus will increase arterial pressure and heart rate?

A

Posterior and lateral

81
Q

What are the 2 routes for diffusion of (releasing and inhibiting) hormones once produced by hypothalamic nuclei?

A

1) Diffusion into capillaries of the primary plexus of the hypophyseal portal system. From here they’re carried to the secondary plexus for distribution to target cells in the anterior pituitary
2) Diffusion into the capillary plexus of the infundibular process to the posterior pituitary. Oxytocin and vasopressin are released by exocytosis

82
Q

Stimulation of the LHA (lateral hypothalamic nuclei in tuberal group) causes what?

A

Thirst and eating, and increased general activity levels, sometimes leading to overt rage and fighting

83
Q

Stimulation of the VMH (ventromedial hypothalamus) and surrounding areas causes what?

A

Satiety, decreased eating and tranquility

84
Q

Stimulation of the thin periventricular region (immediately adjacent to the third ventricle) leads to what?

A

Fear and punishment reactions

85
Q

Stimulation of the anterior- and posterior-most portions of the hypothalamus cause what?

A

Sexual drive

86
Q

What causes the sensation of thirst?

A

Cells in the thirst centre of the LHA are stimulated by rising osmotic pressure of the ECF (fluid electrolytes here become too concentrated), causing the sensation of thirst

87
Q

In which part of the hypothalamus is the temperature of blood flowing through measured?

A

Anterior, particularly preoptic, hypothalamus

88
Q

What are the 6 major functions of the hypothalamus?

A

Regulation of eating and drinking
Control of body temperature
Regulation of circadian rhythms and states of consciousness
Production of hormones
Regulation of emotional and behavioural patterns
Control of ANS

89
Q

What tests can you use to determine the extent of hypothalamus lesions?

A 
MRI
Blood tests (for hormone and electrolyte concentrations)
90
Q

What are the 2 theories behind appetite regulation?

A

1) ‘Glucostat’ theory: short-term regulation of appetite. Glucose metabolism in hypothalamus determines food intake (volatile fatty acids in ruminants)
2) ‘Lipostat’ theory: long-term regulation of appetite. Satiety signals are conveyed to hypothalamus when fat deposits increase in size (secrete leptin)

91
Q

Factors which make an animal eat more are referred to as what?
Factors which make an animal eat less are referred to as what?

A

More=orexigenic

Less=anorexigenic

92
Q

Explain the role of leptin

A

Released from fat cells into the blood in amounts reflecting the ‘fatness’ of the animal
As an animal gets fatter, more leptin is secreted, binds to receptors in the arcuate nucleus, suppresses appetite, stimulates metabolic rate, promoting weight loss

93
Q

What is the role of NPY (neuropeptide Y)?

A

Appetite stimulant

94
Q

How does leptin suppress food intake?

A

By inhibiting NPY production or secretion in the arcuate nucleus, thus decreasing appetite. Also by stimulating melanocortin production (these decrease food intake).

95
Q

Where are orexins released from?

A

Lateral hypothalamic area (LHA)

96
Q

What is the role of melanocortins?

A

Decrease food intake

97
Q

What is the role of corticotropin-releasing hormone (CRH)?
Where is it released from?
It is released in response to what?

A

Appetite suppressant
Released from paraventricular nucleus (PVN) in hypothalamus
Released in response to melanocortins

98
Q

How is an animal signalled to terminate a meal?

A

Gastric stretch receptors in stomach suppress food intake.
Nucleus of solitary tract in the brainstem integrates sensory messages from GI tract (via vagus nerve) with hypothalamic inputs

99
Q

What does the stomach secrete when it is empty and full?

A

Ghrelin (empty)
PYY3-36 (full)
Changing levels of these signals enable an animal to feel full before a meal has been fully digested and absorbed, helping to prevent overeating

100
Q

How does insulin act as a satiety signal?

A

Released in response to high blood glucose levels, and stimulates tissue uptake of glucose

101
Q

What is the function of the cerebellum?

A

Evaluates how well movements initiated by motor areas in the cerebrum are being carried out (by UMNs of pyramidal and extrapyramidal tracts).
It compares intended movements with what is actually happening, and functions to minimise the differences. When they are not carried out correctly, it detects the discrepancies and sends feedback signals to motor areas of cerebral cortex via connections with the red nucleus, thalamus and LMNs in ventral horn of spinal cord.

102
Q

The pyramidal tract involves movements caused by contractions of which kinds of muscles?
What about the extrapyramidal tract?

A

Distal flexor muscles

Proximal extensor muscles

103
Q

What are the 3 layers of the cerebellar cortex?

A

Molecular layer
Purkinje cell layer
Granular layer

104
Q

Do the caudal, middle and rostral cerebellar peduncles contain axons that are afferent or efferent to the cerebellum?

A

Caudal and middle=afferent (to the cerebellum)

Rostral=efferent (away from cerebellum)

105
Q

Where do the axons in the caudal cerebellar peduncles go to and from?

A

From vestibular apparatus of inner ear and proprioceptors throughout the body to the cerebellum.
Extend from inferior olivary nucleus of medulla and spinocerebellar tracts of spinal cord.

106
Q

Where do the axons of the middle cerebellar peduncles go to and from?

A

From pontine nuclei to the cerebellum.

107
Q

Where do the axons of the rostral cerebellar peduncles go to and from?

A

From the cerebellum to the red nuclei of the midbrain and to several thalamic nuclei.

108
Q

What are the 2 primary groups of input (afferent) axons to the cerebellum?

A

Mossy fibre axons (via the pontine nuclei)

Climbing fibre axons (from the inferior olivary nucleus)

109
Q

The output of the deep nuclei of the cerebellum is modified by inhibition from what?

A

Purkinje cell axons

110
Q

The deep nuclei of the cerebellum have excitatory output to what?

A

Pyramidal and extrapyramidal systems

111
Q 
Vestibulocerebellum:
What does it coordinate?
Afferent input is from where?
Efferent output is to where?
Lesions cause what?
A

Balance and eye movements
Vestibular and visual systems
Vestibular nuclei in brainstem
Swaying posture, wide-based stance, falling to the side when moving

112
Q 
Spinocerebellum:
What does it coordinate?
Afferent input is from where?
Efferent output is to where?
Lesions cause what?
A

Muscle tone and movement
Via spinal cord spinal cord from muscle and cutaneous receptors, visual, auditory and vestibular systems
Via deep cerebellar nuclei to pyramidal and extrapyramidal systems
Hypermetria and hypertonus (spasticity), resulting in exaggerated spinal reflexes

113
Q 
Cerebrocerebellum:
What does it coordinate?
Afferent input is from where?
Efferent output is to where?
Lesions cause what?
A

Planning of limb movements
Inputs from motor and sensory cerebral cortices by way of corticopontine-cerebellar system
Outputs return to motor cerebral cortices by way of thalamus
Lesions cause loss of synchrony in movement: dysmetria, overshooting of body parts, intention tremor

114
Q

Which virus can cause cerebellar hypoplasia?

A

Feline panleukopenia virus

Virus destroys actively dividing granule cells and sometimes the Purkinje cell layer

115
Q

How is cerebellar development different in precocial and altrical neonates?

A

Precocial=cerebellum is almost complete

Altrical=cell devision continues for weeks after birth

116
Q

What does ‘working memory’ involve?

A

Comparing current sensory data with relevant stored knowledge and manipulating that information

117
Q

What does short-term memory involve?

A

Transient modification in the functioning or activity of existing synapses, such as temporary alteration in the amount of neurotransmitter released in response to stimulation.
Caused by modification of different membrane channel proteins in pre-synaptic terminals of specific afferent neurones, thus causing a change in neurotransmitter release

118
Q

What does long-term memory involve?

A

New, relatively permanent, functional or structural changes between existing neurons, such as enhanced synaptic connections.
Requires activation of specific genes that control protein synthesis. These proteins are needed for the formation of new synaptic connections.

119
Q

How does habituation occur (in the formation of STM)?

A

Decreased responsiveness to a harmless stimulus. Occurs through closing of pre-synaptic Ca2+ channels, decreasing quantity of neurotransmitter released. Animal learns to ignore stimulus.

120
Q

How does sensitisation occur (in the formation of STM)?

A

Increased responsiveness to mild stimuli following a strong, noxious stimulus. A form of learning by conditioning. Occurs through indirectly enhanced entry of Ca2+ into the pre-synaptic terminal. Animal learns something dangerous is in the vicinity.

121
Q

What is long-term potentiation?

A

Behavioural stimulation can last for several days if repeated noxious stimulation persists, leading to prolonged increase in strength of existing synaptic connections in activated pathways.

122
Q

What are the neurological benefits of animals having environmental enrichment?

A

Have more opportunity to learn so have greater branching and elongation of dendrites in brain regions involved in memory storage, providing more surface area for synaptic connections

123
Q

What is meant by cognition?

A

The ability to think and mentally process and manipulate knowledge through learning, memory, planning and other means

124
Q

What are the 5 classic signs of CDS?

A

Disorientation, alterations in social Interactions, Sleep-wake cycle disturbances, House-soiling, and changes in Activity (DISHA)

125
Q

Describe the 4 main neurological features of canine Alzheimer’s disease

A

1) Brain atrophy: widened sulci, thinned tissue and dilation of ventricles resulting from neuron loss or changes in neuronal density due to reduced neurogenesis
2) Senile (b-amyloid) plaques: the b-amyloid peptide is produced by enzymatic cleavage of the amyloid precursor peptide and laid down as insoluble deposits outside the neuron. If this happens in excess, it impairs synaptic function.
3) Neurofibrillary tangles: excess phosphorylation of the tau protein causes microtubules to disintegrate when the protein binds to them, forming clumps
4) Oxidative damage: the production of free radicals, leading to oxidative damage to proteins, lipids and nucleotides in neurons, can lead to their dysfunction

126
Q

Which neurones release acetylcholine?

A

All preganglionic neurones
Somatic motor neurones
Postganglionic neurones of the parasympathetic system

(Postganglionics of the sympathetic system release adrenaline/noradrenaline)

127
Q

What types of drugs would be used to treat urinary incontinence? (2)
Give an example of a drug from each type

A 
Alpha agonists (to increase action of urethral sphincter), eg Bethanechol, neostigmine 
Anticholinergics/ muscarinic antagonists (to decrease activity of detrusor muscle and stop it contracting), eg atropine, propantheline
128
Q

What secondary effect is caused by activation of beta receptors?

A

Increased cAMP

129
Q

What secondary effect is caused by activation of:
Alpha-1 receptors
Alpha-2 receptors

A

Alpha-1 receptors: activates phospholipase C

Alpha-2 receptors: decreases cAMP

Year 2 Semester 2 (16 decks)

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