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Brain Power: Beyond Adam > Neurophysiology > Flashcards

Neurophysiology Flashcards

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1
Q

Which receptor cell type is responsible for the ff stimullus:

  1. Tap, Flutter 5-40 Hz
  2. Deep pressure, Vibration 60-300 Hz
  3. Motion
  4. Sustained pressure
A
  1. TOUCH– Flutter 5-40 Hz: Meissner
  2. TOUCH– Vibration 60-300 Hz: Pacinian
  3. TOUCH– Motion: Hair follicle
  4. TOUCH– Sustained pressure: Ruffini corpuscles
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2
Q

Which receptor cell type is responsible for the ff stimullus:

  1. Vestibular– Balance: Angular acceleration
  2. Vestibular– Balance: Linear acceleration
A
  1. Vestibular– Balance: Angular acceleration
    Hair cells SC canal
  2. Vestibular– Balance: Linear acceleration
    Hair cells Otolith organs
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3
Q

What kind of pain is elicited?

  1. Glutamate for rapid localization
  2. Glutamate and substance P, dull, intense, unpleasant
A
  1. First/ fast/ epicritic pain

2. Second/ slow/ protopathic pain

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4
Q

What kind of pain is mediated by:

  1. ASIC
  2. TRPM8
  3. P2X, TRPA1
  4. TRPV1
A
  1. ASIC: Acid pain
  2. TRPM8: Cold
  3. P2X, TRPA1: Mechanical
  4. TRPV1: Acid and Heat
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5
Q

Differentiate:

  1. Hyperalgesia
  2. Allodynia
A

Hyperalgesia is an exaggerated response to a noxious stimulus, and allodynia is a sensation of pain in response to a normally innocuous stimulus

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6
Q

Where is the only place in the body where arterioles are readily visible?

A

Retina during fundoscopy

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7
Q

What are the components of the extrafoveal portion of the retina?

A
  1. Outer nuclear layer: Rods and cones
  2. Outer plexiform layer
  3. Inner nuclear layer: Bipolar cells, amacrine cells
  4. Inner plexiform latyer
  5. Ganglion cell layer: Midget and diffuse ganglion cells
  6. Outer nerve fibers
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8
Q

What kind of photoreceptor cell is most prominent in the fovea?

A

Cones

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9
Q

What induces hyperpolarization in cones? Light or dark?

A

Light.

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10
Q

In the dark what is the movement of the Na+?

A

From the inner to the outer segment

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11
Q

What are the two components of rhodopsin? Which one is an aldehyde of vitamin A?

A

Retinal and opsin

Retinal

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12
Q

When light hits what happens to retinal?

A

The only action of light is to change the shape of the retinal, converting it to the all-trans isomer from an all cis isomer.

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13
Q

What is the process of bleaching?

A

After 11-cis retinal is converted to the all-trans configuration, it separates from the opsin in a process called bleaching. This changes the color from the rosy red of rhodopsin to the pale yellow of opsin.

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14
Q

Where do the axons of a group of ganglion cells in the retina that contain melanopsin go? 2 answers.

A

The axons of these melatonin-containing photosensitive retinal ganglion project via at least two pathways. One, their axons can travel via the optic nerve, optic chiasm, and optic tract (bypassing the lateral geniculate nucleus, LGN) to terminate in the olivary pretectal nucleus. From here neurons synapse on parasympathetic preganglionic neurons in the Edinger—Westphal nucleus to mediate the pupillary light reflex (described below). Two, the axons of melatonin-containing photosensitive retinal ganglion cells can project to the suprachiasmatic nucleus of the hypothalamus, where they form connections that synchronize a variety of endocrine and other circadian rhythms with the light-dark cycle (Chapter 14).

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15
Q

Fill in

  1. Change in retinal due to light
  3. Activation in phosphodiesterase
  4. Decrease in cGMP
  7. Decreased release of synaptic transmitter
  8. Response of bipolar cells and other neural elements
A
  1. Change in retinal due to light
  2. Activation of transducin
  3. Activation in phosphodiesterase
  4. Decrease in cGMP
  5. Closure in Na channels
  6. Hyperpolarization
  7. Decreased release of synaptic transmitter
  8. Response of bipolar cells and other neural elements
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16
Q

What is the range of wavelength of visible light?

A

397 to 723 nm

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17
Q

When should strabismus be corrected before complete loss of visual acuity occurs in the suppressed eye? The cortical phenomenon called “Suppression scotoma”

A

6 years old

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18
Q

Why can occipital lesions spare macular central vision?

A

because the macular representation is separate from that of the peripheral fields and very large relative to that of the peripheral fields. Therefore, occipital lesions must extend considerable distances to destroy macular as well as peripheral vision.

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19
Q

There are 6 layers of the lateral geniculate nucleus. Which layers are part of the magnocellular pathway? Which layers are from the contralateral eye?

A

Magno 1, 2

Contralateral eye 1,4,6

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20
Q

Which layers of the LGN detect movement depth and flicker? Which are for color, texture, shape and fine detail?

A

Depth: 1-2 MAGNOCELLULAR
Color: 3-6
PARVOCELLULAR

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21
Q

Blindness with preservation of the pupillary reflex is usually due to a lesion in which visual pathway?

A

Bilateral lesions posterior to the optic tract

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22
Q

Which visual projection area?

  1. Primary visual cortex
  2. Motion
  3. Shape, color, texture
  4. Direction of movement
  5. Direction and speed
  6. Shape
  7. Color vision
A
  1. Primary visual cortex V1
  2. Motion V3
  3. Shape, color, texture V4
  4. Direction of movement V5
  5. Direction and speed V6
  6. Shape LO
  7. Color vision V8
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23
Q

Vision from V1 divides roughly to a dorsal parietal pathway and a ventral temporal pathway. What are the functions of these?

A

Dorsal: Motion

Ventral: Shape and recognition of faces

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24
Q

What are the primary colors?

A

Red Green Blue

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25
Q

What region of the visual projection area is responsible for color vision? Can lead to achromatopsia?

A

V8

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26
Q

How is color blindness inherited?

A

X-linked

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27
Q

The young helmhotz theory of color vision indicates that there are how many types of cones?

A

The Young–Helmholtz theory of color vision in humans postulates the existence of three kinds of cones, each containing a different photopigment and that are maximally sensitive to one of the three primary colors, with the sensation of any given color being determined by the relative frequency of the impulses from each of these cone systems.

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28
Q

What are the functions of the superior colliculi?

A

The superior colliculi, which regulate saccades, are innervated by M fibers from the retina.

The superior colliculi are constantly active positioning the eyes, and they have one of the highest rates of blood flow and metabolism of any region in the brain.

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29
Q

What type of astrocytes are in white and gray matter?

A

White: fibrous
Gray: Protoplasmic

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30
Q

What proteins that lock onto one another compacts the myelin sheaths?

A

Po or Myelin protein zero

The myelin is then compacted when the extracellular portions of a membrane protein called protein zero (P0) lock to the extracellular portions of P0 in the apposing membrane.

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31
Q

What proteins are attached to microtubules to help with the orthograde and retrograde transport of substances?

A

Dynein and kinesin

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32
Q

At rest what is them membrane potential? Which is more negative inside or outside? Close to the resting potential of which ion?

How is resting membrane maintained?

A

-70mV
Inside negative
Potassium
Because there are more open K+ channels than Na+ channels at rest, the membrane permeability to K+ is greater.

Steady ion leaks cannot continue forever without eventually dissipating the ion gradients. This is prevented by the Na, K ATPase, which actively moves Na+ and K+ against their electrochemical gradients.

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33
Q

Determine which fiber type

  1. Largest diameter and fastest
  2. For touch and pressure, second largest
  3. For proprioreception and somatic motor
  4. Pain and temperature (2 answers)
  5. Motor to muscle spindles
  6. Preganglionic autonomic
  7. Post ganglionic sympathetic
  8. Most susceptible to local anesthetics
  9. Most susceptible to pressure
A
  1. Largest diameter and fastest A alpha
  2. For touch and pressure, second largest A beta
  3. For proprioreception and somatic motor A alpha
  4. Pain and temperature (2 answers) A delta and C
  5. Motor to muscle spindles A gamma
  6. Preganglionic autonomic B
  7. Post ganglionic sympathetic C
  8. Most susceptible to local anesthetics C
  9. Most susceptible to pressure A
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34
Q

How does lidocaine and cocaine work in local anesthesia?

A

This usually occurs as a result of blockade of voltage-gated Na+ channels on the nerve cell membrane.

Nociceptive fibers (unmyelinated C fibers) are the most sensitive to the blocking effect of local anesthetics. This is followed by sequential loss of sensitivity to temperature, touch, and deep pressure. Motor nerve fibers are the most resistant to the actions of local anesthetics.

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35
Q

Correlate the numerical with the letter classification of nerve fibers

A

Ia
Muscle spindle, annulo-spiral ending
Aα

Ib
Golgi tendon organ
Aα

II
Muscle spindle, flower-spray ending; touch, pressure
Aβ

III
Pain and cold receptors; some touch receptors
Aδ

B has no number correlate (preganglionic autonomic)

IV
Pain, temperature, and other receptors
C

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36
Q

Which proteins are attached to:

  1. Z-line
  2. M-line
A
  1. Z-line: Actin

2. M-line: Myosin

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37
Q

The overlap of myosin and actin forms which band?

How about the lighter bands between these?

A

A band, in the middle of which is the M line

DONT FORGET A (H) BAND M LINE MYOSIN

Lighter bands are I bands bisected by the Z line

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38
Q

What are the functions of the ff troponins?
T
I
C

A

T: Bind actin to tropomyosin
I: Inhibit binding of actin to myosin
C: Bind to calcium– facilitates contraction

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39
Q

Which muscle protein?

  1. Binds actin to the Z line
  2. It connects the Z lines to the M lines and provides scaffolding for the sarcomere. It contains two kinds of folded domains that provide muscle with its elasticity.
  3. It adds structure to the Z lines in part by binding the Z lines to the plasma membrane.
A
  1. Actinin
  2. Titin
  3. Desmin
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40
Q

What does dystrohpin bridge?

A

F actin and the dystroglycan sarcoglycan complex. This dystrophin–
glycoprotein complex adds strength to the muscle by providing
a scaffolding for the fibrils and connecting them to
the extracellular environment.

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41
Q

What is the resting membrane potential of skeletal muscle?

A

-90mv

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42
Q

Regarding calcium in muscle contraction:

  1. What two receptors must interact for it to be released?
  2. Where is it released from?
  3. What pumps it back into the #2?
  4. Where does it bind to enable muscle contraction?
A
  1. What two receptors must interact for it to be released? Dihydropyridine receptor and ryanodine receptor
  2. Where is it released from? Terminal cisterns of the sarcoplasmic reticulum
  3. What pumps it back into the #2? SERCA– Sarcoplasmic endoplasmic reticulum Ca++ ATPase
  4. Where does it bind to enable muscle contraction? Troponin C on actin fiber
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43
Q

What receptor is pathologic in malignant hyperthermia?

A

Ryanodine receptors

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44
Q

Determine which type of muscle: Type 1, 2a, 2b

  1. Fast oxidative glycolytic
  2. White
  3. Red
  4. Fast myosin atpase activity
  5. Large
  6. High calcium pumping capacity
  7. Low oxidative capacity
  8. Motor unit fast but resistant to fatigue
  9. Most susceptible to atrophy with inactivity
A
  1. Fast oxidative glycolytic: 2a
  2. White: 2b
  3. Red: 1 and 2a
  4. Fast myosin atpase activity: 2a and 2b
  5. Large diameter: 2a and 2b
  6. High calcium pumping capacity of SR: 2a and 2b
  7. Low oxidative capacity: 2b
  8. Motor unit fast but resistant to fatigue: 2a
  9. Most susceptible to atrophy with inactivity 1
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45
Q

Besides glucose and lipids what other energy rich phosphate compound can the muscles use for contraction?

A

Phosphorylcreatine

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46
Q

Regarding ATP in muscle:

  1. How many kcal are brought about by hydrolysing ATP and H2O
  2. Glucose + 2ATP via anaerobic pathway results in?
  3. Glucose +2ATP via aerobic pathway results in?
A
  1. How many kcal are brought about by hydrolysing ATP and H2O –> 7.3
  2. Glucose + 2ATP via anaerobic pathway results in? –> Lactic Acid + 4 ATP
  3. Glucose +2ATP via aerobic pathway results in? –> 40ATP + 6 CO2 and 6 H2O
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47
Q

End to end adhesion of cardiac muscle fibers are called?

A

Intercalated disks

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48
Q

Identify the ion channel most responsible for the following phases cardiac muscle contraction

  1. Phase 0
  2. Phase 1
  3. Phase 2
  4. Phase 3
  5. Phase 4
A
  1. Phase 0: Upstroke– opening of voltage gated Na+ channels
  2. Phase 1: Closure of Na and opening of K channel
  3. Phase 2: Prolonged plateau phase– Slower but prolonged opening of Ca++ channels
  4. Phase 3– final repolarization: closure of the Ca++ channel and slow delayed K efflux
  5. Phase 4: Resting membrane potential– open K with NaK ATPase maintaining gradient
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49
Q

What are the equivalent structures of Z lines in smooth muscles?

A

Dense bodies

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50
Q

Whereas in striated muscles Ca++ binds to troponin C– where does it bind for smooth muscle?

A

Calmodulin– Smooth muscle

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51
Q

What type of smooth muscle has “pacemaker activities”?

A

Unitary (single-unit) smooth muscle similar to uterus, GI tract, ureter and bladder

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52
Q

What is another name for the substance secreted by endothelial cells to relax smooth muscles– EDRF endothelial derived relaxing factor?

A

Nitric oxide

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53
Q

What are the contents of these synaptic vesicles

  1. Small clear synaptic vesicles
  2. Small with dense core
  3. Large with a dense core
A
  1. Small clear synaptic vesicles: ach, glycine, GABA, glutamate
  2. Small with dense core: catecholamines
  3. Large with a dense core: neuropeptides
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54
Q

Before a vesicle fuses with a presynaptic cell membrane to release contents what proteins must lock together?

A

Synaptotagmin-1 is localized to synaptic vesicles and is the trigger for their calcium-induced exocytosis. Activation causes the fusion of the SNARE complex detailed below

Synaptobrevin (V SNARE) in the vesicle membrane locks with syntaxin and SNAP 25 (T SNARE) in the terminal cell membrane; GTPases regulate a multiprotein complex that includes Rab and Sec1/Munc18-like proteins as part of the fusion process.

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55
Q

How does the MOA of the two clostridium species vary?

A

Tetanus toxin binds irreversibly to the presynaptic membrane of the neuromuscular junction and uses retrograde axonal transport to travel to the cell body of the
motor neuron in the spinal cord. From there it is picked up by the terminals of presynaptic inhibitory interneurons. The toxin
attaches to gangliosides in these terminals and blocks the release of glycine and GABA.

Botulinum
toxins A and E cleave synaptosome-associated protein-25 (SNAP-25). This is a presynaptic membrane protein needed for fusion of synaptic vesicles containing acetylcholine to the terminal membrane, an important step in transmitter release.

Botulinum toxin B cleaves synaptobrevin, a vesicle-associated membrane protein (VAMP). By blocking acetylcholine release at the neuromuscular junction, these toxins cause flaccid paralysis.

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56
Q

Slow post synaptic potentials are usually due to manipulation of the conductance of which ion channel?

A

Potassium

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57
Q

What is the inhibitory neuron in the spinal cord and what does it secrete? How about in the cerebellum?

A

Renshaw cell– glycine

Basket cells

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58
Q

The entry of what ion triggers the release of Ach from the vesicles of the presynaptic junction?

A

Calcium (Voltage gated ion channels open when motor neuron action potential is activated)

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59
Q

What ion channels are blocked in Lambert Eaton Syndrome?

A

Presynaptic voltage gated Calcium ion channels

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60
Q

How do aminopyridines work in LEMS?

A

Also, the use of
aminopyridines facilitates the release of acetylcholine
in the neuromuscular junction and can improve muscle
strength in LEMS patients. This class of drugs causes
blockade of presynaptic K+ channels and promote activation of voltage-gated Ca2+ channels.

61
Q

What do varicosities in the endings of the post ganglionic autonomic neurons on smooth muscles do?

A

Varicosities, mitochondria

62
Q

What neurotraonsmitter is made from the ff:

  1. Tyrosine
  2. Tryptophan
  3. alpha ketoglutarate
  4. Glutamate
A
  1. Tyrosine: NE, Epi, Dopamine
  2. Tryptophan: Serotonin
  3. alpha ketoglutarate: Glutamate
  4. Glutamate: GABA
63
Q

What are the two types of presynaptic receptors?

A

Autoreceptors: Ligand is the NT released by the presynaptic terminal
Heteroreceptors: Ligand is the NOT the NT released by the presynaptic terminal

64
Q

Identify the main source of the ff neurotransmitters:

  1. Norepinephrine
  2. Serotonin
  3. Dopamine
  4. Acetylcholine
A
  1. Noradrenergic neurons in the locus coeruleus innervate the spinal cord, cerebellum, several nuclei of the hypothalamus, thalamus, basal telencephalon, and neocortex.
  2. Serotonergic neurons in the raphe nuclei project to the hypothalamus, limbic system, neocortex, cerebellum, and spinal cord.
  3. Dopaminergic neurons in the substantia nigra project to the striatum and those in the ventral tegmental area of (Tsai) the midbrain project to the prefrontal cortex of the limbic system.
  4. Cholinergic neurons in the basal forebrain complex (Nucelus basalis of Meynert and septal nuclei) project to the hippocampus and the neocortex and those in the pontomesencephalotegmental cholinergic complex project to the dorsal thalamus and the forebrain.
65
Q

What are the three ionotropic glutamate receptors?

A

AMPA: Na+
Kainate: Na+
NMDA: Ca++ –> Leads to excitotoxicity

The release of glutamate and its binding to AMPA or kainate receptors primarily permits the influx of Na+ and the efflux of K+, accounting for fast excitatory postsynaptic potential (EPSP).

The Mg+ block in the NMDA receptor is displaced with the influx of Na+ resulting in the activation of the receptor. The NMDA receptor then permits the influx of relatively large amounts of Ca2+ along with Na+.

Afterwards the Ca++/calmodulin kinase complex phosphorylates AMPA receptors, increases their conductance and moves them into the synaptic cell membrane from storage sites.

This is the MOA of long term potentiation. :-)

66
Q

What do riluzole, memantine and amantadine have in common?

A

NMDA receptor antagonists

67
Q

What enzyme facilitates the decarboxylation of glutamate into GABA?

A

glutamate decarboxylase (GAD)

68
Q

Which GABA receptor:

  1. Increases Chloride conductance
  2. Has Baclofen as an agonist and increases K+ conductance
A

GABA A

GABA B

69
Q

Besides prolonging the opening of Cl- channel GABA A how else do barbiturates work?

A

Suppress AMPA receptors

70
Q

How does glycine facilitate its inhibitory effects in the brainstem and spinal cord?

How about it’s excitatory effects in the CNS?

A

Increase in Cl- conductance

Makes NMDA more sensitive to the actions of glutamate

71
Q

It is synthesized in the nerve terminal from choline and acetyl-CoA by the enzyme ______________

A

Choline acetyltransferase (ChAT)

72
Q

Identify which drug affects inhibits the following transporters all invovled in the release of Ach into the cholinergic synapse:

  1. Choline transporter CHT
  2. Vesicle associated transporter VAT
  3. Vesicle associated membrane proteins VAMP
A
  1. Choline transporter CHT: Hemicholinium
  2. Vesicle associated transporter VAT: Vesamicol
  3. Vesicle associated membrane proteins VAMP: Botulinum toxin
73
Q

Which receptor of Ach is involved in the following?

  1. Muscle contraction
  2. Blocked by tubocurarine
  3. Blocked by atropine
A
  1. Muscle contraction: Nicotinic M (N2)
  2. Blocked by tubocurarine: Nicotinic M (N2)
  3. Blocked by atropine: Muscarinic

Nicotinic N1 are receptors found in the autonomic system (Preganglionic).

74
Q

___________ is
the only small-molecule transmitter that is synthesized in synaptic vesicles instead of being transported into the vesicle after
its synthesis.

A

Norepinephrine

Once dopamine is synthesized, it is transported into the
vesicle by the VMAT. Here the dopamine is converted to norepinephrine
by dopamine β-hydroxylase.

75
Q

What is the rate limiting step in the formation of NE?

What is the enzyme involved and what inhibits this enzyme?

A

What is the rate limiting step in the formation of NE? Formation of dopamine from tyrosine

What is the enzyme involved and what inhibits this enzyme? Tyrosine hydroxylase– inhibited by metyrosine.

76
Q

Identify which drug inhibits the following enzymes/transporters all involved in the release of NE into the noradrenergic synapse:

  1. Tyrosine hydroxylase
  2. Vesicular monoamine transporter
  3. Vesicle associated membrane protein
A
  1. Tyrosine hydroxylase: Metyrosine
  2. Vesicular monoamine transporter: Reserpine
  3. Vesicle associated membrane protein: Guanethedine
77
Q

What drugs inhibit the reuptake of NE via the NET (Norepinephrine transporter)?

A

Cocaine and TCAs

78
Q

What two enzymes are responsible for the degradation of epinephrine and norepinephrine?

A

The former reaction is catalyzed by monoamine oxidase (MAO) and the latter by catechol-O-methyltransferase (COMT).

79
Q

What pathway of dopamine release is involved in psychiatric disturbances?

How about for movement?

A

Mesocortical system, it arises primarily in the ventral tegmental area, which projects
to the nucleus accumbens and limbic subcortical areas.
The mesocortical system is involved in reward behavior and addiction and in psychiatric disorders such as schizophrenia

Nigrostriatal system

80
Q

Serotonin is synthesized from which amino acid?

A

Tryptophan

81
Q

How is serotonin cleared from the synaptic cleft?

A

5HT transporter then in the nerve terminal is inactivated by MAO or repackaged and sent back out

82
Q

Which serotonin receptor?
1. High affinitity for antidepressants
2. Platelet aggregation and smooth muscle contraction
3. GI receptors and vomiting in the area postrema
4. Present in the gastrointestinal
tract, where they facilitate secretion and peristalsis, and in the brain.

A
  1. High affinitity for antidepressants: 5HT6
  2. Platelet aggregation and smooth muscle contraction: 5HT2a
  3. GI receptors and vomiting in the area postrema: 5HT3
  4. Present in the gastrointestinal
    tract, where they facilitate secretion and peristalsis, and in the brain. 5HT4
83
Q

Whereas depression is alleviated by blocking serotonin reuptake– how is psychosis related to dopamine?

A

Overstimulation of D2 receptors can lead to psychosis.

84
Q

Substance P is found in high concentrations in the endings of primary afferent neurons in the spinal cord. What is its function there?

A

It is the mediator at the first synapse in the pathways for pain transmission in the dorsal horn.

85
Q

Which opioid receptor has the highest affinity for

  1. Endorphins
  2. Enkephalins
  3. Dynorphins
A
  1. Endorphins: Mu
  2. Enkephalins: Kappa
  3. Dynorphins: Gamma
86
Q

Endogenous cannabinoids to induce euphoria and an antinociceptive effect act on which cannabinoid receptor?

A

CB1

CB2 is in the periphery not CNS

87
Q

What type of nerve in the sympathetic system:

  1. Preganglionic axons
  2. Post ganglionic axons
A
  1. Preganglionic axons: B

2. Post ganglionic axons: C

88
Q

What NT is released?

  1. Preganglionic sympathetic
  2. Preganglionic parasympathetic
  3. Posganglionic sympathetic
  4. Posganglionic parasympathetic
  5. Alpha motor neurons
A
  1. Preganglionic sympathetic: Ach
  2. Preganglionic parasympathetic: Ach
  3. Posganglionic sympathetic: Ach or NE
  4. Posganglionic parasympathetic: Ach
  5. Alpha motor neurons: Ach
89
Q

Where are the IML columns of the sympathetic division located?

A

T1 to L3/4

90
Q

Name the 5 autonomic ganglia in the brainstem and indicate if PS or S

A
  1. Midbrain CN3: Edinger westphal nucleus PS– ciliary ganglion for pupillary constriction
  2. Medulla CN 7: Superior salivatory ganglion PS– sphenopalatine ganglion for lacrimal and nasal glands AND Submandibular ganglion for submandibular and sublingual glands
  3. Medulla CN9: Inferior salivatory ganglion PS– Otic ganglion for parotid glnad
  4. Medulla CN10: Dorsal motor nucleus of vagus PS to the lung, stomach, SI and colon
  5. Medulla CN10: Nucleus ambiguus PS to the SA and AV nodes of the heart
91
Q

Which sympathetic post-ganglionic neurons use acetylcholine?

A
  1. Sympathetic postganglionic neurons that innervate sweat glands
  2. Sympathetic postganglionic neurons that end on blood vessels in some skeletal muscles and produce vasodilation when stimulated (sympathetic vasodilator nerves)
92
Q

How does the PS and S affect the ff?

  1. Salivary glands
  2. Male sex organs
A
  1. Salivary glands: PS profuse watery secretion S thick viscous and amylase secretion
  2. Male sex organs: Point and Shoot
93
Q

What are the types of Ach receptors? Where are they commonly found?

A

Nicotinic: autonomic ganglia Nn (N1) and Nm (N2) neuromuscular junction
Muscarinic: in heart, muscle, and glands

94
Q

What do the ff have in common? Sarin gas and soman gas

A

Both are similar to parathion and malathion– organophosphates that function as cholinesterase inhibitors

95
Q

What is the immediate treatment for organophosphate poisoning? What can be given prophylaxis?

A

Atropine

Pyridostigmine

96
Q

How do the effects of Inocybe mushroom differ from the Amanita muscaria mushroom differ?

A

Inocybe is Excessive activation of the cholincergic system
Amanita is antimuscarinic – similar to atropine toxicity: “red as a beet” (flushed skin), “hot as a hare” (hyperthermia), “dry as a
bone” (dry mucous membranes, no sweating), “blind as a bat”
(blurred vision and cycloplegia), and “mad as a hatter” (confusion
and delirium).

97
Q

What are the components of the horner syndrome resulting from interruption of the sympathetic pathway?

A

The hallmark of Horner syndrome is the triad of anhidrosis
(reduced sweating), ptosis (drooping eyelid), and miosis
(constricted pupil). Symptoms also include enophthalmos
(sunken eyeball) and vasodilation.

98
Q

What is the Raynaud phenomenon?

A

An episodic reduction in blood flow primarily to the fingers, often during exposure to cold or during a stressful situation.

99
Q

What organs are exclusively innervated by the
Sympathetic AS
PS AS

A

S: Adrenals, pilomotor, sweat glands
PS: Lacrimal, Ciliary (for accommodation), Naspharyngeal gland

100
Q

What brain structures provide direct input to the Intermediolateral nucleus for the sympathetic system?

A
  1. Hypothalamic paraventricular nucleus
  2. Pontine A5 cell group
  3. Rostral ventrolateral medulla
  4. Medullar raphe nucleus
101
Q

What model drug?

  1. Blocks Ach synthesis by blocking choline synthesis
  2. Blocks NE syntheisis by blocking tyrosine hydroxylase
  3. Prevents storage of Ach
  4. Prevents storgae of NE
A
  1. Blocks Ach synthesis by blocking choline synthesis: hemicholinium
  2. Blocks NE syntheisis by blocking tyrosine hydroxylase: metyrosine
  3. Prevents storage of Ach: Vesamicol
  4. Prevents storgae of NE: Reserpine
102
Q

Which adrenoreceptor is activated by:

  1. Clonidine
  2. Dobutamine
  3. Salmeterol, albuterol, terbutaline
A
  1. Clonidine: Alpha 2
  2. Dobutamine Beta 1
  3. Salmeterol, albuterol, terbutaline: Beta 2
103
Q

What drug blocks the ff adrenoreceptors:

  1. Alpha 1
  2. B1 and B2
  3. Beta 1> beta 2
A
  1. Alpha 1: Prazosin, Terazosin
  2. B1 and B2: Propranolol
  3. Beta 1> beta 2: Atenolol, metoprolol
104
Q

What is the MOA of atropine, ipatropium, tropicamide?

A

Binds to and blocks MUSCARINIC receptors

105
Q

Identify the location of hair cells are responsible for:

  1. Hearing
  2. Horizontal acceleration
  3. Vertical acceleration
  4. Rotational acceleration
A
  1. Hearing
  2. Horizontal acceleration
  3. Vertical acceleration
  4. Rotational acceleration
106
Q

Where is the endolymph formed and how does the content differ from the perilymph?

A

Stria vascularis

High K

107
Q

When the shorter stereocilia are pushed toward the taller ones, the entry of which ions cause depolarization?

A

Calcium

Potassium

108
Q

What are the 3 cell types in the olfactory epithelium?

A

Sustentacular cells
Oflactory neurons
Basal cells (Which become olfactory neurons later on)

109
Q

What cells of the olfactory bulb send axons to the cortical areas for olfaction?

A

Tuft and mitral cells

Cortex: medial most temporal lobe– uncus

110
Q

How many olfactory genes are there?

A

500– accounting for the variety in smells

111
Q

What percentage of individuals have abnormalities in smell sensation? 65 to 80
more than 80

A

50%

>75%

112
Q

Which papillae?

  1. Rounded structures most numerous at the tip of the tongue
  2. Prominent structures arranged in a V on the back of the tongue
  3. Posterior edge of the tongue
A
  1. Rounded structures most numerous at the tip of the tongue: Fungiform
  2. Prominent structures arranged in a V on the back of the tongue: Circumvallate
  3. Posterior edge of the tongue: Foliate

NB: Circumvallate papillae work closely together with von Ebner glands to form a functional complex that is important in actual taste detection

113
Q

What nerve conducts taste from the anterior part of the tongue?

A

Chorda tympani branch of the facial nerve

114
Q 
How is signal transduction work for the different tastes?
Salty
Sour
Sweet
Bitter
Umami
A

Salty: Na+ movement through ion channels (ENaC– epithelial sodium channel)
Sour: H+ movement through ion channels

The rest are mediated by G protein coupled receptors:
Sweet
Bitter
Umami: mGluR4 metabotropic glutamate receptor

115
Q

What taste has the lowest taste threshold?

A

Bitter substances

116
Q

What does activation of the Agamma motor neurons to muscle spindles do?

A

They increase the dynamic sensitivity of the muscle spindle Aalpha (1a) endingsWh

117
Q

Which muscle sensors are mainly for

  1. Detection of static and dynamic changes in muscle length
  2. Detect muscle tension
A
  1. Detection of static and dynamic changes in muscle length: Muscle spindles– 1a, 2 Abeta and Agamma
  2. Detect muscle tension: Golgi tendon organs
118
Q

What is the alpha gamma coactivation concept?

A

The muscles can be made to contract via stimulation of the α-motor neurons that innervate the extrafusal fibers or the γ-motor neurons that initiate contraction indirectly via the stretch reflex.

Increased γ-motor neuron activity thus increases spindle sensitivity during stretch.

In response to descending excitatory input to spinal motor circuits, both α- and γ-motor neurons are activated. Because of this “α–γ coactivation,” intrafusal and extrafusal fibers shorten together, and spindle afferent activity can occur throughout the period of muscle contraction

119
Q

How do gamma motor neurons play into the Jendrassik maneuver?

A

Increased gamma motor neuron discharge is initiated by afferent impulses from the hands

120
Q

Where are golgi tendon organs located?

A

They are located in the fascicles of the a tendon– there are 3-25 muscle fibers per tendon organ

121
Q

Up to a point the harder a muscle is stretched the stronger is the reflex contraction– however when the tension becomes great enough contraction suddenly ceases and the muscle relaxes.

What is this phenomenon and what is the receptor involved for this?

A

Inverse stretch reflex– c/o the Golgi tendon organ

122
Q

What are the mechanisms for clonus?

A
  1. Damage to the pathways to the Renshaw cells that normally inhibit contraction of antagonist muscles
  2. Stretch reflex-inverse reflex sequence c/o golgi
  3. Hyperactive muscle spindles that initiate contraction right after muscle relaxation because of persistent stretch applied with foot dorsiflexion
123
Q

What muscle receptor is the main contributor to tone in muscles?

A

A gamma motor neuron discharge to intrafusal muscle fibers

hypotonic if low discharge and hypertonic with high discharge

Hyperactive intrafusal muscle fiber– trying to passively flex the elbow results in contraction in the triceps– but when stretch is too much the inverse muscle stretch reflex supervenes and the muscle suddenly relaxes

124
Q

What are the types of memory?

A

Declarative/ Explicit memory
Semantic (facts)– lateral and anterior temporal cortex, prefrontal cortex
Episodic (Events)– hippocampus, medial temporal lobe, neocortex

Non-declarative/implicit memory
Procedural– striatum, motor cortex
Priming– neocortex
Associative learning (conditioned reflex–Pavlov)– amygadala and cerebellum
Nonassociative (habituation)– reflex pathways

125
Q

T or F? Hippocampus is not involved in the storage of long term declarative memory

A

T

126
Q

How does long term potentiation work? Involving schaeffer collateral from CA1 and a pyramidal neuron in CA2.

A
  1. Glutamate is released
  2. Depolarization results in Mg+ being displaced from NMDA receptor
  3. Ca++ enters NMDA
  4. Ca++/calmodulin kinase phosphorylates AMPA receptors, increases their conductance and moves them into the synaptic cell membrane from storage sites
127
Q

What parts of the brain undergo neurogenesis?

A

Olfactory bulb

Hippocampus

128
Q

What part of the brain is concerned with encoding and recalling emotionally charged memories?

A

Amgydala

129
Q

Confabulation or “honest lying” results from lesions in?

A

Ventromedial prefrontal cortex

130
Q

T or F: Short term explicit memory involves the hippocampus while long therm memories involve the entire neocortex.

A

T

131
Q

Enumerate the 5 genes associated with the development and progression AD?

A

Presenilin 1 on chromosome 14
Presenilin 2 on chromosome 1
Amyloid precursor protein on chromosome 21
TRANSMITTED ADW

Trisomy 21
Apolipoprotein E4

132
Q

Where are NF tanlges and amyloid plaques located in AD?

A

NF are intracellular while AD are extracellular

133
Q

What are the new terms for dominance of hemispheres?

A 
Categorial hemispheres (language, analytic processes)
Representational hemisphere (visuospatial relations)
134
Q

What percentage of left handed people will have the left as the categorical hemisphere?

How about right handed people?

A

70%
15% right
15% no preference

96%
4% right

135
Q

Where is the lesion with anomic aphasia?

How about with prosopagnosia?

A

Angular gyrus

Right inferior temporal lobe

136
Q

What is the only inihbitory thalamic nucleus with no projections outside the cortex?

A

Thalamic reticular nucleus

137
Q

What layer of the cortex do thalamic axons synapse on?

A

Layer 4

138
Q

What are the two waves in evoked cortical potentials? Which one is highly localized and highly specific in its location?

A

Primary evoked potential

Diffuse secondary response

139
Q

PGO or pontogeniculo-occipital spikes are large phasic potnetials that originiate in teh cholinergic neurons in the pons and pass rapidly to the LGB and from there to the occipital cortex. When do they occur?

A

REM sleep

140
Q

What percentage of sleep is REM in premature infants? Full term neonates? Young adult? Elderly?

A

80
50
25
20%

141
Q

What are the 4 key clinical features of narcolepsy?

What is lacking or at low levels in narcoleptic patients?

A
  1. Sudden loss of voluntary muscle tone (cataplexy)
  2. Irresistible urge to sleep during the daytime
  3. Sudden onset REM sleep

Hypocretin producing neurons in the hypothalamus

142
Q

T or F. Patients with OSA experience a reduction in total sleep time.

A

FALSE:

OSA is not associated with a reduction in total sleep
time, but individuals with OSA experience a much greater time in stage 1 NREM sleep (from an average of 10% of total sleep to 30–50%) and a marked reduction in slow-wave sleep (stages 3 and 4 NREM sleep). The pathophysiology of OSA includes both a reduction in neuromuscular tone at the onset of sleep and a change in the central respiratory drive.

143
Q

Treatment for excessive daytime sleepiness with narcoleptic patients?

Associated Cataplexy?

Treatment for Willis Ekbon disease/ Periodic limb movement disorder

A

Treatment for excessive daytime sleepiness with narcoleptic patients?

  1. Modafinil
  2. Methyphenidate
  3. Methamphetamine (?)

Associated Cataplexy?
Gamma hydroxybutyrate
Imipramine

Treatment for Willis Ekbon disease/ Periodic limb movement disorder:
Dopamine agonists

144
Q

What is candidate gene for childhood absence epilepsy?

How about generalized epilepsy with febrile seizures?

A

GABRB3

Mutation in a subunit gene of the GABA receptor

SCN1A and SCN1B mutation– Sodium channel subunit genes

145
Q

What AED functions by reducing the low threshold T-type Calcium currents in the thalamic neurons?

Which one functions by decreasing Ca entry into cells and reducing glutamate release?

A

Ethusuximide

Gabapentin

146
Q

During wakefulness and sleep describe the balance between monoamines and ach.

A

Awake: NE from locus ceruleus and serotonin from raphe nuclei predominate over pontine Ach

REM: Ach in the pontine reticular formation are dominant

NREM: Ach in the pontine reticular formation have equal dominance as the monoaminergics above

147
Q

In the awake state– what is the balance between histamine and GABA?

A

High histamine
Low GABA

In NREM the inverse is true
Histamine is from the tuberomamillary nucleus of the hypothalamus.

148
Q

How does ramelteon work in treating insomnia?

A

It functions as a melatonin receptor agonist– it is more effective than melatonin in treating insomnia!

149
Q

Which nucleus of the hypothalamus is responsible for the regulation of the the cyclic activity of the circadian rhythms?

What are the two main inputs to the nucleus

A

Suprachiasmatic nucleus

Light from the retinohypothalamic tract and melatonin from the pineal gland

Brain Power: Beyond Adam (4 decks)

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