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Gross Anatomy > Neuroscience 3 > Flashcards

Neuroscience 3 Flashcards

1
Q

What are the layers of the eyeball from outside in?

A

Sclera, choroid, retina, vitreous body

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2
Q

What is the pathway for light waves as they enter the eye?

A

Cornea, Aqueous humor, Lens, Vitreous humor

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3
Q

The opthalmic artery enters the bony orbit via the optic canal and gives off the:

A

central artery of the retina

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4
Q

Occlusion of the opthalmic artery may result in:

A

ipsilateral blindness

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5
Q

Where is the nucleus of CN III?

A

Tegmentum of the midbrain

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6
Q

CN III innervates the motor fibers of the:

A 
Superior rectus
Medial rectus
Inferior rectus
Inferior oblique
Levator palpebrae
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7
Q

CN III innervated the PS fibers of the:

A

Ciliary muscle

Sphincter pupillae muscle

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8
Q

What is “down and out” and what nerve is out?

A

External strabismus, CN III is out, and eye is down and out due to unopposed action of superior oblique (4) and lateral rectus (6). This also can cause diplopia

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9
Q

What is ptosis? What CN damage is associated with it?

A

Droopy eyelid, CN III or Horner’s syndrome

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10
Q

What is mydriasis and what CN damage is associated with it?

A

Dilated pupil, CN III, can also have blurred vision (impaired accommodation)

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11
Q

Damage to CN IV can result in:

A

Vertical diplopia, patient can’t look down ie when going down stairs

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12
Q

True or False: CN IV and CN VI only have motor input.

A

True

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13
Q

What is the onlyCN to emerge on the dorsal surface of the brain stem, with contralateral projection?

A

Trochlear, CN IV

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14
Q

What is internal strabismus and what CN damage is associated with it?

A

Eye deviates medially due to unopposed action of medial rectus muscle, damage to CN VI - abducens

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15
Q

Nucleus of CN VI is located in:

A

the pons

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16
Q

Ophthalmic nerve is also known as:

A

V-1 of trigeminal nerve, CN V

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17
Q

Name the branches of the ophthalmic nerve:

A
  1. Tentorial (meningeal branch)
  2. Lacrimal
  3. Frontal
  4. Nasociliary
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18
Q

What is papilledema and what are some conditions that cause it?

A

Swelling of optic disc, associated with tumor, bleeds, impaired CSF reabsorption, increased CSF production, ventricular obstruction
typically bilateral with visual acuity unaffected unless extreme case

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19
Q

A relaxed ciliary muscle causes the lens to become __1__ and is used for __2__.

A
  1. Lens is less convex

2. Far vision focus

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20
Q

A contracted ciliary muscle causes the lens to become __1__ and is used for __2__.

A
  1. Lens more convex

2. Near vision focus

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21
Q

Gray matter is composed of:

A

neuronal cell bodies

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22
Q

White matter is composed of:

A

axons

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23
Q

Where is the limbic lobe in the brain?

A

Directly above the corpus collosum (cingulate gyrus)

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24
Q

The precentral gyrus is also known as:

A

primary motor cortex

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25
Q

The postcentral gyrus is also known as:

A

the primary somatosensory cortex

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26
Q

Warnicke’s areas includes:

A

the supramarginal gyrus

the planum temporale

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27
Q

The primary visual cortex is on the banks of the:

A

calcarine sulcus (covers the lingual sulcus and the cuneus)

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28
Q

The middle cerebral artery supplies:

A 
Primary motor
Primary somatosensory
(for the above **not leg and foot)
Broca's
Wernicke's
Primary Auditory
Frontal lobe
Superolateral portion of temporal lobe
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29
Q

The anterior cerebral artery supplies:

A

Primary Motor and Primary somatosensory - leg and foot areas

Medial surface of cortex

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30
Q

The posterior cerebral artery supplies:

A

Inferior and medial portions of the cerebral cortex
Primary visual cortex
Temporal lobe areas responsible for memory
Thalamus and Midbrain

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31
Q

The lenticulostriate arteries supply:

A

The basal ganglia

Internal capsule

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32
Q

The blood supply of the pons come from:

A

The basilar artery

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33
Q

The base of the pons contains axons of the corticospinal tract and what CN’s?

A

CN VI and VII

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34
Q

What is the blood supply of the medulla?

A

PICA, AICA

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35
Q

The CSF flows into the 4th ventricle where it exits the __1__ into the sub-arachnoid space through three holes in the lining of the ventricles and the pia mater: __2__ and __3__.

A
  1. ventricular system
  2. foramen of magendie (medial)
  3. foramina of Luschka (lateral)
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36
Q

Eventually, CSF is reabsorbed into the venous system through:

A

the arachnoid villi

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37
Q

The subcortical gray matter of the thalamus includes:

A
  1. Pulvinar
  2. Anterior tubercle
  3. Lateral geniculate body (visual from eye to V1)
  4. Medial geniculate body (auditory info from Heschel’s)
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38
Q

The lenticular nucleus (putamen and globus pallidus) and the striatum (putamen and caudate nucleus) make up the gray matter of the:

A

basal ganglia

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39
Q

What are the symptoms of Parkinson’s Disease:

A
  1. shuffling gait
  2. limb rigidity
  3. masked expression
  4. difficulty initiating movements
  5. pill rolling tremor of hands
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40
Q

Where is the lesion implicated in Parkinson’s disease found?

A

Substantia nigra - basal ganglia

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41
Q

Uncontrollable hand writhing movements and mental status changes such as dementia siggest what diagnosis?

A

Huntington’s Disease (putamen and caudate nuclei)

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42
Q

Wild, flailing movements of the limbs are suggestive of what diagnosis of the basal ganglia?

A

Hemiballism (subthalamic nucleus)

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43
Q

The internal structures of white matter include:

A
  1. corpus callosum
  2. fornix
  3. anterior commissure
  4. posterior commissure
  5. optic tract
  6. optic chiasm
  7. optic nerve
  8. corona radiata
  9. Internal capsule
  10. Crus Cerebri
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44
Q

What is this? The funnel in which axonal tracts carry information from the thalamus to the cortex, and from the cortex to the striatum, brain stem (corticobulbar) and spinal cord (corticospinal).

A

Internal Capsule

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45
Q

Damage to what part of the internal capsule results in symptoms of sensory loss and paralysis?

A

Posterior Limb

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46
Q

What makes up the lenticulate nucleus?

A

Putamen, globus pallidus - part of basal ganglia

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47
Q

Lenticulostriate arteries and/or the anterior choroidal artery supply the:

A

posterior limb of the internal capsule

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48
Q

What is the cause of retinitis pigmentosa?

A

Degeneration of rods, then cones due to mutations in rhodopsin gene

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49
Q

What are the symptoms of macular degeneration?

A

Loss of central vision and acuity

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50
Q

What is the leading cause of vision loss?

A

Age-related macular degeneration

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51
Q

Blocked, blurred vision is a symptom of?

A

Diabetic retinopathy

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52
Q

What is the treatment for diabetic retinopathy?

A

Laser surgery etc.

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53
Q

The common retinal disorders are:

A

retinitic pigmentosa
macular degeneration
diabetic retinopathy

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54
Q

The visual system is very good at detecting spatial:

A

contrast

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55
Q

ON center cells increase their discharge rate to luminance _____ in the receptive field center

A

increments

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56
Q

____ center cells increase their discharge to luminance decrements in the receptive field center.

A

Off

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57
Q

Receptive fields of ganglion cells have a __1__. They come in 2 types: on-center and off-center ganglion cells.

A
  1. center and antagonistic surround
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58
Q

Where does an on-center ganglion cell cell have its excitation?

A

Center

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59
Q

Where does an an off-center ganglion cell have its excitation?

A

Periphery

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60
Q

Bipolar cells have what instead of APs?

A

Graded potentials

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61
Q

Graded depolarization of bipolar cells leads to increase ___1___ release at their synapses and ___2___ of ganglion cells they contact.

A
  1. glutamate

2. depolarization

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62
Q

On-center bipolar cell __1__ in light (and __2__ in dark)

A
  1. depolarizes

2. hyperpolarizes

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63
Q

Off-center bipolar cell __1__ in light (and __2__ in dark)

A
  1. hyperpolarizes

2. depolarizes

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64
Q

Center and surround receptive fields are constructed neurally where?

A

At the level of the retinal bipolar cells (receiving synaptic input from cones)

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65
Q

In hyperpolarization of off-center bipolar cells, what is hyperpolarizing and what NT release is lessening?

A

cones are hyperpolarizing (leads to BC hyperpolarizing), glutamate release goes down

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66
Q

Cone hyperpolarization in on-center bipolar cells results in:

A

BC depolarization (also glutamate DECREASE)

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67
Q

What determines the the on/off center properties of bipolar cells?

A

Glutamate receptors

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68
Q

On-center bipolar cells have what kind of glutamate receptors?

A

Metabotropic

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69
Q

Off-center bipolar cells have what kind of glutamate receptors?

A

Ionotropic (AMPA, kainate)

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70
Q

What cells connect bipolar cells to cone cells?

A

Horizontal cells

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71
Q

Horizontal cells have what kind of potentials?

A

Graded

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72
Q

Horizontal cells to what for bipolar cells?

A

Provide lateral inhibition/antagonism in that they tend to antagonize the bipolar cells’ response to light

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73
Q

Cones synapse on __1__ to form receptive field centers, and on horizontal cells to form receptive field __2__.

A
  1. bipolar cells

2. surrounds

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74
Q

What is the basis for trichromatic color vision?

A

short (blue), medium (green) and long (red) cone cells

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75
Q

What are cone opsins?

A

GPCR superfamily where the cis-11- retinal chromophore sits

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76
Q

No green detection comes from:

A

no expression of M opsin, deuteranopia

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77
Q

No red detection comes from:

A

no expression of L opsin, protanopia

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78
Q

What kinds of ganglion cells carry color information?

A

Parvocellular cells

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79
Q

What kind of cells are luminance encoding?

A

Magnocellualr cells

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80
Q

Blue on/yellow off cells are:

A

koniocellular cells

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81
Q

The class of “intrinsically photosensitive retinal ganglion cells” play important roles in non-image forming vision such as:

A
  1. Inform ambient light intensity
  2. Synchronize circadian rhythms
  3. control the pupil response
82
Q

What is declarative memory?

A

Remembered events, images, cognitive skills that can be summoned at will, and is available to consciousness

83
Q

Patient HM suffered what complication of epilepsy surgery?

A

Anterograde amnesia

84
Q

Autopsy of RB revealed what area of the brain that contributed to his amnesia for declarative memory?

A

CA1 area of the hippocampus

85
Q

Spatial learning and memory (in rodents) depends on:

A

the hippocampus

86
Q

What are the brain areas involved in declarative memory?

A

Hippocampus and its subcortical connections to the mammillary bodies and dorsal thalamus

87
Q

Short-term storage of declarative memory is __1__ while long-term storage of declarative memory is thought to take place in __2__.

A
  1. Hippocampus and related structures

2. Wernicke’s, temporal cortex…other cortical sites

88
Q

The physical embodiment of long-term memory is the:

89
Q

What determines the engram?

A

Long term changes in efficacy of synaptic transmission

90
Q

What is the theory behind long-term potentiation?

A

Brain changes that aid in consolidation of declarative memory.

91
Q

What is LTP?

A

long lasting increase in synaptic strength that provides an attractive neural mechanism for certain learning and memory

92
Q

Where is LTP observed?

A

Cerebral cortex, hippocampus, cerebellar cortex

93
Q

NMDA receptor activation is required for _____ of LTP.

94
Q

_____ receptors are required for the expression of LTP (after induction)`

95
Q

What kinds of synapses have been studied w/r/t their expression of LTP?

A

Schaffer Collateral-ca1 synapses in the hippocampus

96
Q

Why are Ca1 pyramidal neurons given to LTP?

A

They show 1. specificity and 2. associativity. LTP requires strong activity in both presynaptic and postsynaptic neurons

97
Q

The NMDA receptor channel can only open when:

A

the depolarization is sufficient - high intensity and high frequency to remove the Mg2+ ion

98
Q

What ion is most directly responsible for LTP in the short term?

A

Ca, which travels through the NMDA receptor and activates AMPA receptor insertion in the postsynaptic membrane

99
Q

What is most directly responsible for LTP in the long-term?

A

Changes in gene expression and synthesis of new proteins associated with synaptic growth

100
Q

What is LTD?

A

Long-term depression, a long-lasting decrease in synaptic strength

101
Q

LTD has what effect on AMPA receptors?

A

Internalization of them from the postsynaptic membrane (opposite of LTP)

102
Q

Where is LTD seen?

A

Same areas as LTP, Schaffer collateral-CA1 synapses in the hippocampus

103
Q

In LTD, what kinds of Ca2+ changes occur?

A

Small and slow rises of Ca2+ intracellularly, which correspond to activation of phosphatases instead of kinases.

104
Q

A tumor that produces profound personality changes might involve what gyrus?

A

Middle frontal gyrus

105
Q

The supramarginal gyrus is directly above what in the brain?

A

Wernicke’s area

106
Q

The superior temporal gyrus is associated with what sensory modality?

107
Q

Squirming and fidgeting, but still having control over things like touching a hand to a nose on command indicates a lesion of:

A

Basal ganglia

108
Q

What cranial nerve runs close to Wernicke’s area and can be implicated in a lesion?

A

Trigeminal, CN V

109
Q

A lesion in the right posterior cerebral artery can result in what visual problem?

A

left homonymous hemianopia

110
Q

The ventroposterolateral nucleus receives:

A

axons whose cell bodies are in the gracile and cuneate nuclei on the opposite side

111
Q

The 3rd ventricle is associated with what part of the brain?

A

Diencephalon

112
Q

What is a synaptic active zone?

A

Site were special vesicles are docked.

113
Q

What is a PSD, postsynaptic density?

A

Lots of electrons at postsynaptic cell, many receptors

114
Q

An AP in the motor neuron produces a depolarization of the muscle cell called:

A

an endplate potential, EPP

115
Q

What is a MEPP made of?

A

discrete packet of ACh, many packets of ACh make an EPP

116
Q

NT release significantly depends on:

A

Rise in intracellular Ca channels from opening of voltage-gated channels

117
Q

Blocking voltage-gated Ca channels, for example with certain toxins, eliminates the postsynaptic response because:

A

no NT is released

118
Q

What is Lambert-Eaton myasthenic syndrome?

A

Skeletal muscle weakness and fatigue, happens to cancer patients.

119
Q

What is the cause of Lambert-Eaton syndrome?

A

Reduction in ACh release resulting from a loss of voltage-gated calcium channels in the presynaptic terminal of motor neurons due to an autoimmune reaction where antibodies bind to calcium channels

120
Q

Small molecule NTs such as amino acids have a clear core or dense core? Where are they synthesized?

A

Clear core, made in nerve terminal

121
Q

Neuropeptides have a clear core or a dense core? Where are they made?

A

Dense core, made in cell body and transported to nerve terminal

122
Q

Where is the PSD located?

A

Target zone

123
Q

A form of short-term synaptic plasticity known as facilitation results from:

A

prolonged elevation of presynaptic Ca

124
Q

Facilitation is also known as:

A

paired pulse facilitation

125
Q

Why can Ca build up in the synaptic terminal?

A

Because it takes longer to clear Ca from the target cell than to invite it in.

126
Q

Synaptic facilitation is a __1__ in synaptic strength that occurs when two or more __2__ invade the presynaptic terminal within a few ms of each other. Because of facilitation, the second EPSP is __3__ than the first. It results from prolonged elevation of presynaptic __4__ following synaptic activity.

A
  1. rapid increase
  2. APs
  3. larger
  4. Ca2+
127
Q

Synaptic facilitation means that when APs arrive in close succession, Ca2+ builds up and allows:

A

more NT release in response to a subsequent AP.

128
Q

Is facilitation observed if two APs are far apart in time?

129
Q

What is the major excitatory NT in the CNS? What kinds of receptors does it use?

A

Glutamate, has both ionotropic and metabotropic receptors

130
Q

How do we get receptor diversity?

A

Diff arrangements of subunits

131
Q

AMPA receptor channels are selectively activated by __1__ and mediate a __2__ EPSP via the flow of Na and K ions down their electrochemical gradient.

A
  1. AMPA

2. fast

132
Q

Which is faster, AMPA receptors or NMDA receptors?

133
Q

What ions produce an EPSP in a NMDA receptor?

A

K, Ca and Na

134
Q

Why do NMDA receptors not typically open?

A

Because they are blocked by Mg and the membrane must be sufficiently depolarized for the Mg to come off.

135
Q

What kind of receptor channels are AMPA and NMDA?

A

Ionotropic

136
Q

In most glutamate receptors, an EPSP is made by:

A

both AMPA and NMDA receptors opening

137
Q

What is CREB?

A

A transcription factor, influences by intracellular Ca influx at the synaptic terminal

138
Q

What does CREB activity tell us?

A

Calcium and other 2nd messengers can modify neuronal function by regulating gene transcription.

139
Q

What is the major inhibitory NT in the CNS?

140
Q

GABA-A receptors mediate:

A

a fast IPSP via the flow of Cl ions down their ec gradient

141
Q

GABA-B receptors mediate:

A

a slow signal (bc they are G-protein linked)

142
Q

What is the effect of pentobarbital?

A

Induces a large IPSP (synaptic GABA channel open for a longer period of time)

143
Q

What is the function of dendrites?

A

Increases the receptive surface of the neuron

144
Q

How do PSPs differ from APs?

A

PSPs are small, graded potentials

145
Q

Anterograde transport requires ATP via:

146
Q

Retrograde transport requires ATP via:

147
Q

True or False: Electrical synapses are often bidirectional.

148
Q

Where in the CNS are electrical synapses found?

149
Q

How can a signal can be amplified?

A

Chemical synapse can amplify a signal - allow for temporal and spatial summation

150
Q

Associate synaptobrevin with:

151
Q

Associate T-SNARES with:

A

SNAP-25 and syntaxin

152
Q

V-SNARES and T-SNARES help exocytosis in what kind of synapse?

153
Q

Botulinim toxin creates muscle weakness by cleaving:

A

SNAP-25 or synaptobrevin

154
Q

A muscarinic ACh receptor elicits what effect on cardiac muscle?

A

Slows heart rate (as opposed to ionotropic Ach receptor) which increases it)

155
Q

If the reversal potential is more + than the threshold, what happens?

A

excitation results

156
Q

Inhibition occurs if the reversal potential is:

A

more (-) than the threshold

157
Q

What is decremental conduction?

A

Before EPSPs can reach the cell soma, a large amount of potential is lost because dendrites are thin and leaky tp electric current

158
Q

A lesion in Meyer’s loop produces what VF?

A

Pie in the sky phenomenon or homonymous quadrantanopia

159
Q

The left VF is dealt with by what hemisphere of the brain?

A

Right (and vice versa)

160
Q

Where does spatial contrast originate?

A

Center-surround receptive fields

161
Q

What are the first neurons to receive light input?

A

The striate cortex

162
Q

What part of the brain is involved in the regulation of circadian rhythms?

A

hypothalamus

163
Q

What is one main place where optic radiations originate?

A

LGN, lateral geniculate nucleus

164
Q

What is the central point of the vertical meridian in the retina?

165
Q

The LEFT optic tract contributes to what portions of the VF?

A

Temporal vision of left VF and Nasal vision of right VF

166
Q

The RIGHT optic tract contributes to what portions of the VF?

A

Temporal vision of the right VF and nasal vision of the left VF.

167
Q

A lesion in the striate cortex looks like?

A

Macular sparing, homonymous hemianopia

168
Q

Where would a lesion be that produces quandrantanopia?

A

LGN, VF defect is contralateral to lesion…Meyer’s loop lesion applies here

169
Q

The primary visual cortex is located:

A

around the calcarine sulcus

170
Q

True or False: P, M and K ganglion cells all have center-surround organization.

171
Q

The magno pathway has what shaped cells?

A

Parasol cells

172
Q

The parvo pathway has what shaped cells?

A

Midget cells

173
Q

The M pathway is known for:

A

Luminance, contrast detection and motion

174
Q

The P pathway is known for:

A

Spatial acuity and color

175
Q

How are P and M cells arranged in the LGN?

A

Layers, with K layers in between

176
Q

True or False: The K pathway is not involved in color processing.

177
Q

Color vision is based on cone-:

A

opponency. We see green as the absence of red, blue as the absence of yellow etc.

178
Q

The K pathway carries what color information?

A

Blue-yellow

179
Q

Can a single cone cell inform both color and intensity?

180
Q

The neocortex has how many layers?

181
Q

How does cortical circuitry run in the primary visual cortex?

A

Vertically, includes inputs from LGN, and resident pyramidal cells, and cells that run information back to the LGN

182
Q

LGN inputs enter V1 and terminate:

A

in layer 4. Contralateral and ipsilateral effects alternate like stripes (ocular dominance columns)

183
Q

What are ocular dominance columns?

A

Groups of cells that all receive input from one eye. They line up all next to one another like stripes.

184
Q

What is orientation tuning?

A

Our cortical neurons react more to certain angles that we observe.

185
Q

What is retinotopy?

A

Retinal mapping

186
Q

What kind of organization is suggested by retinotopy, orientation tuning and ocular dominance?

187
Q

What is a special characteristic of V1 of the primary visual cortex?

A

CO, cytochrome oxidase blobs

188
Q

What is contained in CO blobs?

A

Unoriented color cells

189
Q

Within V1, what are two anatomically segregated pathways?

A

CO blobs and interblobs (there are more)

190
Q

What is the icecube model?

A

Functional representation of architecture of V1 proposed by Hubel and Weisel.

191
Q

What is a hypercolumn?

A

For example, an orientation hypercolumn is a complete set of orientation columns that span all possible preferred angles of orientation

192
Q

Retinotopy is essential for delineating:

A

visual space/VF

193
Q

Ocular dominance is essential for delineating:

194
Q

Orientation is essential for delineating:

A

contour extraction

195
Q

What is one suggested reason for why there are more than 30 separate visual cortical areas in the brain, rather than a large V1?

A

Map shouldn’t get too crowded with information organization. Diff cortical areas have different strengths.

196
Q

Semaphorins are mostly:

A

repellant (non-diffusible)

197
Q

Ephrins have what effect on cells?

A

Collapse of growth cone

198
Q

__1__ and __2__ guide projections from the retina to the optic tectum.

A
  1. Ephs
  2. Ephrins
    Axons in the temporal retina are repulsed by ephrin, but axons in the nasal retina are blind to ephrin because they lack the Eph receptor
199
Q

Netrins play a key role in commisural axonal crossing in the:

A

developing spinal cord

200
Q

In order for axons to not recross the midline, upregulation of what occurs, which reacts to slits in the midline?

201
Q

The highest level of form vision for primates appears to be:

A

face recognition

202
Q

Lesions in certain parts of the temporal cortex produce yield prosopagnosia, which is:

A

the inability to recognize faces

Gross Anatomy (5 decks)

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