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NEUROSci Winter > Midterm 1 > Flashcards

Midterm 1 Flashcards

1
Q

Where is the pain sensitivity within the skull restricted to

A

Pain sensitivity in the skull is restricted tot he intracranial meninges

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2
Q

What are the three layers of the Meninges

A

Dura mater
Arachnoid mater
Pia Mater

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3
Q

Describe the dura mater

A

Thickest, outermost layer, protective, impermeable
Made of two layers: Periosteal layer, Meningeal layer

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4
Q

Describe the two layers of the Dura mater

A

Periosteal: attached to inner surface of skull, continuous with periosteum (outside) on outside of skull bones and cranial sutures
Meningeal layer: covering brain, penetrates spaces in cerebral hemispheres

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5
Q

Describe the arachnoid mater

A

Middle layer, impermeable, adjoins dura (not tightly bound- potential subdural space) separated from Pia by Subarachnoid space that is filled with CSF

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6
Q

Describe the Pia mater

A

Delicate, permeable, innermost, resting on the brain surface
vascular membrane that adheres closely to brain

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7
Q

What are the two important partitions that arise from the meningeal layer

A

Falx cerebri, tentorium cerebelli

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8
Q

Describe the Falx cerebri

A

Sickle-shaped fold separating the cerebral hemispheres. The superior convex border forms floor of superior sagittal sinus; inferior border houses inferior sagittal sinus
Restrict brain displacement

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9
Q

Tentorium cerebelli

A

Fits between the cerebellum and the occipital lobes; separates the posterior cranial fossa from the rest of the cranial vault. Arches upward along median line to become continuous with falx cerebri to form straight venous sinus
Restrict Brain displacement

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10
Q

What is the location, usual cause, and symptoms of an epidural hemorrhage

A

Location: tight potential space between the dura and the skull
Cause: rupture of the middle meningeal artery during head trauma
Symptoms: initially no symptoms (lucid interval), within hours the hematoma compresses the brain and increases ICP, which leads to herniation and death. (unless surgery)

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11
Q

What is the location, usual cause, and symptoms of an subdural hemorrhage

A

Location: potential space between the dura and the loosely adherent arachnoid
Cause: rupture of bridging veins that pass through en route to dural sinuses (vulnerable to shear injury)
Same symptoms has epidural

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12
Q

What are acute and chronic subdural hematomas/hemorrhages

A

Acute: can occur with high velocity impact
Chronic: seen in elderly where brain atrophy allows the brain to move freely (bridging veins susceptible to injury). Slow bleeding over weeks/ months allows brain to accommodate so symptoms often vague: headache, cognitive impairment, unsteady gait.

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13
Q

What is the time frame each blood is seen in the brain: hyperdense, isodense, hypodense

A

hyperdense: More dense than surrounding brain tissue, acute/ recent injury
Isodense: 1-2 weeks
Hypodense: 3-4 weeks

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14
Q

What separates the Pia from the Arachnoid mater

A

Subarachnoid space (CSF)

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15
Q

Where are all cerebral arteries and veins (aneurysm site, may hemorrhage)

A

subarachnoid space, sending off branches that penetrate into the brain

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16
Q

How is the Arachnoid connected to the Pia

A

Delicate threads called trabeculae

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17
Q

What are arachnoid granulations

A

site where CSF diffuses into the venous sinuses

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18
Q

What layer fuses with the ependyma to form the choroid plexus

A

Pia mater, arteries carry sheath of pia as they enter the parenchyma

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19
Q

Where does pain from headaches come from

A

No pain receptors in brain, so pain comes from trigeminal and first three cervical nerves innervating the meninges and vasculature
Dura above the tentorium by the trigeminal ganglion
Dura below the tentorium by cervical nerves

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20
Q

What innervates the dura above and below the tentorium

A

Above: trigeminal ganglion
below: cervical nerves (1-3)

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21
Q

What do migraines depend on

A

depend on the activation of the trigeminal afferents that densely innervate the meninges

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22
Q

Meningitis and meningiomas

A

Inflammation of the meninges and tumors in the meninges

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23
Q

Effects of space-occupying lesions

A

Increased ICP and stretching of dura

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24
Q

What is a cluster headache

A

Lancinating or boring periorbital pain. More sever than childbirth

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25
Q

How does a hangover affect the meninges

A

toxic effect on meninges

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26
Q

Where do immune cells reside? how does inflammation affect immune cells?

A

Meningeal spaces
Inflammation = activation of immune cells. When immune cells are activated, they release things that lower the threshold of activation of pain fibres

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27
Q

Which arteries are responsible for posterior and anterior circulation

A

Anterior: internal carotid artery
Posterior: vertebral artery

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28
Q

Which arteries supply each cerebral hemisphere

A

carotid and vertebral arteries supply each cerebral hemisphere

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29
Q

What is the Circle of Willis? What is anastomosis

A

Anterior and posterior blood supply combines at the circle of Willis. Circle of WIllis provides overlapping blood supply and alternative routes for blood flow.
Anastomosis (circulatory connection between 2 blood vessels) protects the brain when part of vascular supply is blocked

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30
Q

Which cerebral arteries are important for anterior circulation and posterior circulation

A

Anterior: middle cerebral artery, anterior cerebral artery
Posterior: Posterior cerebral arteries

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31
Q

which cortical area does the MCA supply

A

most of the lateral convexity of the cortex (except the leg area of motor homunculus) and white matter, including the frontal, parietal, temporal, and occipital lobes of the insula

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32
Q

which cortical area does the ACA supply

A

The cortex and white matter of the medial frontal and parietal lobes and the anterior corpus callosum
A strip of cortex (1inch) wide on later surface

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33
Q

which cortical area does the PCA supply

A

The occipital lobes and portions of the medial and inferior temporal lobes and the posterior corpus callosum

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34
Q

How do deep structures receive blood

A

Deep structures receive blood directly from branches of the internal carotid artery and proximal portions of the cerebral arteries

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35
Q

what is the most common site of infarction/ ischemia

A

MCA

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36
Q

How does gray matter of the cerebral cortex and underlying white matter receive blood

A

supplied by branches of more distal cerebral arteries

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37
Q

What does in infarction in the MCA result in

A

Contralateral Hemiparesis and hemisensory loss (mainly in face and arm)

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38
Q

What is hemineglect? How does it happen?

A

Unawareness of space and the patient’s own body contralateral to the lesion. Patients may seem unaware or deny the handicap. This may include unawareness of quite dramatic impairments such as blindness or paralysis. May not take care of the contralateral side of the body, deny own limbs, ignore objects in the contralateral visual field
Happens by an infarct in the right hemisphere MCA
Patients may experience anosognosia (denying or unaware of their handicap)

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39
Q

What is parietal neglect syndrome

A
  • Failure to recognize side of body contralateral to injury
  • May not bathe contralateral side of body or shave contralateral side of face
  • Deny own limbs
  • Objects in contralateral visual field ignored
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40
Q

What is Aphasia? What is the cause

A

Inability to comprehend or formulate language
Caused by infarct in left hemisphere MCA

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41
Q

What is Broca’s aphasia

A

Difficulty producing speech, comprehension intact

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42
Q

What is Wernicke’s aphasia

A

difficulty comprehending speech, speech fluent, well structured, grammar and syntax adequate by nonsensical.

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43
Q

What does an infarct in the ACA result in

A

Contralateral hemiparesis: paralysis or weakness of one side of the body
Hemisensory loss involving mainly the leg and foot
Personality changes (frontal lobe)

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44
Q

What does an infarct in the occipital region of the PCA result in

A

Hemianopsia or visual agnosia

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45
Q

What is hemianopsia

A

Loss of vision for one half of the visual field

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46
Q

What is visual agnosia

A

Inability to recognize or interpret objects in the visual field

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47
Q

What does an infarct in the temporal region of the PCA result in

A

memory impairment

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48
Q

What is prosopagnosia? What part of the cortex is damaged? what is the most common cause

A

Inability to identify facial characteristics or not able to recognize a face at all. Damage to the inferior temporal cortex. Most common cause is a PCA stroke

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49
Q

What is a stroke

A

death or dysfunction of brain tissue due to vascular disease

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50
Q

What is an infarction

A

neuronal death

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51
Q

What is ischemia

A

insufficiency of blood supply

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52
Q

what is anoxia

A

reduced oxygen supply

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53
Q

what is an embolus

A

Material carried from one point to lodge in another
(blood clot, air, or fat forms somewhere and travels to lodge somewhere else)

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54
Q

What is an embolism

A

Embolus becomes lodged in an artery and obstructs flow

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55
Q

describe hemorrhagic. what does it lead to

A

bleeding from a vessel (high chance if you have hypertension or aneurysm)

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56
Q

Describe occlusive and what does it lead to

A

Closure of a vessel
(high chance if you have Atherosclerosis or thrombosis

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57
Q

What is tissue plasminogen activator (tPA)

A

A protease enzyme that catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown

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58
Q

What does intraparenchymal hemorrhage mean

A

within the brain

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59
Q

What does extraparenchymal hemorrhage mean

A

at the brain surface

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60
Q

What is an intracranial aneurysm

A

Weakness in the wall of a cerebral vasculature causes a localized dilation or ballooning of the blood vessel

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61
Q

How could you fix a cerebral aneurysm

A

endovascular coiling or surgical clipping

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62
Q

What is endovascular coiling

A

A catheter is inserted in the artery and guided to the aneurysm, a stent is released to prevent the coil from blocking flow, the catheter is guided to the aneurysm to be filled with coil, the coil fills the aneurysm to prevent further growth and rupture

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63
Q

What is surgical clipping?

A

Using a clip on the base of an aneurysm, preventing blood flow into the aneurysm
(very invasive, requires craniotomy)

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64
Q

Where do superficial veins, deep veins, and the superior sagittal sinus drain into

A

Superficial –> Super sagittal sinus and cavernous sinus
Deep –> Great vein of Galen
Superior sagittal sinus –> 2 transverse sinuses –> sigmoid sinus –> jugular vein

Venous blood drains into a system of valve channels called dural venous sinuses

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65
Q

Homeostasis of the the three fluid compartments are regulated by what?

A

Blood-brain and blood-CSF barriers

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66
Q

Describe the vasculature of the arachnoid mater

A
  • The arachnoid mater is an epithelial layer that provides a barrier between the peripheral vasculature of the dura mater and the CSF present in the subarachnoid space through tight junctions and efflux pumps
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67
Q

Describe the vasculature of the dura matter

A
  • The dura mater contains lymphatics and fenestrated blood vessels that lack tight junctions.
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68
Q

Describe the vasculature of the pia mater

A
  • The pia mater meningeal blood vessels lack astrocytic ensheathment, but their endothelial cells are connected by tight junctions.
  • The Pial arteries penetrating the brain are covered by a densely packed perivascular layer of astrocytic foot processes; Veins exiting the parenchyma have a perivascular space flanked by astrocytic foot processes as well as endothelial basement membranes (BMs). The pial BM is only present in the superficial (brain surface) portion of the veins.
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69
Q

What are the three intracranial fluid compartments

A

CSF compartment, interstitial compartment of the brain, intracellular compartment of the brain

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70
Q

What is the choroid plexus

A

Specialized capillary networks that secrete CSF

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71
Q

What are the cellular constituents of the choroid plexus? What constituent secretes CSF

A

Blood vessels and pia form the core and the choroid epithelium secretes CSF

72
Q

What is the total CSF production (mL/ day)? what is the total volume? how many times does it turn over per day

A

500mL/day (~0.5mL/min)

73
Q

What is the total CSF production (mL/ day)? what is the total volume? how many times does it turn over per day

A

500mL/day (~0.5mL/min)
~150 mL
3 times

74
Q

What junctions bind choroid epithelial cells to each other

A

tight junctions

75
Q

What are the two sequential stages of CSF formation?

A

1: ultrafiltration of plasma across the fenestrated capillary into the ECF beneath the basolateral membrane of the choroid epithelial cell
2: Choroid epithelial cells secrete fluid into the ventricle

76
Q

CSF occurs with a net transfer of _____ and ______ that drives water movement _______

A

NaCl, NaHCO3, Isosmotically

77
Q

describe the two step process of the net secretion of Na from plasma to CSF

A

1: Na-K pump in choroid plexus epithelia apical membrane moves Na+ out of the cell into the CSF
2: Active movement of Na+ out of cell generates an inward Na+ gradient across the basolateral membrane, energizing basolateral Na+ entry through the Na-H exchange and Na+- coupled HCO-

78
Q

What is the route of cerebrospinal fluid circulation

A

Lateral ventricle –> foramina of Monro –> third ventricle –> cerebral aqueduct –> fourth ventricle –> Foramina of Magendie and Luschka –> subarachnoid space, over brain

79
Q

How is CSF absorbed

A

absorbed by dural venous sinuses through arachnoid granulations

80
Q

How do the granulations function?

A

Granulations appear to function as pressure-sensitive, one-way valve that allow CSF to go to venous blood

81
Q

At what pressure does CSF formation and absorption change

A

CSF formation is insensitive to changes in the pressure of the CSF
Absorption of CSF increases steeply at presures around 70 mmH20

82
Q

What happens when absorption exceeds formation

A

Lower CSF volume decreases intracranial pressure

83
Q

how can small and large intracranial masses be compensated for?

A
  • Small intracranial masses can be compensated for by reductions in intracranial CSF and blood volume without causing much rise in intracranial pressure (flat part of curve).
  • Larger masses overcome compensatory mechanisms and lead to a steep rise in intracranial pressure, causing reduced cerebral perfusion and, ultimately, herniation and death (right-most part of the curve)
84
Q

what is the equation for cerebral perfusion pressure

A

CPP= MAP - ICP

85
Q

What is a lumbar puncture (spinal tap)

A

A needle is inserted between the fourth and fifth lumbar vertebrae and into the subarachnoid space. CSF flows through the needle which attached to a manometer and the fluid is allowed to rise

86
Q

What is the normal intracranial pressure

A

65-195 mm CSF (H20)
3-15 mm Hg

87
Q

What is papilledema

A

Optic disc swelling caused by increased intracranial pressure
elevated ICP is transmitted to the optic nerve sheath, obstructing axonal transport and venous return in the optic nerve.
Pressure on the optic nerve head forces it inward

88
Q

What is hydrocephalus? What are the three things it can result from

A

excess CSF in the intracranial cavity
1: excess CSF production (rare)
2: obstruction of flow at any point in the ventricles or subarachnoid space
3: decrease in reabsorption when granulations are damaged or clogged

89
Q

Communicating hydrocephalus vs noncommunicating hydrocephalus (common)

A

Communicating: Caused by impaired CSF reabsorption in the arachnoid granulations, obstruction of flow in the subarachnoid space, or rarely by excess CSF production
Noncommunicating: Caused by obstruction in ventricular system

90
Q

What is the treatment for hydrocephalus

A

involves a procedure that allows CSF to bypass the obstruction and drain the ventricles.
A more permanent treatment is a shunt, in which the tubing passes from the lateral ventricle and is then tunneled under the skin to drain into the peritoneal cavity. A valve prevents backflow

91
Q

Where are the three main barrier sites? What is the physical barrier caused by?

A

1: brain endothelium forming the blood-brain barrier
2: Arachnoid epithelium forming the middle layer of the meninges
3: Choroid plexus epithelium which secretes CSF
Physical barrier caused by tight junctoins

92
Q

What are the three proteins in the tight junctions of the BBB? which molecules do they let pass

A

Claudins, occludings, and junctional adhesion molecules
Non-water soluble

93
Q

What are the three ways entry into the brain is achieved

A

1: Diffusion of lipid soluble substances
2: Facilitative and energy-dependent receptor-mediated transport
3: Ion channels and exchanger

94
Q

What is anosmia? how can it be acquired

A

Loss of the ability to detect one or more odors
congenital, sinus infection or inflammation, head injury, toxins, aging, neurodegenerative conditions, chemotherapy, eating disorders, diabetes,

95
Q

Describe the olfactory epithelium

A

Layer of olfactory receptor cells, supporting cells, and basal cells.
Odorants dissolve in the mucus layer and contact the cilia of the olfactory cells. Axons of the olfactory cells penetrate the bony cribiform plate on way to CNS

96
Q

what is the molecular mechanism of odorant transduction

A

Odorant receptor –> activates Golf (G-protein) –> activates Adenylyl cyclase, which converts ATP to cAMP –> activates Na/Ca channel –> activates Cl- channel and Na/Ca exchanger

97
Q

Describe the 3 steps of transduction in olfactory receptor neurons

A

1: odorants generate a slow receptor potential in the cilia
2: receptor potential propagates along the dendrite and triggers a series of action potentials in the soma
3: action potentials propagate along the nerve axon

98
Q

how do ~950 functional receptor proteins discriminate tens of thousands of odors given that each receptor allows for the binding of different odors more or less readily?
3 Hypotheses

A

Olfactory population coding
Olfactory spatial maps
Olfactory temporal coding

99
Q

What is olfactory population coding

A

Each receptor cell expresses a single receptor protein. Each one responds to many odors with differing preferences. Brain distinguishes between odors using a combination of responses

100
Q

describe the central olfactory pathway

A

Olfactory receptor neurons send axons into the two olfactory bulbs, each bulb contains 2000 glomeruli. 25, 000 olfactory axons converge on the dendrites of about 25-100 olfactory neurons within each glomerulus

101
Q

What is olfactory spatial maps

A

Receptor neurons expressing a particular receptor gene all send their axons to the same glomeruli extremely accurately. So the glomeruli within each bulb is an orderly map of the receptor cells in the epithelium expressing a particular receptor protein. the smell of an odor is converted into a specific map within the bulb

102
Q

What is olfactory temporal coding

A

odor information encoded by the detailed timing of spikes within cells and between groups of cells as well as number, pattern, rhythm, and synchronicity of spikes

103
Q

what are the two ways mitral cells can be tuned

A

Only care about the about the position of side chains
Only care about the type of side chain

104
Q

What is lateral inhibition

A

Using inhibitory interneurons to enhance contrast

105
Q

why can individuals mitral cells become more sharply tuned

A

Mitral cells synapse with granule cells that can enhance the contrast between strongly activated and faintly activated glomeruli

106
Q

Is the segregation of information in the olfactory bulb maintained in the olfactory cortex

A

no

107
Q

Why don’t humans have a blind spot

A

Brain fills in blindspot based on given info, brain fills in image

108
Q

T/F we don’t just passively perceive the world, we actively generate it

A

true

109
Q

what are the 5 classes of neurons

A

Rods, cones, horizontal cells, bipolar cells, amacrine cells

110
Q

What is the most direct route for transmitting visual information

A

Photoreceptor, bipolar cell, and ganglion cell

111
Q

What are horizontal and amacrine cells used for

A

Mediates lateral interactions in the inner and outer layers respectively

112
Q

Rods vs Cones

A

Rods: 1000x more sensitive to light. Contains more disks that make vision possible in low light. Produce a reliable response to a single photon. 100 million. low spatial resolution. Only rods are illuminated at low lighting
Cones: Responsible for color, contains one of 3 photopigments. Cones enable us to see in daylight.~5 million

113
Q

Peripheral retina vs Central retina

A

Peripheral: much higher ratio of rod to cones, higher ratio of photoreceptors to ganglion cells, peripheral retina are much more sensitive to low light

Central: Cones only, low ratio of photoreceptors to ganglion cells, specialized for high resolution resolution

114
Q

What is the fovea? why is there no image blur

A

area of the retina responsible for high visual acuity in the center of the macula
Lateral displacement of cells above photoreceptors reduces scattered light

115
Q

Are rods or cones more densely present in the fovea

A

Cones

116
Q

What is protanopia and deuteranopia

A

both have difficulties in red and green
Protanopia: impairment in perception of long wavelength(red)
Deuteranopia: impairment in the perception of medium wavelengths(green)

117
Q

What are the three uses for melanin

A

1: reduces photo-oxidative stress
2: primary nourishment
3: increased visual acuity

118
Q

Describe the removal of photoreceptor disks by the pigment epithelium

A

The tips of photoreceptors are in the pigment epithelium. Disks move from the inner segment to outer segments over a 12 day period. Expended disks are shed from the outer segment and phagocytosed. Photopigment from the disks are then cycled back to newborn photoreceptor disks

119
Q

What is retinitis pigmentosa? what are the hall marks? cause and cure?

A

Progressive vision loss due to gradual degeneration of photoreceptors.
Hallmarks: night blindness, loss of peripheral vision, dark clumps of pigment within the retina. Visual defects begin in the periphery and enlarge leading to tunnel vision and can progress to blindness
Unknown cause and no cure

120
Q

What is macular degeneration

A

Progressive loss of central vision

121
Q

How does light affect a cone cell (hyper or depolarization)

A

hyperpolarization

122
Q

Describe the depolarization of cells in the dark,
How does light affect it

A

cGMP in the outer segment are high, it binds to Na channels keeping them open and allowing sodium to enter, depolarizing the cell.
Absorption of photons leads to a decrease in cGMP, closing the channels and resulting in hyperpolarization

123
Q

describe the retinoid cycle

A

Following photoisomerization, all-trans-retinal is converted to all-trans retinol –> all-trans retinyl ester –> 11-cis retinol –> 11-cis retinal –> transported back to outer segment where it recombines with opsin

124
Q

What molecule is responsible for photoreceptor light adaptation. How does it modulate it

A

Calcium, calcium-mediated inhibition
Calcium channels close in the light, leading to a reduction in calcium. As a result photoreceptor’s sensitive to photon capture is reduced

125
Q

What is the Calcium light adaptation pathway

A

Ca/Na channel brings calcium into the cell which inhibits rhodopsin kinase and guanylate cyclase and reduces the affinity of cGMP for their gated channels
Preventing GTP –> cGMP
Preventing phosphorylation of Rh

126
Q

Which cells make up the outer nuclear layer, the inner nuclear layer, and the ganglion layer

A

Outer: rods and cones
Inner: bipolar and horizontal
Ganglion: ganglion

127
Q

What molecules do photreceptor, ipolar and horizontal cells release

A

Photoreceptor and bipolar cells release glutamate
Horizontal cells release GABA

128
Q

Which retinal processing cell fires APS

A

ganglion cells

129
Q

What are the two classes of bipolar cells

A

mGluR6 and AMPA

130
Q

Are mGluR6 and AMPA cells OFF or ON

A

mGluR6- ON, depolarized when light is on
AMPA- OFF, depolarized when light is off

131
Q

What is a receptive field and how is it located

A

The receptive field is a location on the retina which causes spiking in the ganglion cell’s firing rate.
A small spot of light is projected onto various parts of the retina, and detecting the changes in firing rate

132
Q

What is the direct pathway from photoreceptor to bipolar cells

A

Bipolar cell receives direct synaptic input from a cluster of photoreceptors, constituting the receptive field center.

133
Q

What is the indirect pathway from photoreceptor to bipolar cells

A

Light hits the surrounding receptive field causing the the surround photoreceptors to hyperpolarize. This causes hyperpolarization of horizontal cells to release GABA on the bipolar cell which hyperpolarizes the bipolar cell.

134
Q

What determines whether a ganglion cell is ON or OFF?

A

Determined by the bipolar cell
On bipolar = On ganglion

135
Q

What are mach bands? explain them

A

Our system exaggerating the borders so we can see borders
Certain cells will have their whole surround in the lighter region but when part of it is in the darker region it will have less inhibition and will have higher firing rates. (For ON ganglion)

136
Q

What is the function of the hypothalamus

A

Regulation of circadian rhythms

137
Q

What is the function of the pretectum

A

reflex control of pupil and lens

138
Q

What is the function of the superior colliculus

A

Orienting the movement of head and eyes

139
Q

______ receives a selective input from the retina that is necessary and sufficient for photic entrainment of circadian rhythms

A

Suprachiasmatic nucleus receives a selective input from the retina that is necessary and sufficient for photic entrainment of circadian rhythms

140
Q

T/F retinal photoreceptors are require for circadian photoreception

A

false, ganglion cells send signals to the suprachiasmatic nucleus

141
Q

What opsin-like pigment is expressed in photosensitive ganglion cells

A

melanopsin

142
Q

Do ganglion cells respond slow or fast

A

slow with a big barrage of action potentials

143
Q

Describe the pupillary light reflex pathway

A

When light is shone in one eye, it will have a direct response and the opposite eye will have a consensual response. This is because the resopnse is mediated by the parasympathetic innervation of the iris. The signal travels down an afferent pathway back to the nuclei which talk to the other nuclei through a bilateral effect causing a reaction in both eyes.

144
Q

Would the defect be in the afferent or efferent pathway if:
1. There was a failure to elicit a response (either direct or indirect) to stimulation of the right eye if both eyes respond normally to stimulation of the left eye.
2. There is a direct response in the left eye without a consensual response in the right eye.

A
  1. Afferent pupillary defect
    2: Efferent pupillary effect
145
Q

retinal signals converge on the _____

A

tectum

146
Q

what is the optokinetic response

A

combination of a slow-phase and fast-phase eye movements. Initial slow phases in the direction of the stimulus, followed by fast, correctve phases (return saccade)

147
Q

What is a saccade

A

Fast eye movements that present various parts of the visual scene to the fovea (foveation)
Line up or fovea at all time

148
Q

describe the sensorimotor integration in the superior colliculus

A

Neurons in a particular region of the superior colliculus are activated by specific visual stimuli in a limited region of visual space. Which leads to the generation of a saccade by activating upper motor neurons that move the eye enough to align the foveae

149
Q

what is blindsight

A

blindness in the visual cortex, completely perceptually blind

150
Q

P-type vs M-type ganglion cells
(population, size of receptive field, conduction velocity, type of firing, color?, Type of resolution, what aspects are it good for)

A

P-type: 90% population, small receptive fields, slow conduction velocity, sustained firing to the presentation of visual stimuli, can transmit information about colour. Important for high spatial resolution vision and detailed analysis of the shape, size and colour of object
M-type: 5% population, large receptive field, fast conduction, transient bursts of action potentials to the presentation of visual stimuli, cannot transmit information about colour. High temporal resolution, such as evaluating the location, speed and direction of rapidly moving objects

151
Q

Which hemisphere does the right visual field project to

A

left hemisphere

152
Q

how are images from the pupil projected on to the retina

A

inverted and left-right reversed

153
Q

Which axons of ganglion cells in the retina cross in the optic chiasm

A

nasal retina axons

154
Q

Which ganglion correspond to which layer of the LGN

A

M-type: –> magnocellular (1,2)
P-type –> Parvocellular (3-6)

155
Q

visuotopic organization of the striate cortex is found in the ______ _______ _______

A

right occipital lobe

156
Q

describe the layers of the striate cortex

A

6 principle layers
layer 4 has several subdivisions ABC

157
Q

Which layer is dominated by spiny stellate neurons? Which layer to lateral geniculate axons terminate most heavily in? Where do neurons in layer 4C terminate? where do axons of layer 2/3 terminate? 6? Connections with extrastriate cortex arise primarily from neurons in layers ___ and ____? Descending projections to the lateral geniculate nucleus arise from layer ___ neurons, while those projecting to the superior colliculus reside in layer __?

A

4C
4C and 4A
4B and 2/3
5
4C
2/3 and 4B
6, 5

158
Q

Which layers of the lGN does the contralateral eye project to? which layers do the ipsilateral eye project to?

A

Contralateral projects to 1, 4, 6
Ipsilateral: 2, 3, 5

159
Q

Which sublayer do parvocellular layers project to in the primary visual cortex? Magnocellular?

A

Parvocellular: 4CB
Magnocellular: 4CA

160
Q

Which layer is responsible for receiving segregated inputs from the eyes, and then sending their neurons to more superficial layers to synapse on those layers

A

Layer 4

161
Q

Where does the mixing of pathways from the two eyes first occur

A

in the striate cortex, in layer 4

162
Q

Which layers are binocular

A

4/3

163
Q

What is the head bob called by pigeons which is prompted by seeing the surrounding environment moving relative to the bird

A

motion parallax

164
Q

How is a net magnetic field created that changes in time and gives rise to an electric current that is ultimately measured in MRI (3 steps)

A

1: water protons spin around their axes, creating individual random magnetic fields
2: vertical magnetic field is applied, protons align to create a net magnetic field that is small and vertical
3: a radio frequency pulse is applied in the horizontal direction to make the protons wobble around the vertical axes

165
Q

How do MRI measurements work (3 steps)

A

Place subject in vertical magnetic field, then a horizontal radio frequency pulse is applied so that they rotate in the horizontal plane in phase with one another
2: the horizontal is turned off and the protons begin to move out of phase leading to a decay in the measured current
3: after the withdrawal of the horizontal pulse, the protons will realign with the vertical magnetic field
Different tissues will have different rates of decay T2 (~30ms)

166
Q

What is an fMRA based on? What does it measure?

A

BOLD effect: blood oxygen level dependent signal

Measures blood flow

167
Q

The BOLD signal reflects changes in the ratio of ___ to ___

A

ratio of oxyhemoglobin to deoxyhemoglobin

168
Q

is deoxyhemoglobin or oxyhemoglobin paramagnetic

A

deoxyhemoglobin

169
Q

what is the ratio of oxyhemoglobin in a resting neuron and an activated neuron?

A

Resting: even ratio
Activated: more oxyhemoglobin

170
Q

How would an increase in neuronal activity affect dephasing? What would an fMRI reveal?

A

Increase in neuronal activity = increased oxygenated blood
This decreases deoxyhemoglobin concentration, causing dephasing to occur more slowly and hence slowing down the decay of the measured electric current.
This results in an fMRI image of the location of metabolic activity as revealed by the changes in deoxyhemoglobin concentration

171
Q

How would increased deoxyhemoglobin affect dephasing

A

Increased deoxyhemoglobin = increased dephasing

172
Q

What is neurovascular coupling

A

the active process linking local neuronal activity to orchestrated increase in blood flow

173
Q

fMRI bold signals are sensitive to which type of hemoglobin

A

deoxyhemglobin

174
Q

What is the vascular evolution (pathway) of stimulus-evoked functional hyperemia

A

First capillaries respond and dilate to increase total Hb
Then arterioles will dilate
Then venous outflow will increase (increasing blood flow)
Deoxyhemoglobin decreases next

175
Q

What happens in the following times of stimulus-evoked functional hyperemia?
t < 1, t< 2s, 2s < t< 6s, t>6s, t>10s

A

t < 1 = stimulus?
t < 2 s = arterioles dilate, venous flow speed increases
2-6s = venous outflow is seen as an increase in HbO and decrease in HbR. Veins do not notably dilate
t>6= for prolonged stimulation, pial arteries return to baseline. Parenchymal hyperemia remains
t>10 = Reponse returns to baseline

176
Q

what are the mechanisms for blood flow change?
4 ways

A

1: direct action of neuronally derived substances such as glutamate and nitric oxide on the vasculature
2: cellular mediators of neurovascular coupling, such as astrocytes, interneurons, and pericytes
3: afferents from the basal forebrain via acetylcholine release
Vsoactive substance by cortical interneurons including VIP and NO

177
Q

What mediates the rapidly propagated retrograde vasodilation mechanism during functional hyperemia

A

endothelial hyperpolarization

NEUROSci Winter (3 decks)

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