Final Exam Flashcards
(114 cards)
1
Q
what is the path of light?
A
cornea -> aqueous humor -> lens -> vitrous humor -> focused on retina by lens and cornea
2
Q
what is the retinal pigment epithelium (RPE)?
A
monolayer of pigment-producing cells with dendritic-like projections
- melanin absorbs light and minimizes scatter of photons between photoreceptors (prevents light hitting all PRs, high acuity vision)
- provides nutrients, removes wastes, supplies and regenerates retinal chromophore
3
Q
what are the 4 structural components of photoreceptor cells?
A
- cell body (layer 4)
- inner segment (layer 2): rich in ER and mitochondria
- outer segment (layer 2): where light hits first; contains stacks of membrane-rich discs rich in photopigment (opsin) protein
- synaptic terminal (layer 5)
4
Q
what are the 2 types of photoreceptors? how do they differ?
A
scotopic (rods) and photopic (cones)
- rods have a higher density of opsin, making them more sensitive to light (activated by a single photon; sensitive to amount of light)
5
Q
what is the maximum sensitivity of each type of cone? rods?
A
- blue (short): 419 nm
- green (medium) 533 nm
- red (long): 564 nm
- rod: 500 nm (doesn’t provide info about wavelength, only # of photons b/c only one type of rod)
6
Q
what part of the retina is cone density the highest? where is the optic disc?
A
- cone density highest at fovea (0 degrees)
- optic disc: ~20 degrees into nasal retina; anatomical blind spot (optic nerve where all RGCs converge)
7
Q
what is the initial event in phototransduction?
A
photoisomerization of the retinal chromophore (located between TM protein 6-7 of GPCR)
- 11-cis retinal gets hit with a photon of light and photoisomerizes into all-trans retinal, revealing the G protein binding site
8
Q
what are the steps of phototransduction?
A
- hv binding isomerizes cis-retinal to trans-retinal, actives rhodopsin (GPCR)
- rhodopsin activates transducin (G protein) which activates phosphodiesterase (PDE)
- PDE cleaves cGMP -> GMP
- CNG channels close (loses cation influx)
- cell hyperpolarizes, reduces glu release that normally occurs in the dark
9
Q
how does phototransduction stop?
A
- rhodopsin kinase phosphorylates opsin, stopping the cascade
- arrestin binds opsin to stop it
10
Q
how does chromophore regeneration occur (what is the visual cycle)?
A
- isomerized all-trans retinal must be reconverted to cis-retinal in order to regenerate functional PRs
- occurs in RPE cells (rods+cones) and Muller cells (cones)
- once cis-retinal is resynthesized, carried back to PRs via retinal binding protein (RBP)
- cis-retinal binds to opsin in PRs, reseting the cycle
11
Q
what is the circuitry of the retina?
A
- PRs synapse onto bipolar cells and horizontal cells
- bipolar cells synapse on RGCs
- RGCs turn into the optic nerve
12
Q
what do horizontal cells do?
A
inhibitory; turn off neighbouring signals when strongly activated (lateral inhibiton)
13
Q
what generally occurs in the presence of light?
A
glutamate release is decreased which excites bipolar cells and generates AP in retinal ganglion cells
14
Q
what is the structure of opsin proteins?
A
GPCRs = apoprotein + retinal
- 7 TM spanning proteins
- extracellular N-terminus, intracellular C-terminus and G-protein binding domain
- difference in spectral sensitivity due to differences in AA sequence (3 types of cone opsins)
15
Q
what makes a GPCR an opsin?
A
have a retinal binding site
- K296 = lysine residue required to be an opsin
16
Q
what is the purpose of lateral inhibition? how does it work?
A
provides higher acuity for stimulus
- neuron excited to the greatest degree has inhibitory collaterals to inhibit neighbouring neurons
17
Q
how do ON bipolar cells work?
A
ON bipolar cells fire in the presence of light, exciting RGCs
- have metabotropic glutamate receptors
- in the dark, mGluR activation keeps Na+ channels (TRPM1) closed -> hyperpolarizes them (mGluRs are inhibitory)
- in the light, they depolarize due to release Glu release and opening of TRPM1 channels
18
Q
how do OFF bipolar cells work?
A
in the dark, OFF bipolar cells are depolarized and have a baseline firing rate
- have ionotropic glutamate receptors (iGluRs) -> ion channels when activated keeps OFF bipolar cells depolarized
- in the dark, they are depolarized
- in the light, they hyperpolarize due to reduced Glu release and closing of iGluRs
** OFF bipolar cells are turned off by light and result in decreased RGC firing**
19
Q
what are the types of receptive fields?
A
- each ganglion cell has a receptive field that contains a centre region and a surround region
- PRs can hyperpolarize or depolarize bipolar cells (depending on the type of bipolar cell)
1) on-centre/off-surround
2) off-centre/on-surround
20
Q
what occurs when you shine light in the centre of an on-centre/off-surround field?
A
shining light on the centre will hyperpolarize the cone, decreasing NT release, turning off mGluRs resulting in opening of TRPM1 channels -> ON-bipolar cell depolarizes, releasing NT and RGC fires
an on-centre/off-surround is turned on when you shine light in the centre
21
Q
what occurs when you shine light in the centre of an off-centre/on-surround field?
A
shining light on the centre will hyperpolarize the cone, decreasing NT release, closing iGluRs resulting in hyperpolarization of the OFF bipolar cell, which reduces NT release and decreases AP firing by the RGC
an off-centre/on-surround is turned off when you shine light in the centre
22
Q
what is the organization of the surround?
A
photoreceptor that synapses onto a horizontal cell that synapses onto a central cone
23
Q
what occurs in the surround of an on-centre/off-surround receptive field if light is shone on the surround?
A
- light on the surround hyperpolarizes the PR and decreases glu release onto H cells
- H cells stop inhibiting the centre PR, increasing glu release from the PR, closing TRPM1 channels and reducing AP firing from the RGC
24
Q
what occurs in an on-centre/off-surround field in the dark?
A
- dark depolarizes centre cone and hyperpolarizes bipolar cell
- dark depolarizes surround cone, release glu onto H cell
- H cell provides some inhibition (GABA) onto centre cone
- some excitation + some inhibition = baseline firing
25
what occurs in an off-centre/on-surround field in the dark?
- dark depolarizes centre cone and depolarizes bipolar cell (glu binds iGluRs, cation influx, depol.)
- dark depolarizes centre cone, releasing glu onto H cell
- H cell provides some inhibition (GABA) onto centre cone
- some excitation + some inhibition = baseline firing
26
what happens when you shine light on the surround of an off-centre/on-surround receptive field?
- light hyperpolarizes the surround cone, reducing glu release onto H cell
- reduced activation of H cell reduces GABA release onto centre cone
- increases glu release onto off-bipolar cell
- glu binds iGluRs, increasing cation influx and depolarizing the BC
- increased glu release onto RGCs, increased firing
27
why do we see Mach bands as a gradient?
the receptive field over the dark band receives more surround inhibition because part of the surround is in the
brighter area. Therefore, the excitatory response is less and this results in our seeing that area as darker
28
what is contrast? how do we see it?
difference in luminance or wavelength of the focal object and other objects within the field of view
- cone opponent receptive fields
29
what is constancy? what is assimiliation?
- constancy: perceived colour of an object remains relatively constant under varying illumination conditions
- assimilation: tendency for colour to take on tinges of another colour when juxtaposed alongside it
30
what happens when you shine green light onto the centre of an on-centre/off-surround field with green in the centre and red in the surround?
- green light hyperpolarizes the centre cone, reducing glu release onto on bipolar cell
- TRPM1 channels open in on bipolar cell, increasing firing in the RGC (green perceived)
31
what happens when you shine red light onto the surround of an on-centre/off-surround field with green in the centre and red in the surround?
- red light hyperpolarizes the surround cone, reducing glu release onto the H cell
- reduced H cell activation reduces GABA release onto centre cone
- increases glu release from centre cone onto on bipolar cell
- mGluRs activated, TRPM1 channels inhibited, reduced NT release onto RGC
- reduced perception of green
32
what are protanopes? what are deuteranopes?
- protanopes: missing LWS opsin (red)
- deuteranopes: missing MWS opsin (green)
- inability to distinguish between red and green, making them appear yellowish or brownish
- present in 8% of males
33
what are tritanopes? why is it rare?
- missing SWS opsin (blue)
- doesn't involve sex chromosomes
34
why is colour blindness more prevalent in males?
- opsins are coded for in the X chromosome
- males have only 1 X chromosome (unlike females)
- have no back up copy if gene duplication goes wrong
35
how is the dress perceived differently by different people? how does lighting affect perception?
- older females see W/G
- younger males see B/B
- cool illuminant favours W/G
- warm illuminant favours B/B
- W/G seen by people with larger pupils
36
what is the ratio between PRs and RGCs in foveal and extrafoveal regions? how does this affect acuity?
- fovea: 1:1 ratio (small RF, high resolution, low sensitivity)
- extrafoveal: 15-45 PRs per RGC (large RF, dim light, low acuity)
37
what are the types of ganglion cells?
- P cells: GCs project to parvocellular layers of LGN; exhibit cone opponency, small RF, sustained firing, colour, form, fine details
- M cells: GCs project to magnocellular layers of LGN; more sensitive to luminescence (amount of light), large RF, phasic, contrast and movement
38
what separates the nasal retina from the temporal retina?
fovea
39
where hemispheres do different parts of the retina reach?
- temporal retina travels to ipsilateral hemisphere (uncrossed info)
- nasal retina travels to contralateral hemisphere (info crosses at optic chiasm)
40
how is our binocular FOV imaged on the retina? why is this important?
binocular segment of target imaged on both retinas:
- left half of target imaged on left nasal retina and right temporal retina
- right half of target imaged on right nasal retina and left temporal retina
- stereopsis (depth perception) relies on different images from each eye
41
how is our monocular FOV imaged on the retina?
monocular segment of target imaged on nasal retina of ipsilateral eye
ex) left monocular segment imaged on left nasal retina
42
how is information from the left visual field conveyed to the right side and vice versa?
corpus callosum
43
what is the lateral geniculate nucleus? what is it composed of?
termination site of GC projections
- 6 layers that receive input from ipsi/contralateral eye
- colour vision processing starts here (cone opponent responses)
44
what are the layers of the LGN?
- magnocellular layers (1,2): receive input from M cells about movement and brightness
- parvocellular layers (3-6): receive input from P cells about colour and form
45
where does visual input go after the LGN?
tp V1 via the optic radiation/geniculostriate pathway
- LGN output ends in layer 4
46
what are ocular dominance columns?
cortical neurons in a column respond to one eye selectively
47
what is the dorsal stream?
where pathway; associated with:
- representation of object location
- motion
- control of the eyes and arms, especially when visual info is being used to guide saccades or reaching
- V1 -> V2 -> V5/V6
48
what is the ventral stream?
what pathway; associated with:
- form recognition and object representation
- storage of LTM
- V1 -> V2 -> V4
49
what is a simple cell in V1?
responds best to a bar of light in a particular orientation
50
what creates a striate cortex receptive field?
- LGN projects to layer 4 of V1 where input converges onto simple cells (orientation selective)
- simple cell input converges onto complex cells with direction specificity (ex. sensitive to a band of light moving in one direction but not the other)
51
what kind of input converges onto complex cells?
multiple simple cell inputs that may or may not have the same orientation specificity
52
what are orientation columns? what are cortical blobs?
- orientation columns: contain neurons with similar orientation selectivity
- blobs: concerned with colour vision, receive input from cones and have RFs with spectral opposition
53
how do different aspects of vision work together to display feature extraction?
- ganglion cells extract the edges
- higher cortical cells like simple/complex cells extract lines, corners and motion
54
what is the hippocampal formation? what makes it up? what is its function?
- archicortex (older part of brain, 3 layers - molecular, pyramidal, polymorphic)
- made of hippocampus, dentate gyrus, and subiculum
- main input from entorhinal cortex
- memory storage output offloading
- site of STM formation and LTM consolidation
55
what is the entorhinal cortex?
bridge between hippocampal formation and higher cortical areas
- important for LTM storage
56
what happened to patient H.M.?
- developed seizures following head injury as a child
- bilateral removal of medial temporal lobes to stop seizures
- developed anterograde amnesia (inability to form new memories) and retrograde amnesia (couldn't recall some old memories)
- unchanged personality
- could not follow the plot of a TV show, could modify old memories
57
what do H.M.'s deficits prove?
ability to form new fact and event memories relies on MTL; cognitive function and motor memory do not
58
what are the different types of memory?
- episodic
- semantic
- declarative
- non-declarative
- explicit
- implicit
59
what is episodic memory? what is semantic memory?
- episodic: autobiographical events that can be recalled (ex. 10th bday)
- semantic: fact-based memory (ex. recalling Royal family names)
60
what is declarative vs non-declarative memory?
- declarative: broader term, memories that can be verbalized
- non-declarative: less consciously accessible, not easy to verbalize (ex. riding a bike)
61
what is explicit vs implicit memory?
- explicit: person is aware of memory
- implicit: person is unaware (ex. motor skills)
62
why was H.M. unable to form long-term memories?
- stimulation of entorhinal cortex, which projects to dentate gyrus of hpc leads to increased EPSPs in dentate gyrus over time (LTP + Hebbian)
- H.M. removed bilateral MTLs, eliminating these mechanisms for LTM formation
63
how is plasticity relevant in olfaction?
people without olfactory cortex can still perceive smell
- different regions of the brain take on the responsibility of lost areas = plasticity
64
how do the brain areas associated with learning change over time?
- 1 day after learning, most associations involve hpc (involved in fear-associated learning)
- 36 days after learning, connections involved cerebral cortex and thalamus (older memories stored in thalamocortical connections)
65
what is the dorsolateral PFC responsible for?
- planning and organizing of flexible behaviours (ones that require modification in response to real world context)
- uses working memory
- regulates input-behavioural output
66
what is the dorsomedial PFC responsible for?
- role in conflict
- updating goals in response to new rules (Stroop test)
- adaptability
67
what is the ventrolateral PFC responsible for?
- inhibition of unwanted actions
- lesions = impulsivity
- Tourette's (cannot suppress urges), OCD (unable to ignore thoughts), clinical depression
68
what is the orbitalfrontal responsible for?
- receives sensory information (various modalities), evaluates and determines value
- role of reward -> DA pathways project here (VTA and SNpc project here)
ex) food poisoning: past experience of eating is given a value to determine if eating again is worth it
69
what is the big picture flow of information of the PFC?
sensory info collected and evaluated in OFC -> laterally/rostrally to other PFC regions for planning -> premotor/motor/other
70
what can occur due to PFC damage?
- impaired goal-setting, project initiation, planning and execution of tasks
- lack attention, insight
- euphoric or manic, lack typical inhibition of inappropriate behaviour
- may be quiet or apathetic
- dysexecutive vs disinhibition syndrome
71
what is working (transient) memory?
active and temporary representation of info maintained for the short term to help you make decisions
- holding station to remember something long enough (can be kept there through rehearsal)
- temporary retention of info just experienced or just retrieved from LTM
- ex) searching for your phone and avoiding places you've checked, planning your day
72
what is executive function/cognitive control?
manipulation and application of working memory for planning, task switching, attention, appropriateness in response to changing environmental conditions or demands
73
what is dysexecutive syndrome?
damage to lateral PFC; disrupted ability to think and plan
- deficits in executive function and working memory (normal LTM and skill-learning)
- STM deficits (patient K.F.); failure to recall short sequences
- inability to perform tower of Hanoi
- denial of deficit
74
what is disinhibition syndrome?
damage to OFC, DMPFC, or VLPFC
- typical cognitive functioning, working memory
- euphoric, manic, inappropriate social behaviour and responses to social cues
- inappropriate laughter, lacking a filter, TMI
- overly outwardly expressive
- disinhibition of normally repressed behaviours
75
who is Phineas Gage? what happened to him?
- explosion drove a tamping rod through his left PFC
- left (dominant) VMPFC lesion
- became frequently angry, impulsive, lacked planning, socially-inappropriate behaviour
76
what does visual working memory involve?
coordination between DLPFC (motor association) and either posterior parietal (spatial) or inferior temporal (identity) visual association areas
77
how do neurons store information? how is this beneficial?
we have categories and networks of neurons
ex) firing for steve carrell but not whoopi goldberg (only fires to white guy comedians)
- beneficial for memory preservation; loss of one column will not cause total loss
78
what brain areas does language involve? what can occur due to damage at these regions?
- Wernicke's area: comprehension, auditory association (damage causes receptive/fluent aphasia)
- Broca's area: production, motor association (damage causes expressive/non-fluent aphasia)
79
how is interhemispheric transfer affected when the optic chiasm is split?
- imaged flashed in right eye only will only be sent to right hemisphere
- information is still transferred to left hemisphere via corpus callosum
80
how is interhemispheric transfer affected when the optic chiasm is split and the corpus callosum is severed?
- imaged flashed in right eye only will only be sent to right hemisphere
- since optic chiasm is split, visual info cannot reach left hemisphere
- since corpus callosum is severed, interhemispheric transfer cannot be complete
81
what would happen in the interhemispheric transfer task when a patient with a severed CC is asked to locate an item flashed in the LEFT monocular visual field ?
image flashed in left monocular visual field would end up in the right side of the brain
- ipsilateral communication between visual cortex and motor areas
- motor cortex controls contralaterally, so patient can pick up correct object only with left hand
82
what would happen in the interhemispheric transfer task when a patient with a severed CC is asked to locate an item flashed in the RIGHT monocular visual field ?
image flashed in right monocular visual field would end up in left side of the brain
- ipsilateral communication between visual cortex and motor areas
- motor cortex controls contralaterally, so patient can pick up correct object only with right hand
83
what would happen in the interhemispheric transfer task when a patient with a severed CC is asked to verbally identify the object flashed in the right monocular visual field?
- info ends up in left visual cortex
- ipsilateral communication between visual cortex and language areas
- patient will be able to correctly identify object
84
what would happen in the interhemispheric transfer task when a patient with a severed CC is asked to verbally identify the object flashed in the left monocular visual field?
- info ends up in right visual cortex
- info cannot be projected to language regions b/c they are left dominant (Broca's, Wernicke's)
- patient will not be able to identify object
85
is the parietal lobe lateralized?
YES; there is a dominant side (usually left)
86
what happens when there is damage to the dominant parietal lobe?
Gerstmann syndrome:
- left/right confusion
- agraphia (can't write)
- acalculia (can't calculate)
- anomia (can't recall words)
87
what happens when there is damage to the non-dominant parietal lobe?
- spatial problems
- contralateral neglect
- neglecting parts of the body
- denial of any such deficiency
- anosognosia (unaware of deficit)
88
what happens when there bilateral damage to the parietal lobe?
Balint's syndrome:
- ocular apraxia (can't control gaze)
- inability to integrate components of a visual scene
- optic ataxia (inability to accurately reach for an object)
89
how does neural coding create rhythms?
activated neuronal groups engage in rhythmic synchronization that leads to sequences of excitation and inhibition within precise temporal windows
90
what is phase locking?
the tendency of a neuron to fire action potentials at particular phases of an oscillation -> creates rhythms
- sending neuron excitability should be paired with receiving neuron excitability
- cells are in sync and are more likely to communicate because of this
91
what is rate coding vs spike-time coding?
- RC: avg # of spikes per unit time; as stimulus intensity increases, the firing frequency increases
- STC: precise timing of single spikes, calculated by dividing # of spikes by temporal window (duration of an individual spike)
92
why is phase-locking important?
without it, overexcitability or oversynchronization can cause epilepsy
93
what do electroencephalograms (EEGs) measure?
field potentials: collective electrical activity of large # of distant neurons
- flatline EEG = brain death
94
what are and at what frequency do the following waves occur:
a) beta
b) alpha
c) delta
d) REM
a) beta: 15-30 Hz -> oscillations seen only in wakefulness and REM (awake, eyes open, active state/processing)
b) alpha: 8-14 Hz -> oscillations reflect inhibition or idling
c) delta: 1-4 Hz -> oscillations strongly expressed during sleep
d) REM: 15-30 Hz -> every ~90 min slow wave sleep changes to low-voltage fast activity resembling beta (like you're awake)
95
what kind of EEG abnormalities are caused due to epilepsy?
- tonic and clonic states of grand mal: consciousness lost, coincident with increases in muscle tone; followed by jerked movements
- petite mal: transient loss of consciousness, spike and wave activity (staring off into space)
96
what is the Ascending Reticular Activating System (ARAS)? what do lesions to this system cause?
promotes wakefulness (WAKE ME UP); excitatory NTs
- 2 pathways: yellow and red
- lesions cause profound sleepiness
97
how does the ARAS yellow pathway project?
ACh
- originates in pons and is a major input to the thalamus
98
how does the ARAS red pathway project?
DA, 5-HT, NA, His
- activates cerebral cortex to facilitate processing input from thalamus
- bypasses thalamus
- activates lateral hypothalamic area (LHA) and basal forebrain (arousal)
99
what does the LHA contain?
orexigenic (ORX) neurons (feeding and hunger)
- project widely thru CNS; feeding behaviour and arousal, regulate ARAS
100
what is the ventrolateral preoptic (VLPO) nucleus? what happens when there are lesions to this area?
promotes sleep (anterior hypothalamus); sends GABA to brain regions that promote arousal
- innervates LHA including orexigenic neurons that regulate activity of ARAS
- GABAergic and galaninergic neurons
- lesions result in insomnia
101
how are ARAS and VPLO related?
form a flip-flop switch that allows relatively rapid transitions between sleep and wakefulness through mutual inhibition
102
how is the VPLO activated? how is it inhibited during wakefulness?
- activated by serotonin and adenosine that accumulate during wakefulness
- receives input from ARAS regions that release ACh and NE, which inhibit VPLO during wakefulness
103
what occurs during the sleep-wake cycle?
1) melanopsin receptors in the eye respond to the presence of light by transmitting signals to the SCN
2) light-induced activation of the SCN prevents the pineal gland from producing melatonin
3) light-dark entrainment
104
what are intrinsically photosensitive retinal ganglion cells (ipRGCs)?
third class of photoreceptor that function in non-image forming vision
- opsin expressed = melanopsin -> TRPC6/7
- project to the SCN -> body's central pacemaker
- functionally blind people can still photo-entrain (day-night cycle)
105
what is the suprachiasmatic nucleus (SCN)?
located in the anterior hypothalamus; contains a 24 hour clock controlled by a gene turnover cycle; influences:
- other organs through pituitary (endocrine interface)
- other rhythms through pineal gland
- sleep wakefulness through ARAS
clock in SCN can be reset by sunlight
106
why do we need sleep? why is it evolutionarily advantageous?
- deprivation causes hallucinations/psychosis
1) maintenance of immune system function
2) clear the brain of waste that accumulates during the day
3) synaptic connections made during daily activity need to be strengthened or pruned (critical for learning and memory)
107
what are the symptoms of Alzheimer's?
after ~65 years; order of occurrence:
- memory loss
- decline in non-memory aspects of cognition (word-finding, visuo-spatial issues, impaired judgement)
- with progression: further decline, wandering, trouble handling money and bills, inability to carry out daily tasks, personality changes
- confusion, inability to recognize family, impulsivity
- inability to communicate
108
what are possible causes of Alzheimer's disease?
- 2/3 cases are women
- 5% linked to rare genetic mutations (ApoE4, usually early onset)
- CVD, diabetes, high BP, depression increase risk
- link to diet, exercise
- link to menopause (estrogen protects brain from aging; stimulates function and may decrease plaque formation)
- often unknown cause (likely combo of lifestyle, environment, genetics)
109
what is the mechanism of Alzheimer's?
involves amyloid-beta plaques and neurofibrillary tangles (tau - messed up microtubules)
- AB accumulation results from imbalance in synthesis, aggregation, and clearance
- forms oligomers (pore-like structures with channel activity, can kill cell)
- alter glutamate receptors and cause excitotoxicity (cell is so excited that it is toxic due to Ca2+ handling)
- mitochondrial/lysosomal failure -> caspases (induce apoptosis)
- tau proteins stabilize MTs; hyperphosphorylation leads to NF tangles
110
how does Alzheimer's cause loss of plasticity?
AB oligomers accumulate in synapse
- AB activates mGluRs -> lead to internalization of AMPARs -> weakens synapse
- AB inhibits NMDARs -> less excitation (blocked Ca2+ influx) -> LTD
111
what is BAN2401?
drug that reduced plaques and slowed dementia progression
- must be early administration when less plaques are present
112
what are symptoms of schizophrenia?
16-30, 1% of pop
- enlarged ventricles, abnormal hpc
- positive symptoms: hallucinations, delusions, thought and movement disorders
- negative symptoms: reduced expression of emotion, reduced feelings of pleasure, difficulty sustaining activities, reduced speaking
- cognitive symptoms (PFC): poor executive function, trouble focusing, problems with working memory
113
what are potential causes of schizophrenia?
- loss of grey matter and reduced synapses (small frontal cortices)
- thought to involve excessive synaptic pruning
- decrease DA in PFC and excess DA release in other pathways associated with psychotic episodes
- treatments include antipsychotics that block D2 receptors
114
what is the possible mechanism for schizophrenia?
association with complement component 4 (C4)
- complement proteins are part of the immune system and play an important role in targeting foreign antigens for destruction
- C4 proteins localize to neuronal synapses and dendrites in humans
- C4 protein levels elevated in schizos
