Last Unit (Cognition) Flashcards
anterograde amnesia
INability to form new memories, but tend to seem cognitively intact. No loss of previously formed memory.
- due to hippocampal lesion
(ie: anti-epileptic surgery –> bilateral removal of part of temporal lobe, including hippocampus)
- due to hippocampal lesion
prosopagnosia
failure to recognize faces
= due to lesion in ventral occipitotemporal/temporal lobes
* can still see face as a face, and even recognize objects, but can’t identify specific people by face.
key modulators of memory storage
- Norepinephrine/Epinephrine
- Glucocorticoids (–> hippocampal LTP)
* 1 & 2: “inverted U-shape” response (improve memory) - opioids (impair memory)
declarative memory
“explicit” memory.
semantic or episodic memory, fact-like;
encoded in language or visual images (conscious modalities).
– uses hippocampus.
procedural memory
“implicit” memory.
acquisition of motor skills performed without conscious awareness; especially long-lasting.
ie: riding a bike
short term memory
memory stored for only seconds to minutes
long term memory
memory stored for days to years
Lateral Hypothalamic Area (“LTA”)
releases orexin to inhibit NTS
–> increase food intake
stimulated by neurons from Arcuate Nucleus
+ NPY - Melanocortin (POMC)
Lesion to LTA
aphagia (stop eating)
- decrease activity in motivation and motor systems for eating
Paraventricular Nucleus (“PVN”)
releases CRH (corticotropin-releasing hormone) to +stimulate NTS
–> DEcrease food intake.
stimulated by neurons from Arcuate nucleus
* uses GABA interneuron to switch to opposite signal as LTA
+ (- to GABA) Melanocortin - (+ to GABA) NPY
Arcuate Nucleus
in hypothalamus, sends neurons (+ and -) to LTA and PVN;
- melanocortin (POMC) neurons +stimulated by Leptin!
- -> can + or - influence food intake.
Leptin
endocrine hormone, = adiposity signal (long-term modulator);
increases sensitivity of NTS by stimulating POMC neurons (and inhibiting NPYs) in ARC.
–> inhibits food intake (satiety signal)
* encoded by ob gene*
CCK (cholecystokinin)
satiety signal, increases NTS activity DIRECTLY;
–> inhibits food intake.
Also stimulates:
1. Gallbladder contraction (bile release)
2. Pyloric constriction (holding food in stomach)
3. Gastric contractions (“””)
Satiety signals
- mostly stimulate NTS activity*
Short term: oropharyngeal Rs, gastric distention Rs, intestinal nutrient Rs, hepatic nutrient Rs
Long term: Leptin, CCK (direct to hypothalamus)
Ghrelin
hunger stimulating signal –> increase food intake;
stimulates NPY neurons (in ARC).
* increased production in Prader-Willi patients => hyperphagia and obesity!*
Ventral Stream (cortical pathway)
higher order pathway for Object Recognition,
- includes V4, TEO and TE (parts of Inferotemporal lobe “IT”)
- responds to whole objects/complex shapes
- NOT retinotopic, many opiate Rs
- familiarity/recentness increases response strength
- response INvariance!
Response invariance
same cortical response elicited by same (complex) shape ~regardless of orientation, size, position, etc.
Lesion to Ventral Stream:
=> visual agnosia can see, but not process whole objects correctly. - can copy but not recognize/name object => +/- prosopagnosia * ie: "Kluver-Busy" Syndrome*
Dorsal stream
higher order cortical pathway for spatial cognition,
esp. in MT/MST, 7a, and LIP regions (post. parietal lobe).
* respond to trace memories and shift memory images to keep world “stable” despite changes in visual gaze
lesions to dorsal stream
=> optic ataxia (Balint syndrome) and hemispatial neglect;
- can’t process multiple visual stimuli at same time
- decreased accuracy when reaching for targets
- -> perception AND mental imagery objects = cut in half.
Hemi-spatial Neglect
due to lesion in posterior parietal cortex (dorsal stream),
object-centered neglect of 1/2
- no awareness (visual, mental, proprioceptive, etc.) of 1/2 of visual field/body, etc.)
Frontal lobe role in cognitive processesing
controls executive function and working memory.
Lesions to Frontal Lobe change cognition by…
==> Dysexecutive syndrome
- disinhibition/impulsivity, - emotional impairment
- poor planning ability - poor handle on abstract/changing rules.
Dorsal-Lateral PreFrontal Cortex lesions:
decrease working memory ability.
* also decreased planning and problem solving.
macroglial cells (types)
- Astrocytes
- oligodendrocytes/schwann cells
- oligodendrocyte progenitor cells
General characteristics of glial cells
- selectively permeable to K+
- have ion channels and receptors (mostly metabotropic)
ie: glutamate, GABA, ACh, DA, 5-HT, ATP, endocannabinoid Rs - neuron signaling to glia (evoke Ca2+ response in glial cells)
- communicate with other glial cells in network
(propagate Ca2+ wave across many glia) - able to divide
Glial cell functions (general)
- insulate neurons (myelin)
- prevent excitotoxicity (Glutamate-glutamine cycle)
- metabolic support (Lactate shuttle hypothesis)
- maintain microenvironment for neurons (regulate extracellular K+, CO2 sensor)
- Modulate synaptic transmission (tonic release of ATP and glutamate –> LTP!)
- regulate neuronal development (& promote synapse formation)
Influence of Astrocytes on blood vessels (in brain)
- astrocyte endfeet surround blood vessels*
1. promote development – release VEGF (vascular endothelial growth factor)
2. induce blood-brain barrier (tight junctions)
3. regulate blood flow = basis for fMRI!
(release vasoactive factors –> dilation/constriction)
Microglia (function)
= “macrophage of the brain,” derived from mesoderm.
1. survey for damage and remove debris
(gravitate towards damaged areas)
2. prune un-needed synapses (–> neural development/learning)
Schwann cell involvement in PNS re-growth
if fiber tract is severed, Schwann cells guide sprouting axons to target
(assist regrowth ONLY in PNS)
Oligodendrocyte involvement in CNS regeneration
Oligodendrocytes PREVENT regeneration of CNS
- -> release “Nogo” protein to inhibit axon growth
- restore (limited) growth w/: **
- Antibodies to Nogo
- treat with GDNF (glial cell neurotrophic factor)
- transplant similar glia (?)
Epilepsy
= seizure disorder; can occur through injury to brain & scar tissue formation.
- find “Reactive Astrocytes” at sites of epileptogenesis
- reduced K+ regulation
- reduced glutamate uptake/increased GABA uptake
- glutamate release?
brain tumors
most often derived from glial cells –> “Glioma”
(#1 astrocytes, but also oligodendrocytes and ependymal cells)
Gliomas…
- release glutamate, down-regulate glutamate uptake
- Up-regulation of cysteine-glutamate exchange
—-> excitotoxicity and neuron death
Multiple sclerosis
autoimmune disease, attacks oligodendrocytes;
Ag = myelin basic protein
treating parkinson’s with GDNF
GDNF = trophic factor, so can help support dopaminergic neurons in substancia nigra (dying in Parkinson’s).
But… not shown to work in humans.
Astrocytes
type of glial cell in brain,
2 parts:
1. processes - cover neurons and surround synapses
2. end-feet - terminate on pial surface of blood vessels
oligodendrocyte progenitor cells
aka: NG2+ cells (bc express NG2 proteoglycan),
* continue to divide throughout lifespan.
- prenatal: divides into oligodendrocytes AND astrocytes
- adult: divides into only oligodendrocytes
Tripartite synapse
synapse in brain which involves 1) pre- & 2) post-synaptic neurons AND 3) astrocyte.
NTs from pre-synaptic terminal activate astrocytes:
NT–> increase intracellular Ca2+ –> release gliotransmitters (glutamate, ATP)
* Ca2+ wave can spread to other astrocytes in network too!*
glutamate-glutamine cycle
process of recycling glutamate to neurons from synapse via astrocyte;
prevents excitotoxicity
1. Glutamate pumped from synapse into astrocyte by EAAT
(“Essential AA transporter”)
2. glutamine synthetase converts glutamate –> glutamine in astrocyte
3. glutamine taken up by neuron (so can convert to glutamate and use as NT)
Lactate Shuttle Hypothesis
theory that astrocytes convert glucose to lactate for use by neurons (as energy).
- astrocytes take up glucose (and store as glycogen)
- glycolysis in astrocyte to convert glucose to lactate (uses 2 ATP)
- transport into neuron via MCT1/2 (ox. phosph. –> 26 ATP)
GDNF (Glial cell line-Derived Neurotrophic Factor)
trophic factor released by astrocytes to…
- promote growth of spinal cord motor/ANS neurons
- enhance regeneration of CNS neurons
- give trophic support to dopamine neurons in midbrain
Radial Glia
= stem cells for neurons and neuronal progenitor cells;
* promote neuronal migration:
allow neurons to move down processes of radial glial cells.
thrombospondins
released by astrocytes to promote synapse formation
as part of neuronal migration/development
Gliosis
proliferation and differentiation of glial cells in response to injury in brain, esp. of “reactive glial cells.”
= primary response
aphasia (aka: dysphasia)
loss of language skills due to cortical (not physical/mechanical) damage.
prosody
degree of fluency or rhythm in speech
poor prosody = halting, irregular speech patterns
paraphasia
substitution of wrong syllable in word(s) when speaking
ie: “purnpike” instead of turnpike.
* very common
neologia
making up words/speech lacking meaning.
dysarthria
inability to speak due to mechanical/physical limitations affecting mouth and/or throat; have linguistic skills, but poor articulation.
ie: weakness/paralysis, damaged CN X or XII, damaged larynx/tongue/etc.
cerebral dominance
refers to the hemisphere that (more strongly) controls speech and (usually) the dominant hand. 96% of ppl = left side!
* use WADA test to ID side (uses side localized anesthetic)
Pattern: more neuron projections to dominant side
(fewer decussations to opposite side in pyramid)
planum temporale
superior surface of the temporal lobe (posterior to aud. cortex),
= ~5x larger on left (dominant) side!
Broca’s Area
on Left side of frontal lobe, just rostral to the premotor cortex.
Responsible for speech production (= motor association area);
Lesion => non-fluent aphasia.
Sx of lesion to Broca’s Area
“Non-Fluent Aphasia”
–> agramatical & telegraphic speech and writing, loss of rhythm/fluency, little spontaneous speech, poor repetition.
Language comprehension = intact (aware of inability to communicate).
* Also: right hemiparesis (including lower face and hand) if large lesion.
Wernicke’s Area
Language/auditory association area in Left temporal/inferior parietal lobes;
Responsible for language comprehension
(lesion => fluent aphasia)
Sx of Lesion to Wernicke’s Area
“Fluent Aphasia”
–> poor comprehension (can’t follow commands or understand own speech), poor repetition, paraphasias common.
Fluent/rhythmic spontaneous speech that doesn’t make sense,
unaware of errors.
* no motor deficits associated w/ lesion.
Arcuate Fasciculus
bundle of white AND gray matter connecting Wernicke’s area to Broca’s area, runs through inferior parietal lobe.
Lesion => “conduction aphasia”
Sx of lesion to Arcuate Fasciculus
“Conductive Aphasia”
–> paraphasias/problems finding words, poor repetition.
Maintain prosody, awareness/comprehension, and ability to follow complex instructions.
Syntax
ordering/arranging linguistic elements together into appropriate/correct “constituents” (phrases).
- depends on:
1. SLF/Arcuate Fasciculus
2. Uncinate Fasciculus (“UF”) 3. Extreme capsule.
Uncinate Fasciculus
collection of ventral pathways that connect frontal (broca’s) and temporal (Wernicke’s) speech areas.
* esp. important for ability to use syntax*
Sx of Corpus Callosotomy (aka: “split brain”)
Relatively normal f(x), BUT Linguistic association = limited to stimuli processed in left hemisphere.
R visual field stimuli: can be named, identified, repeated, etc.
L visual field stimuli: no conscious awareness of these. Can’t name or ID. DO process but not on conscious/linguistic level
(ie: man who wouldn’t shake doctor’s hand with tack in it, but couldn’t say why)
Hebb’s Rule
(concept of plasticity)
Activity of a pre-synaptic neuron on the post-synaptic neuron can change how the both neurons respond to future stimulation
requires activity in both to occur
Long-term Potentiation
enhance synaptic action
- by repeated, short high freq. stimulation of pre-synaptic afferent fibers
(ie: in Schaffer collateral neurons in hippocampus) - long-lasting effect!
Limitations of Long-term Potentiation (LTP)
- synchronous activation of large enough set of aff. neurons to have noticeable change
- potentiation only if input causes activation
(3. only occurs at dendritic spines)
post-synaptic changes induced by LTP (in Schaffer cells)
input removes Mg block from NMDA R
- -> lets Ca in --> calmodulin activates CaM kinase II 1. binds to AMPA Rs - increase sensitivity - increase # AMPA Rs at membrane 2. activate genes to promote growth of that dendritic spine
effect of NMDA antagonists
no Long-term potentiation
- -> no demonstrated learning
ie: in rats swimming, can’t learn where hidden platform is
Long-term Depression
decreased synaptic action
- by applying brief, repeated slow stimulation.
(homosynaptic OR heterosynaptic)
ie: parallel and climbing fibers for cerebellar cortex
Mechanism of Long-term Depression in cerebellar cortex
(2 parts: parallel and climbing fibers working together)
Parallel fiber: activates AMPA and mGlu Rs
–> activate Protein kinase C
Climbing fiber: lets Ca2+ into cell
Together: phosphorylate Purkinje cell AMPA Rs ==> internalized.
Circuit of papez
(hippocampal formation), needed for declarative memory consolidation and retrieval.
- hippocampus 2. mammillary bodies
- anterior thalamic nucl. 4. cingulate gyrus
(5. back to hippocampus)
- anterior thalamic nucl. 4. cingulate gyrus
emotional modulators
Boost memory:
(“inverted U” shape modulation, w/ x-axis = increasing [ ])
1. NE (on limbics – amydgala, hippocampus)
2. Glucocorticoids (hippocampal LTP)
* Impair memory = Opioid peptides
