Last Unit (Cognition) Flashcards Preview

Neuroscience > Last Unit (Cognition) > Flashcards

Flashcards in Last Unit (Cognition) Deck (69):


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.


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)


key modulators of memory storage

1. Norepinephrine/Epinephrine
2. Glucocorticoids (--> hippocampal LTP)
* 1 & 2: "inverted U-shape" response (improve memory)
3. 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.



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)



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

1. selectively permeable to K+
2. have ion channels and receptors (mostly metabotropic)
ie: glutamate, GABA, ACh, DA, 5-HT, ATP, endocannabinoid Rs
3. neuron signaling to glia (evoke Ca2+ response in glial cells)
4. communicate with other glial cells in network
(propagate Ca2+ wave across many glia)
5. able to divide


Glial cell functions (general)

1. insulate neurons (myelin)
2. prevent excitotoxicity (Glutamate-glutamine cycle)
3. metabolic support (Lactate shuttle hypothesis)
4. maintain microenvironment for neurons (regulate extracellular K+, CO2 sensor)
5. Modulate synaptic transmission (tonic release of ATP and glutamate --> LTP!)
6. 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 (?)



= 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)
- 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.



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).
1. astrocytes take up glucose (and store as glycogen)
2. glycolysis in astrocyte to convert glucose to lactate (uses 2 ATP)
3. transport into neuron via MCT1/2 (ox. phosph. --> 26 ATP)


GDNF (Glial cell line-Derived Neurotrophic Factor)

trophic factor released by astrocytes to...
1. promote growth of spinal cord motor/ANS neurons
2. enhance regeneration of CNS neurons
3. 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.



released by astrocytes to promote synapse formation
(as part of neuronal migration/development)



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.



degree of fluency or rhythm in speech
(poor prosody = halting, irregular speech patterns)



substitution of wrong syllable in word(s) when speaking
ie: "purnpike" instead of turnpike.
* very common



making up words/speech lacking meaning.



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.



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)

1. synchronous activation of large enough set of aff. neurons to have noticeable change
2. 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.
1. hippocampus 2. mammillary bodies
3. anterior thalamic nucl. 4. cingulate gyrus
(5. back to hippocampus)


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