Lecture 36: Learning and Memory, HIppocampus Flashcards
What are three types of memory?
- Short-term memory
- Non-declarative memory (unable to verbalize memories)
-procedural memory (acquisition of physical/cognitive skills like swinging golf club)
-priming
-classical conditioning - Declarative memories (able to put into words)
-contextual/associative
Episodic: associative with PERSONAL experience
Recollection
-non-contextual/non-associative
Semantic memory: general factual knowledge like who’s the president (not in context in self-experience)
Familiarity memory
Semantic memory:
fact memory (like dates of world war) -nonassociative memory
What is Episodic memory:
Associative declarative memory
memory for prior experiences or events
“Mental Time Travel”
Involves autonoetic (self) consciousness)
-events in reference to self and linked to time and space
Anterograde amnesia
inability to learn new information
Retrograde amnesia
inability to remember old memories
What is difference between Recollection vs. Familiarity?
Familiarity is the person is familiar but you can’t recall where you know that person
Recollection is remember errything
What is item vs. associative memory?
Item = you remember item irrespective to any other association Associative = making links…like you saw this while you playing bball, etc.
How is episodic memory stored and applied in the brain?
A. Processing the memory -encoding -storage/consolidation -retrieval B. Distributed among multiple neural networks -medial temporal lobe -frontal -parietal -unimodal sensory areas (auditory, somatosensory, visual) -basal forebrain
What are the medial temporal lobes?
Most important area for memory A. Hippocampal formation -subfields, dentate, subiculum B. Extrahippocampal -entorhinal cortex -parahippocampus -perirhinal cortex Hippocampus located within medial temporal lobe!!!
What are the structures within the hippocampus?
- (CA1, CA2, CA3…stands for cornu ammonis) Subfields
- Dentate
- Subiculum
Hippo looks like a jelly roll!
What are structures in extrahippocampal area?
- Entorhinal cortex
- Parahippocampus
- Perirhinal cortex
Function of hippocampus:
A. convergence of auditory, visual and somatic (unimodal) signals)
-hence hippocampus sits in the middle of memory generation/processing
B. Convergence for multimodal formation
-BINDS neocortical elements like
-pattern completion of partial cue
-critical for associative memory formation
What are the different functions of components of the medial temporal lobe?
Hippocampus = binding
-subiculum = output of the hippocampus
Perirhinal: inputs from ventral visual pathway (“what”)
Parahippocampus: inputs from dorsal visual pathway (“where”)
What is theory of “Dual Process” in how memories has formed?
There are two things that supports memory: recollection and familiarity
Recollection involves retrieval of prior event in spatio-temporal context
-mediated by hippocampus
Familiarity (the feeling you got to know somebody
-mediated by perirhinal lesion
Still a motherfucking theory
What are the different distortions of familiarity?
A. Loss of familiarity -Capgras B. Hyperfamiliarity -Fregoli Syndrome -Reduplicative Paramnesia C. Deja Vu
What is Capgras?
The idea that spouse has been replaced by someone else
Example: wife who says Bob the husband looks like her husband, but does not “feel” like he is her husband
What is the extended hippocampal memory system?
Papez circuit
- fornix
- mamillary bodies
- anterior thalamic nucleus
- posterior cingulate/retrosplenial cortex
What do lesions of the Papez lead to?
- profound memory loss similar to hippocampal lesion
- functional contribution of the circuit is UNCLEAR motherfuckerrr
Wernicke-Korsakoff Syndrome:
The most common type of injury to Papez circuit
Seen in thiamine deficient alcoholics
-petechial hemorrhage in the mammillary bodies…lesion of Papez = amnesia
Symptoms: amnesia caused by lesion of Papez
What are common causes of temporal limbic amnesia?
- Wernicke Korsakoff syndrome
- AD
- hypoxic-ischemic injury
- Posterior cerebral artery stroke
- herpes encephalitis
- hippocampal sclerosis
What type of amnesia do you get when you lesion hippocampus?
Both anterograde and retrograde
Ribot’s Law
known as the fact that patients with retrograde amnesia can remember longer term memory better because overtime, the elements of memory gets stored from medial temporal lobe to neocortex
- explains why people with hippocampal memory loss still have long term memory
- both semantic and episodic memory affected
Whats the role of Frontal lobes in episodic memory formation/retrieval
Specific: ventrolateral frontal lobe
Due to semantic retrievals; being able to say an idea or concept allows us to remember
-so if you impair ventrolateral frontal lobe, you get some sort of amnesia
-specific role of the prefrontal cortex in memory is an area of great debatte
What happens to memory when frontal lobe is lesioned?
Memory gets worse
-greater difficulty on unconstrained tasks at encoding and retrieval
How do you separate MTL and frontal lobes?
- Give the patients a free recall test (both MTL and frontal should be impaired)
- Give recognition or cued recall test (if impaired, the MTL problem…frontal lobe patients can’t retrieve but can remember if given cue)
Also in frontal lobes
–amnesia improves with environmental support
While in MTL lesion
-minimal enhancement in memory performance due to effects of environmental support
Characteristics of Frontal lobe lesion
- normal recognition memory or cue recall
- item memory is normal
- significant enhancement of memory performance with environment support
Characteristics of MTL lesion
All aspects of memory is impaired
How do you differentiate between retrieval and storage memory deficit?
Drill words in these motherfucker
-if patient can recognize items on multiple choice test, the it is just a retrieval deficit (frontal lobe)
if patient CANT recognize items, then there is probably a storage deficit
Unimodal sensory areas involved in memroy
i. Visual
ii. Sound
Significance: Shit you learned as a picture is remembered as a picture…harder to remember as sound and vice versa
What are pathological features of AD?
i. Amyloid Plaques: extracellular accumulation of A(beta)
- abnormal processing of APP (amyloid precursor protein) critical to pathophysiology of Alzheimer’s disease
ii. Neurofibrillary tangles: intracellular, paired helical structures composed of hyperphosporylated tau
- correlate well with disease severity and neuronal death
iii. loss of cholinergic activity
Why is memory loss an early feature of AD?
Because these plaques and tangles takes place earliest in the MTL
-hippocampal atrophy
What are the genetics of AD?
95% are sporadic
-2-5% are Autosomal dominant
Chromosome 21 mutation (trisomy 21) associated with amyloid proteins (just one of 4)
Most common sporadic risk factor = ApoE gene…e4 allele here is associated with onset of AD…e4 is thought to clear amyloid
What is the effect of scopolamine one memory?
Scopolamine is a cholinergic inhibitor that reduces memory performance in healthy subjects
Significance: shows relationship of cholinergic dysfunction to AD and memory loss
Basal forebrain:
collection of structures located rostrally and ventrally to the striatum
Function: produce acetylcholine that are distributed widely throughout the brain
Includes
- nucleus basallis
- band of Broca
- substantia innominate
- septal nuclei
What artery supplies basal forebrain and could have dire consequences on memory if lesioned?
ACA
Treatment for AD?
AChE inhibitors (to increase cholinergic activity)
