G07 --> Memory Flashcards Preview

Lecture series G-post midterm neuro > G07 --> Memory > Flashcards

Flashcards in G07 --> Memory Deck (49):

What is declarative memory?

Declarative --> conscious memory for facts, places and events
involve hippocampal formation, medial temporal lobe and diencephalon


What is non declarative memory (procedural memory) ?

Non-Declarative --> subconscious memory for skills, habits, emotional responses and some reflexes
involves the striatum, cerebellum and amygdala


Describe short term memory

New sensory information is processed into intermediate memory for several seconds then into short term


Describe long term memory

this information, depending on the perceived importance, may be consolidated into long term memory


There are two forms of long term memory, what is the first form?

Explicit declarative memory --> facts and events
happens in the medial temporal lobe


what is the second form of long term memory?

Implicit non declarative memory
(i) Priming -->one stimulus influences a response to another stimulus (neocortex)
(ii) Procedural Skills and Habits (striatum)
(iii) Associative learning classical and operational conditioning -- >emotional responses (amygdala) and skeletal muskulature (cerebellum)
(iv) Non-associative learning: habituation and sensitization (reflex pathways)


What is working memory?

remembering numbers


What is amnesia?

Trauma to the brain may cause loss of memories


what are the two different types of amnesias?

1. Retrograde --> loss of memory of past events before trauma
2. Anterograde --> inability to form new memories following trauma and remember only the past


what is transient global amnesia?

Occurs typically in older men, recent events and information can only remembered for a few minutes. Normally all other functions are NOT impaired. Possible causes; TIA, basilar artery migraine, physical or psychic stress.


what is dissociative amnesia?

psychological reaction (witness of a severe accident or crime)


what is an Engram?

A theory that states how memory is stored as a biophysical/biochemical change in the brain
B. Neural network or fragment of memory in a cluster of neurons connected together


Where is the engram located?

distributed in the neocortex grouped into association areas, which receive input from the primary visual, auditory, and somatosensory cortexes


Where does the sensory information get sent upon entering the neocortex?

the association areas then send new sensory information to medial temporal lobes in the hippocampal formation which then relays it right back to the association area to consolidate into memory.


association areas are considered with what types of memories?

facts, events, places, language
emotions, past events, and ppl
working memory
(note the engram pathway is drawn out and is a great guide for further understanding)


Clinical Cases Reveal Engram Locations: First clinical case--> removal of amygdala, uncus and most of hippocampus to treat epilepsy. resulted in what?

(i) retained IQ, language, long term memory, and ability learn new skills (procedural memory)
(ii) lost ability to make new memories (immediate/short --> long term impairment)


Second clinical case --> lesion to thalamus, medial temporal lobe and mammillary body from fencing sword up the nose. resulted in what?

(i) suffered anterograde amnesia
(ii) Retained his IQ, language, procedural skill learning and 2 years worth of long term memory


Third clinical case --> Stroke/TIA resulting in lesions to the hippocampus suffering marked loss of CA1 neruons. resulted in what?

(i) suffered from anterograde amnesia and unable to form new declarative memories
(ii) IQ, memories, and cognitive ability remained intact


The hippocampus facilitates storage of what?

storage from short term memory into long term memory


Where is the hippocampus located?

located in the hippocampal formation consisting of the dentate gyrus, fields CA1-CA3, the subiculum (parahippocampal gyrus) and of course, the hippocampus.


What is the general pathway for generation of declarative memory?

Cortical association areas --> Entorhinal Cortical Areas --> Dentate Gyrus --> CA3 --> CA1 --> Subiculum (generates back to the entorhinal cortical areas)
(note CA3 and CA1 are the hippocampus and Subiculum is the parahippocampual gyrus)


Passive of information through the declarative pathway look induces what?

induces synaptic plasticity (changing the physiological or morphological state of cells) at synapses on cells of the dentate gyrus, hippocampus and subiculum


what is long term potentiation (LTP)

When CA1 is excited by CA3 impulse trains at high frequencies (100/s), the excitatory synapse undergoes a long lasting increase in synaptic efficiency called long term potentiation (LTP)


Where does this potentiation take place?

on glutamatergic synapses on dendritic spines in the CA1 neuron


LTP is caused by an increase sensitivity to glutamate via what?

via insertion of new AMPA receptors
additionally, due to the formation of new dendritic spines between CA3 and CA1, the increased number of synapses facilitates an increased responsiveness to synapses from CA3 to CA1


Describe very briefly how AMPA and NMDA receptors work?

A single presynaptic impulse can open the AMPA receptors but the NMDAs remain blocked by the resident MG2+ ion however when a train of impulses arrive (tetanic stimulation), it can open the NMDA channel and allows Ca2+ ions to enter


Once Ca2+ enters the NMDA channel what happens?

These Ca2+ ions leads to activation of kinases (PKC and CAMKII) which leads to increase AMPA receptors and eventual LTP


Three elements in the development of LTP at these synapses all of which have origins in the postsynaptic cells -->

(i) increase in AMPA channel conduction (Early)
(ii) increase in the number of AMPA channels (early)
(iii) increase in number of synapses via dendritic spine formation (late)


When glutamate binds to AMPA receptors the channel opens and what cation enters?

Na+ ions and they produce EPSP


What is long term depression (LTD) in the hippocampus?

When CA1 is excited by CA3 impulse trains at low frequencies (temporal summation)(1/sec), the excitatory synapse undergoes a large persistent fall in synaptic efficiency
(this the same synapses showing LTP under intense stimulation will exhibit LTD under weak stimulation)


The use of NMDA receptors is necessary for both LTP and LTD, but what is the critical difference?

calcium concentration
(the amount of NMDA activation dictates Ca2+ thus a direct influence on synaptic strength)


Calcium concentration therefore regulates synaptic plasticity, describe the effect on high frequency stimulation (LTP)

Induces large rises in Ca2+ which activates protein kinase who phosphorylates synaptic proteins (including AMPA receptors) leading to LTP (due to opening of NMDA channels)


describe calcium concentration effect on low frequency stimulation - LTD

Induces very small rises in Ca2+ which activates protein phosphatase which dephosphorylates synaptic proteins (including AMPA receptors) leading to LTD.


What are the three major anatomical sites with functional synaptic connections that play a role in procedural and non declarative memory?

1. Supplemental and premotor cortex
2. Striatum (in basal ganglia)
3. Cerebellum


Describe the role of the purkinje cells in the cerebellum?

are the sole output cells of the cerebellar cortex; each purkinje cell receives two major excitatory inputs


what two fibers are associated with purkinje cells?

Parallel fibers --> found transversing the outer molecular layer and sends an input
Climbing fibers--> makes several hundred synapses on the purkinje's dendrites


When does LTD in the cerebellum occur?

occurs only in parallel fibers that are activated at the same time as the climbing fibers
If the parallel giber is stimulated alone, it will NOT exhibit this LTD plasticity


Describe step by step the mechanism of how LTD is produced. Step 1-->

1. Climbing fiber activation strongly depolarized the purkinje cell dendrite while leads to activation of voltage gated Ca2+ channels


step 2 in the LTD mechanism

2. Parallel fiber activation leads to AMPA activation and subsequent NA influx


Step 3 in LTD mechanism

3 .Parallel fiber activation also leads to stimulation of metabotropic receptors to eventually generate PKC.


Step 4 in LTD mechanism

4. PKC then phosphorylates the AMPA receptor t hat causes them to be internalized where it is the reduction of AMPA channels that cause the decreased sensitivity to glutamate and consequently LTD


In summary the step of LTD mechanism

1. Rise in intracellular calcium arising from the climbing fiber stimulation
2. A rise in intracellular sodium arising from the AMPA channel opening
3. An activation of PKC from glutamate metabotropic receptor activation


Who does Korsakoff's Syndrome occur in?

chronic alcoholics with thiamine deficiency


What anatomically is the reason for Korsakoff's Syndrome?

Atrophy of dorsomedial thalamus and mammillar bodies
may also exhibit lesions in the neocortex, cerebellum and brainstem


What symptoms does one develop who has Korsakoff's syndrome?

Exhibit confusion, confabulation and severe memory impairment.
Anterograde amensia and severe retrograde amnesia probably due to damage to thalamus and hippocampus


What was electroconvulsive therapy used for?

employed to treat severe cases of clinical depression which electrically induces seizures


What was the reasoning for initially trying electroconvulsive therapy?

based on epileptics who are depressed and showed marked improvement in depression following a seizure


what are some side effects from electroconvulsive therapy?

may cause anterograde amnesia dating back several years but usually subsides a few months post treatment


What does neurotoxins from dinoflagellate Pfiesteria Piscicida cause?

released into the water and can cause confusion, decreased concentration, disorientation, and severe memory loss
(Contact may be inhaling or direct contact with the skin)