Role of temporal lobe in memory function

Henry Molasion (patient HM)

had severe temporal lobe epilepsy and underwent bilateral medial temporal lobe surgery = profound amnesia

effect of HM’s surgery

• reduced seizures but severe memory loss

• damage to mesi temporal lobes incl hippo

• profound anterograde amnesia and some retrograde memory impairment

HM’s preserved abilities

• personality and intelligence intact

• normal attention, perception and working memory

• normal immediate verbal memory and arithmetic

• could learn new procedural skills

• language largely preserved though forzen

HM’s memory impairments

• severe anterograde amnesia - no new long-term memories

• some retrograde amnesia - loss of recent past memories

major conclusions from HM

• hippo/medial temporal lobe critical for forming new declarative memories

• memory is multi-system

• amnesia occurs without impairing IQ or perception

• short-term and working memory can remain intact with amnesia

retrograde amnesia

impairment of memories created prior to injury

anterograde amnesia

impairment of memories created after injury and in learning new info

declarative memory

long-term memory involve conscious, intentional recall of factual information, concepts, and events. includes episodic and semantic

procedural memory

long-term memory that enables the performance of tasks without conscious awareness, e.g. playing piano

hippocampus

permanently consolidates memories. structure:

• in medial temporal lobe

• subiculumn - main output region

• cornu ammonis (CA fields) CA1 (closests to sub) >CA2>CA3>CA4 - main circuit

• dentate gyrusinput region - includes CA4

synaptic plasticity

ability of synapses to strengthen or weaken over time = alters presynaptic effect on post

Hebb’s rule

If neuron A repeatedly activates B = synpatic connection between them strengthens and B is easier to activate by A

long-term potentiation

long-lasting increase in synpatic strength - mainly at glutamatergic synapses

• changes neurotransmitter release from presynaptic

• increases receptor number and sensitivity in postsynaptic

• alters protein synthesis in dendrites

long-term depression

Low frequency stimulation at synapse = decrease synaptic strength

Habituation

repeated stimulation reduces strength of synpatic response - mostly reduced neurotransmitter release

Sensitization

single noxious stimulus causes exaggerated synaptic response to repeat presentation of said stimulus

where does LTP occur

• temporal - hippo (esp CA1 and dentate gyrus), entorhinal cortex, amygdala

• prefrontal

• motor cortex

• thalamus

• visual cortex

Papez’s circuit

critical for declarative memory includes

• hippo

• fornix

• mammillary bodies

• anterior thalamic nuclei

• cingulate gyrus

limbic system

Pepez’s and amygdala - emotion, behavior, motivation, long-term memory, and olfaction.

amygdala

supports memory for emotionally arousing experiences, classical fear conditioning and enhances encoding of emotionally sig events

lesions in amygdala

• impaired fear conditioning and enw fear learning

• reduced memory for emotionally charged events

role of frontal lobes in memory

• strategies for encoding and retriving memories

• organising contextual details - source of info and chronological order of events

damage to frontal lobe

• impaired contextual/source memory

• difficulty organising memories in time

• can cause confabulation (false/distorted memories)

damage to thalamus areas

• anterior and medial thalamus - contributes to amnesia

• mammillothalamic tract - impaired episodic memory but short term and intelligence spared

• dorsomedial nucleus - difficulty selecting relevant info for retrieval

• intralaminar/midline nuclei - impaired memory retrieval and semantic memory

Alzheimer’s disease

most common dementia. initial symptom is memory impairment (anterograde amnesia) and progressive loss of cognitive functions over time

progression of Alzhiemer’s

1. hippo and entrohinal cortex - early degeneration = memory deficits

2. neocortex esp frontal and temporal areas esp association cortex

3. subcoritcal areas - nucleus basalis, locus coeruleus and raphe nuclei

cause of neurodegeneration in Alzheimer’s

amyloid plaques and neurofibrillary tangles

• amyloid - made of β-amyloid (Aβ) = high levels are toxic to neurons

• neurofib - formed from abnormal tau protein inside neurons = dysfunction and cell death

• neurofib 1st appear in transentorhinal cortex and entorhinal cortex then spreads to hippo and neocortex