Brain, Behavior, and Experience Ch 12

Henry Molaison

Frequent epileptic seizures. Treatment removed the hippocampal formation, amygdala. Had intact non-declarative memory. Improved on the mirror drawing task. Learned to solve the Tower of Hanoi problem.

Anterograde amnesia

Unable to form new memories

Retrograde amnesia

Few memories decade before surgery

What does amnesia affect

Declarative memory (dates, events)

Consolidation

Brain forms permanent representation of memory

Sensory store

Infinite space, limited duration, quick, sensory coding, and initial recognition

Short-term memory

Working memory, central executive, phonological loop, visuospatial sketchpad.

Long-term memory

Long-lasting memory, explicit declarative memory (semantic, episode), implicit non-declarative memory (procedural (motor memory), priming)

What part of the brain is used with priming

Basal ganglia

Retrieval

Accessing stored memories

Retrieval with glutamate

Glutamate required for consolidation and retrieval. Blocking glutamate receptors prevents consolidation and retrieval.

Prefrontal area

Directs search strategy for retrieval in hippocampus

Place cells

Increase firing when individual is in a specific location in an environment. Collectively form a “spatial map”. Dependent on environmental cues and landmarks. Also found in humans and primates.

Declarative memory in maze

Requires hippocampus. Rat with Hp lesion could not remember which arms it had visited.

Non-declarative memory in maze

Requires striatum. Lesioned rats could not associate light at end of arm with food.

Working memory

Temporary register for information. Delayed match-to-sample tests for assessment.

Prefrontal cortex

Integrates long-term memory with other information. Manages strategies and decision making. Directs working memory traffic in brain. Coordinates sensory and motor systems.

Hebb rule

If an axon of a presynaptic neuron is active while the postsynaptic neuron is firing, the synapse will be strengthened. LTP

Long-term potentiation (LTP)

Synapse becomes stronger over time.

Associative LTP

If a weak synapse and a strong synapse on the same postsynaptic neuron are active simultaneously, the weak synapse will be potentiated.

Rate of stimulation for LTP and LTD

High-frequency stimulation elicits LTP. Low-frequency stimulation elicits LTD.

Memories with LTP and LTD

LTP- forming and recalling memories. Associative LTP- classical conditioning. LTD- forgetting, deleting incorrect information, making space for new memories. Cells that fire together wire together.

Glutamate receptors necessary for LTP

Small stimulation triggers AMPA receptors (short-acting). Large stimulation triggers NMDA receptors (long-lasting)

Consolidation 2 enzymes

CaMKII (establishment of LTP), protein kinase M zeta (maintains long-term memory)

During LTP neurotransmitter release

Postsynaptic nitric oxide release triggers increased presynaptic neurotransmitter release.

Structural changes in LTP

Increased number, enlargement, and growth dendritic spines. Transport of additional AMPA receptors into the spines.

LTP- initiated growth of hippocampus

London taxi drivers with extensive spatial memory have larger posterior hippocampal volume than control individuals. Differences increased proportionally to years as a taxi driver.

Consolidation during sleep

Neurons in the hippocampus and cortical areas repeat firing patterns that occurred during awake learning (non-REM). Sleep-activated genes play roles in protein synthesis, synaptic modification, and memory consolidation. REM: procedural memory.

Extinction

Eliminates useless memories through new learning. Requires activation of NMDA receptors.

Forgetting

Active, adaptive biological process. Enzyme PP1, Rac protein encourage memory loss. May prevent the saturation of synapses.

Reconsolidation

During memory retrieval. Opportunity to refine memory, correct errors (PTSD). Opportunity to create memories that did not occur (false memories)

Dementia with memory

Many show little or no memory loss. Deficits usually reflect motivation on memory tests.

Reverse hypothesis (Cognitive Reserve)

Active lifestyle throughout life promotes neurogenesis. In elderly, this reserve of neurons prevents cognitive declines. Individuals with greater cognitive or brain capacity can compensate for brain changes due to aging, injury or disorder.

Alzheimer’s disease

Progressive brain deterioration, declarative memory loss. Language, visuospatial functions, reason, and aggressive problems. Affects 10% of people over 65, 50% of individuals over 85. Plaques and tangles.

Global loss of neurons in brain

Particularly the temporal/frontal lobes. Enlargement of ventricles. Hippocampus is isolated from the rest of the brain.

Genes in Alzheimer’s

4 genes confirmed in Alzheimer’s disease (50% cases). 3 early onset (<60 years) 1 late onset (>60 years)

Environmental correlates to Alzheimer’s

Lead exposure in childhood, pesticides, chronic stress, mild cognitive impairment, etc.

Treatments for Alzheimer’s

Slow down decline, but cannot reverse effects. 5 approved drugs- Cholinesterase inhibitors (increase available acetylcholine) Memantine (namenda) reduces levels of glutamate. Stem cell and gene therapy options explored.

Detecting Alzheimer’s

Neuropsychological testing, brain scans (PET, MRI) can reveal atrophy in temporal and parietal areas. Biomarkers for plaques is much more promising. 25% of individuals with plaques contract Alzheimer’s within 3 years. Low levels correlate to 2% risk of Alzheimer’s.

Korsakoff’s syndrome

Progressive, irreversible brain deterioration almost always caused by chronic alcoholism. Deficiency in thiamine (vitamin B1). Alcohol reduces absorption of thiamine in the stomach. Cognitive effects: Anterograde amnesia, apathy, confabulation due to confusion between reality and memory.

Amyloid beta proteins

Build up and create plaque which can cause Alzheimer’s

Tau proteins

Go up to cell bodies and create tangles. Kills cell. (fishing lines)