Learning and memory

HM - removed medial temporal lobe for epilsepy. Since surgery, had anterograde amnesia. Unable to remember new events or learn new facts. Able to remember things that happened before surgery. No new declarative long-term memories.

Chemicals generated by endocrine: Transported to brain via bloodtsream. Specific hormones for different emotional states. Adrenalin and noradrenaline affect memory.

Experimental evidence: Pictures better remembered when presented with exciting story, rather than neutral story - advantage disappeared when given noradrenalin antagonist.

Acquiring new behaviour -> Growth of new synapses allows you to...1. Combine info from previously unrelated sources. 2. Respond to old stimuli in new way. 3. Synaptic takeover allows you to re-route info to new pathways and respond to old stimuli in a new way.

Gene-environment interaction - Simple set of rules, produce a large variety of outcomes depending on the environment and exact starting point. Environment can change the rules. To break or not allow positive feedback loop, use nonadrealine antagonists, don't release adrenaline/noradrenaline

Increased neural activity can cause molecular changes at the synapse. Baseline activity - action potentials generated at random intervals, no changes at synapse.

Action potentials become either...1. More frequent (excitation) or 2. Less frequent (inhibition)

How do changes become permanent?

• Increased neural activity - causes lasting structural changes
• Sustained activity (frequent AP's for a long time) can cause...a. Growth of new synapses  b. Synaptic take over

Optimising existing behaviour:

• Increased transmission rate = you react more quickly to important changes in environment
• Decreased transmission rate = you are more likely to ignore unimportant chnages in the environment (lose them)

Cortex: No specific place in cortex where memories are stored. Loss of memory function related to size of lesion. More cortex removed = worse performance on memory tasks. Lesion in v4 = loss of colour perception and memory. Lesion in right fusiform gyrus = impaired facial processing + loss of memory for faces

• Parietal lobe -> Sensori-motor integration, makes decisions about choices
• Frontal lobe -> Motor control + planning, play piano
• Temporal lobe -> Activates neurons + allows you to hear tone
• Occipital lobe -> Vision - read music, connect specific neurons in lobes
• E.g. playing piano (linked + systematic in a specific way)

Diencephalon (Korsakoff's syndrome): Chronic alcoholism - thiamine deficit. Anterograde amnesia, can learn new skills and events, but also have retrograde amnesia, so unaware of condition.

Post Traumatic Stress Disorder (PTSD): Inability to forget - memory becomes dominating. Flashbacks, concentration problems, depression, nightmates. Stress hormones play role.

Amygdala: Limbic system, crucial for emotional memories.

• No longer learn fear response, over-sexed
• Direct contact to hypothalamus, gateway from NS to endocrine system
• If memory becomes strong enough to activate amygdala, fall into positive feedback loop and memory will trigger a stress response.

Model of PTSD:

• 1. Amygdala activated by stress/traumatic experience.
• 2. Amygdala activates hypothalamus
• 3. Hypothalamus activates endocrine system
• 4. Endocrine system releases adrenalin and noradrenalin
• 5. Adrenalin and noradrenalin improve memory of stress/traumatic experience
• Noradrenalin and adrenaline released which improves memory for particular stressful event