Increased neurotransmitter (NT) release by presynaptic axon terminal
Increased number of channels in postsynaptic membrane
Long-term structural changes
Growth of new synapses
Synaptic take-over
Optimising existing behaviour
Increased transmission rate: react more quickly / reliably to important changes in the environment
Decreased transmission rate: better able to ignore unimportant changes in the environment
Acquiring new behaviour
Growth of new synapses: combine information from previously unrelated sources
Synaptic 'take-over': 're-route' information to new pathways
Learning
Forming new connections
No specific place in cortex where new memories are formed or stored
Loss of memory corresponds to size of lesion, loss of memory not specific to site of lesion
Cortical lesions
Lesion in V4 may cause loss of colour perception together with loss of colour memory
Lesion of the right fusiform gyrus may cause loss of face perception together with loss of memory for faces
Anterograde amnesia
Unable to consciously remember anything new that happens, unable to learn new facts
Retrograde amnesia
Lose most memories of their past
Intense negative experiences can damage our brains, especially when they combine threat and helplessness
PTSD
When the memory of a traumatic experience does not 'fade away' over time, but begins to dominate the patient's life
Stress hormones may play a critical role in PTSD
Adrenalin and Noradrenalin
Affect memory
Amygdala
Part of the limbic system, crucial for emotional memories, when damaged animals appear emotionally 'flat', no longer learn a 'fear response', over-sexed
Hypothalamus
Gateway from nervous to endocrine (hormonal) system
Simplified psychobiological model of PTSD
Fear response processed by amygdala, activates hypothalamus, activates endocrine system, releases adrenalin and noradrenalin, improves memory of stress/traumatic experience