Difference Between Habituation and Sensitization:
Habituation: a decrease in response to a repeated, non-threatening, or irrelevant stimulus.
The organism learns to ignore the stimulus because it is not significant.
Reduces attention to unimportant stimuli.
Sensitization: An increase in response to a stimulus, often due to it being intense, harmful, or arousing.
The organism becomes more alert or reactive after exposure to a strong or noxious stimulus.
Enhances response to potential threats.
Kandel’s Three Hypotheses:
Sensory neurons become less responsive.
The sensory neurons stop firing as strongly after repeated stimulation.
Motor neurons become fatigued.
The motor neurons that control the gill reflex eventually get tired and stop responding.
Changes occur between the sensory and motor neurons.
The weakening of the synapse between sensory and motor neurons.
Which Hypothesis Is Correct?:
Changes are occurring between the sensory and motor neurons.
Normally, sensory neurons depolarize as an influx of calcium enters the presynaptic terminal, triggering the release of glutamate into the synapse.
After repeated stimulation, fewer calcium channels open due to inactivation.
Therefore, less calcium is released in the sensory neuron, causing less glutamate release into the synapse.
With less glutamate, ESPSs become smaller and weaker.
Therefore, motor neurons will fire less strongly.
Neural Mechanism for Habituation/Sensitization in Aplysia:
Aplysia is a good animal to study because it has fewer, but larger, neurons.
The gill-withdrawal reflex explains:
The Aplysia’s gill is used for breathing and is covered with a mantle shelf, a protective tissue.
Waste and seawater are released through the siphon, a tube-like structure.
Touching the siphon causes the gill to retract.
Touching the siphon repeatedly leads to a less pronounced reflex or retraction of the gill.
After an electrical shock to the head or tail, an Aplysia will show an increased gill-withdrawal response.
Sensory neurons release more neurotransmitters onto the interneurons and motor neurons, leading to a more intense response.
What Are The Long-Term Changes?:
Typically, Aplysias show 1300 axon terminals synapsed with sensory neurons.
However, Aplysias that have experienced sensitization had 2800 terminals.
Aplysias that have experienced habituation have 800 terminals.
Long-Term Potentiation:
The long-lasting increase in synaptic strength.
Thought to be associated with memory formation.
LTP makes signal transmission faster and stronger.
NMDA and AMPA are receptors for glutamate.
Typically, only NMDA receptors are available to depolarize the postsynaptic membrane.
When the connection is strengthened, AMPA receptors are added to the membrane.
More AMPA receptors allow for a larger response to glutamate.
More AMPA receptors make it easier to reach depolarization (reaching threshold faster).
This is the cellular basis for LTP.
Long-Term Depression:
The long-lasting decrease in synaptic strength that lasts hours or days.
Thought to be associated with learning.
Evidence For LTP As A Mechanism For Long-Term Memory:
Both LTP and memories can last indefinitely.
Both LTP and memories can result from very brief input or events.
LTP is consistent with models proposed by Donald Hebb.
LTP is found in cells thought to be associated with memory formation, such as those in the hippocampus and cerebellum.
NMDA receptors (linked to LTP) are also linked to memory.
Amnesias:
Retrograde amnesia: loss of memories from the past.
Anterograde amnesia: inability to form new memories.
Patient H.M.:
Large areas of H.M.’s hippocampi and temporal lobes were surgically removed.
His personality and IQ were not impacted.
However, he experienced profound retrograde amnesia as well as anterograde amnesia.
His short-term memory was ok.
“Working memory”
Could hold information for a very short amount of time when undistracted.
He could still learn procedural tasks.
Mirror drawing. He improved with practice despite not remembering ever doing it before.
His deficits were in explicit memory tasks.
Concluded that the ability to store memories and the ability to access previously stored memories are in different brain areas.
Procedural memories are dealt with in different brain areas than explicit memories.
Thalamus:
Korsakoff’s Syndrome:
Damage to the thalamus and the mammillary bodies
Caused by a thiamine deficiency due to alcoholism.
Patient N.A.
A fencing foil went up his nose and caused a lesion to their left thalamus.
He had similar amnesia to H.M.
Delayed Non-Matching to Sample Task:
Monkeys with temporal lobe or thalamus damage could not do the DNMS task.
Requires the ability to transfer memories from short-term systems into long-term systems.
Hippocampus:
The right hippocampus is active during spatial memory processing.
May include a 3D representation of the world around us.
The left hippocampus is more active during verbal memory tasks.
Prefrontal Cortex:
Patients with prefrontal cortex damage have issues with the Wisconsin card-sorting task.
Short-term memory issues.
Object permanence studies:
Adult monkeys with prefrontal damage don’t seem to grasp object permanence.
Prefrontal cortex is constantly developing throughout youth and childhood.
Object permanence usually develops in the first year of life.
Basal Ganglia:
Lesions of the basal ganglia impact procedural memories, but not explicit memories.
The opposite of H.M.
Diseases that lead to damage to the basal ganglia typically also have procedural memory deficits.
Huntington’s and Parkinson’s Disease
Cerebellum:
Possibly key to procedural memories.
Motor learning
It is unclear and not currently agreed upon whether damage to the cerebellum leads to deficits in motor learning or simply the performance of that learned task.
Papez’s Circuit:
A network that connects the thalamus, mammillary bodies, and hippocampus.
Believed to be key to forming long memories.
Stress and Memory:
Stress impacts the amygdala.
Has connections to the hippocampus.
Cortisol may damage the hippocampus.
Repression
Flashbacks/flashbulb memories