Behavioral Neuroscience Exam 3 studyguide Chapter 10
● understand what is meant by consolidation, storage, retrieval
○ Consolidation: short-term memories are stabilized into long-term memories (especially in
the hippocampus)
○ Storage: It’s where and how memories are held (in networks of synapses)
○ Retrieval: The process of reactivating stored information for use (hippocampal and
cortical circuits)
● LTP: Hebb rule, what LTP is, in what cases can it be induced, what it does, where it
happens
○ Long-term potentiation: is a long-lasting increase in the strength (efficacy) of synaptic
transmission between two neurons following high-frequency stimulation
🧩
■ cellular mechanism underlying learning and memory
○ Hebb’s Rule: “Cells that fire together, wire together.”
■ If neuron A repeatedly activates neuron B, the connection (synapse) between
them becomes stronger, or simultaneous firing
○ When LTP can be induced:
■ Repeated, rapid stimulation of one set of afferent
■ Stimulation of one set of afferent while depolarizing the cell
■ Simultaneous stimulation of two sets of afferent
● ALL HAVE COOCURRENCE OF STIMULATION
○ Where: hippocampus, cerebellum, amygdala, cortex
● structural changes that occur in neurons during LTP
○ Changes in size and shape of dendrite spine
○ Growth of new spines (allow for more synapses on one axon)
● role of NMDA receptors and magnesium ion in LTP. why is depolarization important?
○ At Rest → Glutamate can bind AMPA and NMDA receptors → AMPA opens → a small
Na⁺ influx → mild depolarization
■ NMDA is blocked by Mg²⁺, so even if glutamate binds, no ions pass through
○ During Strong or Repeated Stimulation → strong depolarization via AMPA receptors →
Depolarization repels the Mg²⁺ ion out of the NMDA receptor channel → Now NMDA
receptors can open fully
■ With NMDA open and glutamate bound → Ca²⁺ and Na⁺ enter the postsynaptic
neuron (The entry of calcium ions leads to long-term potentiation)
○ Depolarization: removes Mg block in NMDA channel
○ Presynaptic changes: increased glutamate release (via nitric oxide feedback)
○ Postsynaptic changes: increased AMPA receptors, spine growth, gene expression
● role of hippocampus and cortex in memory, results of hippocampal damage
○ Hippocampal memory-related functions:
■ Binding sensory information for consolidation
■ Spatial memory of location of objects of behavioral importance
■ Storage of memories (unknown amount of time) → transfers to cortex for
long-term storage
○ Damage:
, ■ Anterograde Amnesia: Inability to form new long-term declarative memories
after the damage
● Famous case of H.M. — could not form new facts or events after surgery
■ Temporally graded retrograde amnesia: Loss of memories formed shortly before
the injury, but older memories (already consolidated) remain intact
● Can recall childhood but not events from the past few months
■ IMPLICIT AND PROCEDUAL MEMORY INTACT
● where different types of memories are stored (declarative, procedural, etc)
○ Declarative/Explicit memory: Hippocampus
■ Episodic: hippocampus & prefrontal cortex
■ Semantic: temporal lobe & parietal cortex
○ Procedural/Implicit memory: basal ganglia
○ Emotional memory: amygdala
○ Working memory: prefrontal cortex
● names of hippocampal formation structures and pathways (but you don't need to identify
them on a diagram or say what is connected to what). know what are the inputs to the
hippocampus and what that tells us
○ main input: entorhinal cortex, which receives highly processed information from
association areas
■ Shows the hippocampus deals with current happenings, processes information,
transfers to the cortex for LTS
○ 3 main structures:
■ Dentate gyrus
■ Area CA3
■ Area CA1
● anterograde amnesia: what causes it, symptoms
○ Korsackoff’s Syndrome: thiamin B1 deficiency (alcoholism) characterized by
inappropriate familiarity and confabulation → damage to cerebral cortex
■ N.A. Korsackoff’s: damaged thalamus
■ N.A. & B.J Korsackoff’s: medial hypothalamus and mamillary bodies
■ H.M. & C.W. Korsackoff’s: damaged hippocampus
● Papez circuit
● What happened to N.A. and where and how is it different from H.M.
○ N.A. and H.M. had the same symptoms but the injury damaged different areas of their
brains (Nick got a fencing needle through his nose into his brain; H.M. had his
hippocampi and amygdali removed due to severe epilepsy)
● why retrieved memories are vulnerable to modification
○ When a memory is stored long-term, it exists as a stable pattern of synaptic connections
(strengthened through LTP); When you retrieve that memory, those neural connections
are reactivated — meaning the memory becomes temporarily unstable or “labile”
● distinguish between the characteristics of four types of learning: stimulus-response, motor,
perceptual, and relational
○ Stimulus-Response learning:
■ classical condition: a US is continually paired with a CS
● understand what is meant by consolidation, storage, retrieval
○ Consolidation: short-term memories are stabilized into long-term memories (especially in
the hippocampus)
○ Storage: It’s where and how memories are held (in networks of synapses)
○ Retrieval: The process of reactivating stored information for use (hippocampal and
cortical circuits)
● LTP: Hebb rule, what LTP is, in what cases can it be induced, what it does, where it
happens
○ Long-term potentiation: is a long-lasting increase in the strength (efficacy) of synaptic
transmission between two neurons following high-frequency stimulation
🧩
■ cellular mechanism underlying learning and memory
○ Hebb’s Rule: “Cells that fire together, wire together.”
■ If neuron A repeatedly activates neuron B, the connection (synapse) between
them becomes stronger, or simultaneous firing
○ When LTP can be induced:
■ Repeated, rapid stimulation of one set of afferent
■ Stimulation of one set of afferent while depolarizing the cell
■ Simultaneous stimulation of two sets of afferent
● ALL HAVE COOCURRENCE OF STIMULATION
○ Where: hippocampus, cerebellum, amygdala, cortex
● structural changes that occur in neurons during LTP
○ Changes in size and shape of dendrite spine
○ Growth of new spines (allow for more synapses on one axon)
● role of NMDA receptors and magnesium ion in LTP. why is depolarization important?
○ At Rest → Glutamate can bind AMPA and NMDA receptors → AMPA opens → a small
Na⁺ influx → mild depolarization
■ NMDA is blocked by Mg²⁺, so even if glutamate binds, no ions pass through
○ During Strong or Repeated Stimulation → strong depolarization via AMPA receptors →
Depolarization repels the Mg²⁺ ion out of the NMDA receptor channel → Now NMDA
receptors can open fully
■ With NMDA open and glutamate bound → Ca²⁺ and Na⁺ enter the postsynaptic
neuron (The entry of calcium ions leads to long-term potentiation)
○ Depolarization: removes Mg block in NMDA channel
○ Presynaptic changes: increased glutamate release (via nitric oxide feedback)
○ Postsynaptic changes: increased AMPA receptors, spine growth, gene expression
● role of hippocampus and cortex in memory, results of hippocampal damage
○ Hippocampal memory-related functions:
■ Binding sensory information for consolidation
■ Spatial memory of location of objects of behavioral importance
■ Storage of memories (unknown amount of time) → transfers to cortex for
long-term storage
○ Damage:
, ■ Anterograde Amnesia: Inability to form new long-term declarative memories
after the damage
● Famous case of H.M. — could not form new facts or events after surgery
■ Temporally graded retrograde amnesia: Loss of memories formed shortly before
the injury, but older memories (already consolidated) remain intact
● Can recall childhood but not events from the past few months
■ IMPLICIT AND PROCEDUAL MEMORY INTACT
● where different types of memories are stored (declarative, procedural, etc)
○ Declarative/Explicit memory: Hippocampus
■ Episodic: hippocampus & prefrontal cortex
■ Semantic: temporal lobe & parietal cortex
○ Procedural/Implicit memory: basal ganglia
○ Emotional memory: amygdala
○ Working memory: prefrontal cortex
● names of hippocampal formation structures and pathways (but you don't need to identify
them on a diagram or say what is connected to what). know what are the inputs to the
hippocampus and what that tells us
○ main input: entorhinal cortex, which receives highly processed information from
association areas
■ Shows the hippocampus deals with current happenings, processes information,
transfers to the cortex for LTS
○ 3 main structures:
■ Dentate gyrus
■ Area CA3
■ Area CA1
● anterograde amnesia: what causes it, symptoms
○ Korsackoff’s Syndrome: thiamin B1 deficiency (alcoholism) characterized by
inappropriate familiarity and confabulation → damage to cerebral cortex
■ N.A. Korsackoff’s: damaged thalamus
■ N.A. & B.J Korsackoff’s: medial hypothalamus and mamillary bodies
■ H.M. & C.W. Korsackoff’s: damaged hippocampus
● Papez circuit
● What happened to N.A. and where and how is it different from H.M.
○ N.A. and H.M. had the same symptoms but the injury damaged different areas of their
brains (Nick got a fencing needle through his nose into his brain; H.M. had his
hippocampi and amygdali removed due to severe epilepsy)
● why retrieved memories are vulnerable to modification
○ When a memory is stored long-term, it exists as a stable pattern of synaptic connections
(strengthened through LTP); When you retrieve that memory, those neural connections
are reactivated — meaning the memory becomes temporarily unstable or “labile”
● distinguish between the characteristics of four types of learning: stimulus-response, motor,
perceptual, and relational
○ Stimulus-Response learning:
■ classical condition: a US is continually paired with a CS
