Biological Psychology Chapter 12: Learning & Memory Lecture Notes PDF

Biological Psychology Thirteenth Edition Chapter 12 Learning & Memory © 2019 Cengage. All rights reserved.  Localized Representations of Memory (1 of 2) Classical conditioning – Pioneered by Ivan Pavlov – Pairin...

Biological Psychology Thirteenth Edition Chapter 12 Learning & Memory © 2019 Cengage. All rights reserved.  Localized Representations of Memory (1 of 2) Classical conditioning – Pioneered by Ivan Pavlov – Pairing two stimuli changes the response to one of them  Conditioned stimulus  Unconditioned stimulus  Unconditioned response  Conditioned response © 2019 Cengage. All rights reserved. Classical Conditioning © 2019 Cengage. All rights reserved.  Amygdala: Plays a crucial role in associating stimuli with emotional responses, especially fear. It's essential for forming conditioned emotional responses. Cerebellum: Involved in the motor learning aspect of classical conditioning, particularly in simple reflexes like eyeblink conditioning. Prefrontal Cortex: Engages in higher-order thinking and is involved in inhibiting or adjusting responses based on learned associations. Hippocampus: Although not directly involved in forming stimulus-response connections, it contributes to forming the context in which conditioning occurs, particularly when multiple stimuli are involved or when spatial or temporal context matters.  Localized Representations of Memory (2 of 2) Instrumental conditioning – Also known as operant conditioning – Individual’s response followed by reinforcer or punishment – Reinforcers  Events that increase the probability that the response will occur again – Punishment  Events that decrease the probability that the response will occur again © 2019 Cengage. All rights reserved. Instrumental Conditioning © 2019 Cengage. All rights reserved.  Dopaminergic Pathways (VTA and Nucleus Accumbens): The ventral tegmental area (VTA) and the nucleus accumbens are central to the brain's reward system. Dopamine release in these areas reinforces behavior that leads to positive outcomes (rewards). Striatum (Basal Ganglia): Involved in habit formation and the reinforcement of action-outcome associations. The basal ganglia help encode the "habitual" aspects of learned behavior. Prefrontal Cortex: Plays a role in decision-making and evaluating outcomes, helping to adjust behavior based on past experiences of reward or punishment. Amygdala: Involved in associating rewards and punishments with emotional responses, making certain consequences more motivating or aversive. Anterior Cingulate Cortex: Important for error detection and conflict monitoring, allowing for learning from mistakes and adjusting behavior to avoid negative outcomes.  Lashley’s Search for the Engram Engram – Karl Lashley believed that specific memories were localized in certain areas of the brain. He thought that if he could identify and damage the exact brain area where a memory was stored, the subject (usually a rat) would lose that particular memory. – Hypothesis disproven Lashley’s experiments showed that learning and memory do not rely on a single cortical area Lashley’s principles about the nervous system – Equipotentiality: all parts of the cortex contribute equally to complex functioning behaviors (e.g., learning) – Mass action: the cortex works as a whole, and more cortex is better © 2019 Cengage. All rights reserved. View of Rat Brain, Showing Lashley’s Brain Cuts in Various Rats © 2019 Cengage. All rights reserved.  Types of Memory Hebb (1949) differentiated between two types of memory: – Short-term memory: memory of events that have just occurred – Long-term memory: memory of events from times further back © 2019 Cengage. All rights reserved. Differences Between Short- and Long-Term Memory Short-term memory has a limited capacity, but long-term memory does not Short-term memory fades quickly without rehearsal, while long-term memories persist Long-term memories can be stimulated with a cue/ hint – Short-term memories cannot Researchers propose all information enters short term memory – The brain consolidates it into long-term memory Later research weakened the distinction between short- and long-term memory – Not all rehearsed short-term memories become long-term memories – Time needed for consolidation varies © 2019 Cengage. All rights reserved.  Our Changing Views of Consolidation Emotionally significant memories form quickly – Locus Coeruleus increases release of norepinephrine – Emotion causes release of epinephrine & cortisol to activate amygdala and hippocampus—enhances consolidation of recent experiences Working memory – Proposed by Baddeley & Hitch as an alternative to short- term memory – Emphasis on temporary storage of information to actively attend to it and work on it for a period of time © 2019 Cengage. All rights reserved. Short-Term Memory Characteristics: Duration: Lasts for about 15-30 seconds without rehearsal. Capacity: Limited to 5-9 items (known as Miller’s Law). Function: Allows immediate recall of information, like remembering a phone number long enough to dial it. Prefrontal Cortex: Responsible for the active maintenance of information for brief periods. It’s critical in keeping things "online" for a short time. Parietal Lobes: Also involved in holding onto certain types of sensory information briefly, especially in spatial memory tasks.  Long-Term Memory Types of Long-Term Memory: Explicit (Declarative) Memory: Conscious memories that can be verbalized. Episodic Memory: Memory of specific events or experiences (e.g., your last birthday). Semantic Memory: General knowledge or facts (e.g., knowing that Paris is the capital of France). Implicit (Non-declarative) Memory: Unconscious memories, such as skills or habits. Procedural Memory: How to perform tasks like riding a bike or playing an instrument. Classically Conditioned Responses: Emotional responses or learned reflexes. Hippocampus: Plays a central role in forming and consolidating new explicit memories. Damage to the hippocampus can result in difficulty forming new long- term memories (anterograde amnesia). Cerebral Cortex: Where long-term memories are stored once consolidated. Different types of memories (e.g., visual, auditory) are stored in corresponding sensory areas. Basal Ganglia & Cerebellum: Important for procedural memory and motor skills.  Working Memory Working memory is a more complex system than short-term memory. It involves not only temporarily holding information but also manipulating it. Working memory is crucial for reasoning, problem-solving, and decision- making. Unlike short-term memory, working memory involves actively processing and manipulating the information, such as doing mental math or holding a conversation while forming responses. Dual Processing: Can handle multiple types of information simultaneously (e.g., visual-spatial data while listening to verbal instructions). Limited Capacity: Similar to STM, it can only handle a few items at a time. Prefrontal Cortex: Essential for the active maintenance and manipulation of information. The prefrontal cortex is crucial for the central executive functions of working memory. Parietal Cortex: Works with the prefrontal cortex in spatial and attentional aspects of working memory. Dorsolateral Prefrontal Cortex (DLPFC): Involved in maintaining and manipulating information over short periods, especially when tasks require complex problem-solving or reasonin Components of Working Memory (Baddeley’s Model): Central Executive: The "manager" that directs attention and coordinates activities of the other components. Phonological Loop: Handles verbal and auditory information (e.g., repeating a phone number to yourself). Visuospatial Sketchpad: Manages visual and spatial information (e.g., mentally rotating objects). Episodic Buffer: Integrates information across modalities and connects working memory with long- term memory.  The Hippocampus and Spatial Memory Navigation depends on your surroundings and your spatial memory Damage to the hippocampus also impairs abilities on spatial tasks such as: – Radial mazes: a subject must navigate a maze that has eight or more arms with a reinforcer at the end – Morris water maze task: a rat must swim through murky water to find a rest platform just underneath the surface © 2019 Cengage. All rights reserved.  Hippocampus and Spatial Memory The hippocampus plays a central role in forming and using cognitive maps— mental representations of spatial environments. It enables you to understand and recall where things are in relation to one another. 1.Place Cells: 1. Inside the hippocampus, there are specialized neurons called place cells. These cells become active when an individual is in a specific location within an environment. 2. When a person or animal moves, different place cells activate, allowing the brain to map out spatial relationships and locations. 2.Memory for Routes and Landmarks: 1. The hippocampus allows us to remember specific routes or paths we’ve taken and to recognize and use landmarks to guide us. 2. This ability helps in learning and recalling not just the current environment but also new environments and spatial layouts. 3.Integration with Other Brain Regions: 1. The hippocampus works closely with other parts of the brain, like the entorhinal cortex, which contains grid cells. These cells provide a grid-like coordinate system to help track movement through space.  Striatum Procedural Memory: Striatum’s Role: The striatum is essential for procedural memory because it helps in learning and automating repetitive tasks through practice. Once a task becomes automatic, the striatum allows it to be performed without conscious effort. Habit Formation: Striatum’s Role: The striatum is heavily involved in forming and storing habits. It helps encode the stimulus-response associations that underpin habit formation, where repeated behaviors become automatic over time. The more a behavior is practiced, the more the striatum strengthens the neural circuits involved, making the behavior habitual. Instrumental (Operant) Conditioning: Striatum’s Role: The striatum plays a key role in reinforcing actions that lead to positive outcomes. It helps encode the associations between actions and rewards, influencing decision-making and reinforcing behaviors based on past experiences of reward or punishment Working Memory: Striatum’s Role: While the prefrontal cortex is the main area responsible for working memory, the striatum contributes to tasks that require the integration of cognitive and motor functions, such as task-switching or learning sequences of actions.  Implicit Memory: The striatum supports memories that are not consciously recalled but influence behavior, such as habits and procedural tasks. The striatum has strong connections with the prefrontal cortex, which is involved in executive functions and decision-making. It also receives input from the dopaminergic neurons of the substantia nigra and ventral tegmental area (VTA), which are critical for processing rewards and reinforcement learning. Outputs from the striatum project back to the thalamus and other areas of the basal ganglia, forming circuits that regulate movement, habits, and learning.  Hippocampus vs. Striatum However, most tasks activate both systems Hippocampal learning at the beginning of a task, but once the task becomes “habitual” or “automatic,” more emphasis on striatum The hippocampus is associated with declarative (explicit) memory, such as the memory of facts and events. In contrast, the striatum is associated with non-declarative (implicit) memory, such as skills and habits. While the hippocampus helps with the formation of memories that require conscious recall (e.g., remembering what you learned in class), the striatum supports memory for tasks that become automatic and routine over time (e.g., driving or typing). © 2019 Cengage. All rights reserved.  Brain Areas for Two Types of Learning Hippocampus Striatum Speed of learning Can learn in a single trial Learns gradually over many trials Type of behavior Flexible responses Habits Based on what type of Sometimes connects information Generally requires prompt feedback? over a delay feedback Explicit or implicit Explicit Implicit learning? What happens after Impaired declarative memory, Impaired learning of skills and damage? especially habits episodic memory © 2019 Cengage. All rights reserved.  OTHER BRAIN AREAS IN MEMORY AND LEARNING Amygdala Function: The amygdala is key for processing emotional memories, particularly those related to fear and pleasure. Role in Learning: It enhances the encoding of memories that are emotionally charged (e.g., traumatic events or joyful experiences). Emotional arousal often strengthens the consolidation of memories. Emotion and Memory: The amygdala interacts with the hippocampus to prioritize the storage of emotionally significant memories. Damage: Damage to the amygdala can impair the ability to remember emotional events, though factual memory may remain intact. Temporal Lobe (Cortex) Function: The temporal lobe, particularly the medial temporal lobe, includes the hippocampus and plays a crucial role in declarative memory and language learning. Role in Learning: It helps in the encoding, storage, and retrieval of explicit memories. It also processes auditory information, which is essential for learning language and music. Damage: Damage to the medial temporal lobe can cause memory deficits, particularly in forming new long-term memories. Cerebellum Function: The cerebellum is involved in procedural memory and motor learning, helping us learn skills and habits, such as riding a bike or playing an instrument. Role in Learning: It helps automate repetitive, coordinated movements and is essential for classical conditioning, particularly in motor tasks. Damage: Damage to the cerebellum can impair motor learning and the ability to perform coordinated movements, but it may not affect explicit memory for facts or events. Parietal Cortex Function: The parietal cortex contributes to spatial learning and memory, helping us navigate our environment. Role in Learning: It is involved in processing sensory information and working with the hippocampus to create cognitive maps of our surroundings. Damage: Damage to the parietal cortex can lead to difficulties in spatial orientation and recalling the spatial layout of environments. Prefrontal Cortex Function: The prefrontal cortex is involved in working memory (the temporary holding and manipulation of information) and higher cognitive functions like decision-making, planning, and problem-solving. Role in Learning: It helps manage and manipulate information in working memory, which is necessary for complex tasks, reasoning, and learning new concepts. Executive Functions: The prefrontal cortex also contributes to goal-directed learning, where individuals use feedback to adjust behaviors to achieve specific outcomes. Damage: Damage to this area can affect short-term memory, attention, and the ability to plan or make decisions. Dopaminergic System (Ventral Tegmental Area and Nucleus Accumbens) Function: The dopamine system is essential for reward-based learning and motivation. Role in Learning: The release of dopamine, particularly in the nucleus accumbens and ventral tegmental area (VTA), signals the brain that a behavior is rewarding, helping to reinforce actions that lead to positive outcomes. Reinforcement Learning: This system helps form associations between actions and their rewarding consequences, which is key for learning new behaviors based on rewards and punishments.  Learning and Memory Processes in the Brain 1.Encoding: 1. Information is first processed and "encoded" in the brain. This involves converting sensory input (visual, auditory, etc.) into a form that can be stored. 2. Brain Areas: Hippocampus (for declarative memories), sensory areas (for initial processing). 2.Consolidation: 1. After encoding, the information must be stabilized to form long-term memories. This often happens during sleep, where memories are replayed and strengthened. 2. Brain Areas: Hippocampus and cortex (especially during sleep). 3.Storage: 1. Memories are stored in distributed networks across the brain, particularly in the areas involved in processing that type of information (e.g., visual memories in the visual cortex, motor memories in the cerebellum). 2. Brain Areas: Sensory cortices, hippocampus, and association areas. 4.Retrieval: 1. Retrieval is the process of bringing stored information back into conscious awareness. This can involve remembering facts, events, or skills. 2. Brain Areas: Prefrontal cortex (for retrieval), hippocampus (for reactivating stored memories).  Learning and the Hebbian Synapse Hebbian synapse – A synapse that increases in effectiveness because of simultaneous activity in the presynaptic and postsynaptic neurons – Such synapses may be critical for many kinds of associative learning If Neuron A repeatedly causes Neuron B to fire, the synaptic connection between these two neurons becomes stronger. Over time, Neuron A will need less stimulation to activate Neuron B, and the connection becomes more efficient. © 2019 Cengage. All rights reserved. Steps of Hebbian Learning: 1.Neural Firing: When the presynaptic neuron (Neuron A) releases neurotransmitters across the synapse, it activates the postsynaptic neuron (Neuron B). 2.Simultaneous Activation: If Neuron A and Neuron B are consistently activated at the same time, the synaptic connection strengthens. 3.Synaptic Potentiation: As this connection strengthens, it becomes easier for Neuron A to excite Neuron B in the future, leading to more efficient communication. Long-Term Potentiation and Short-Term Potentiation in Learning and Memory Long-term potentiation (LTP) and short-term potentiation (STP) are critical processes involved in synaptic plasticity—the ability of the brain to change and strengthen synaptic connections in response to experience. Short-Term Potentiation (STP) Short-term potentiation (STP) refers to the temporary strengthening of synaptic transmission that occurs over a short period, typically lasting from milliseconds to a few minutes. STP does not involve long-lasting changes in the structure or function of the synapse and is typically used for short-term processes, such as immediate memory or working memory. Duration: Lasts seconds to a few minutes, making it a short-lived phenomenon. Cause: Usually results from an increased availability of neurotransmitters (like glutamate) or enhanced responsiveness of postsynaptic receptors. Reversibility: If the increased stimulation ceases, the synaptic strength quickly returns to baseline levels. No Structural Change: STP does not involve structural changes in neurons or synapses. It is mainly a functional change in neurotransmitter release or receptor sensitivity.  Mechanisms of STP: Increased Neurotransmitter Release: With repeated stimulation of a presynaptic neuron, there can be an accumulation of calcium ions in the presynaptic terminal. This extra calcium causes the neuron to release more neurotransmitters into the synaptic cleft. Postsynaptic Changes: The postsynaptic neuron might become more responsive to neurotransmitters, usually through increased receptor activity (e.g., glutamate binding to NMDA or AMPA receptors). Temporary Potentiation: The increased neurotransmitter release temporarily enhances the strength of the synaptic connection, but this effect diminishes as calcium levels return to normal. Short-Term Memory: If you’re memorizing a phone number for a few seconds before dialing it, your brain might use STP. The synaptic connections between neurons involved in storing the number are temporarily enhanced, allowing you to retain the information briefly. Once you dial the number and no longer need to remember it, the potentiation fades, and the synapses return to their normal strength.  Role in Learning and Memory: STP is thought to play a role in the early stages of learning by facilitating rapid, temporary changes in synaptic strength. While STP alone is not sufficient for long-lasting memory, it helps form the initial steps in the learning process by temporarily enhancing communication between neurons. Hippocampus: STP is most commonly studied in the hippocampus, which is critical for learning and memory, especially spatial memory and declarative memory (facts and events). Cerebral Cortex: Plays a role in short-term memory, particularly in areas responsible for sensory processing.  Long-Term Potentiation in Vertebrates Long-term potentiation (LTP) occurs when one or more axons bombard a dendrite with stimulation – Leaves the synapse “potentiated” for a period of time and the neuron is more responsive – https://www.youtube.com/watch?v=4Hm08ksPtMo © 2019 Cengage. All rights reserved.  Long-Term Potentiation Long-term potentiation (LTP) is the long-lasting strengthening of synaptic connections between neurons after repeated stimulation. LTP is considered one of the primary cellular mechanisms that underlie learning and memory in the brain. Key Characteristics of LTP: Duration: LTP can last from hours to days, weeks, or even longer, providing the basis for long-term memory storage. Specificity: LTP is specific to the synapses that are repeatedly activated. Only the synapses involved in the learning process are strengthened. Associativity: Synapses that are activated together can be strengthened together, which may explain how associations are formed during learning. Requires Repeated Activation: LTP typically requires high-frequency stimulation or repeated co-activation of presynaptic and postsynaptic neurons.  Mechanisms of LTP: 1. Postsynaptic Changes: NMDA Receptor Activation: LTP begins with the activation of NMDA receptors, which are glutamate receptors located on the postsynaptic neuron. These receptors are blocked by magnesium ions (Mg²⁺) at rest but are unblocked when the neuron is depolarized, allowing calcium ions (Ca²⁺) to enter the cell. Calcium Signaling: The influx of calcium triggers intracellular signaling pathways that lead to the strengthening of the synapse. This includes the activation of protein kinases, such as CaMKII (calcium/calmodulin-dependent protein kinase II), which plays a key role in LTP induction. AMPA Receptor Insertion: One of the main effects of LTP is an increase in the number of AMPA receptors on the postsynaptic membrane. These receptors are also glutamate receptors and are responsible for fast excitatory neurotransmission. More AMPA receptors mean that the postsynaptic neuron will respond more strongly to neurotransmitters. 2. Presynaptic Changes: Enhanced Neurotransmitter Release: LTP may also involve changes in the presynaptic neuron that increase the release of neurotransmitters. This can happen through retrograde signaling from the postsynaptic neuron to the presynaptic neuron, prompting it to release more neurotransmitter (e.g., glutamate). 3. Structural Changes: Synapse Growth and Formation: Over time, LTP can lead to structural changes at the synapse. Dendritic spines (tiny protrusions on the postsynaptic neuron) can grow or become more stable, providing more surface area for synapses. This structural change underlies the long-lasting nature of LTP.  Role in Learning and Memory: LTP is considered the cellular foundation for long-term memory formation. The strengthening of synapses through LTP allows neurons to communicate more effectively, which is thought to correspond to the formation and storage of long-term memories. Different patterns of LTP might encode different types of information, such as spatial memory, declarative memory, or procedural memory. Learning a New Skill: When learning to play a musical instrument, repeated practice strengthens the neural connections involved in motor skills and auditory processing. Over time, LTP helps these neural pathways become more efficient, so you can play a piece of music more easily and accurately. The strengthened connections support the long-term retention of the skill. The AMPA and NMDA Receptors Before Long-Term Potentiation © 2019 Cengage. All rights reserved.  Properties of Long-Term Potentiation Specificity: only synapses onto a cell that have been highly active become strengthened Cooperativity: simultaneous stimulation by two or more axons produces LTP much more strongly than does repeated stimulation by a single axon Associativity: pairing a weak input with a strong input enhances later responses to a weak input A prolonged decrease in response at a synapse that occurs when axons have been less active than others – Compensatory process: as one synapse strengthens, another weakens © 2019 Cengage. All rights reserved. Associativity in Long-Term Potentiation © 2019 Cengage. All rights reserved.  Long Term Potentiation in Hippocampal Neurons (1 of 2) Glutamate attaches to both receptors. At the AMPA receptor, it opens a channel to let sodium ions enter. At the NMDA receptor, it binds but usually fails to open the channel, which is blocked by magnesium ions. Repeated glutamate excitation of AMPA receptors depolarizes the membrane The depolarization displaces magnesium molecules that had been blocking NMDA receptors Glutamate is then able to excite the NMDA receptors, opening a channel for calcium ions to enter the neuron © 2019 Cengage. All rights reserved.  Long Term Potentiation in Hippocampal Neurons (2 of 2) Entry of calcium through the NMDA channel triggers further changes Activation of a protein sets a series of events in motion More AMPA receptors are built and dendritic branching is increased These changes potentiate the dendrite’s future responsiveness to incoming glutamate © 2019 Cengage. All rights reserved. The AMPA and NMDA Receptors During Long-Term Potentiation © 2019 Cengage. All rights reserved.  Presynaptic Changes Changes in the presynaptic neuron can also cause LTP – Extensive stimulation of a postsynaptic cell causes the release of a retrograde transmitter that travels back to the presynaptic cell to cause the following changes:  Decrease in action potential threshold  Increase neurotransmitter release  Expansion of the axons  Transmitter release from additional sites © 2019 Cengage. All rights reserved. Key Differences Between LTP and STP Long-Term Potentiation Short-Term Potentiation Feature (LTP) (STP) Long-lasting (hours to a Short-lasting (milliseconds Duration lifetime) to minutes) Involves structural Involves temporary Mechanism changes and receptor changes in insertion neurotransmitter release Permanent or semi- Temporary, no structural Changes in Synapse permanent, involving new changes receptor growth Supports short-term Supports long-term Role in Learning memory and immediate learning and memory recall Learning a new language Memorizing a phone Example or skill number briefly  Improving Memory—Drugs Understanding the mechanisms of changes that impact LTP may lead to drugs that improve memory Caffeine, Ritalin, and Modafinil enhance learning by increasing arousal Some herbs have doubtful effects – Ginkgo biloba – Bacopa monnieri © 2019 Cengage. All rights reserved.  Habituation Habituation is a decrease in the strength of a behavioral response after repeated exposure to a benign, non-threatening stimulus. Over time, the organism "learns" that the stimulus is not important, and as a result, it stops responding to it. Synaptic Mechanisms of Habituation: Habituation is thought to result from synaptic depression, where there is a decrease in neurotransmitter release at the synapse between sensory and motor neurons. 1.Reduced Calcium Influx: With repeated stimulation, the amount of calcium that enters the presynaptic neuron during an action potential decreases. Since calcium is necessary for neurotransmitter release, less neurotransmitter is released into the synapse. 2.Decreased Neurotransmitter Release: With less calcium entering the neuron, fewer neurotransmitter-containing vesicles fuse with the presynaptic membrane. This results in a reduced amount of neurotransmitter (like glutamate) being released into the synaptic cleft. 3.Weaker Synaptic Response: On the postsynaptic side, the reduced neurotransmitter release leads to a smaller postsynaptic potential, making it less likely to trigger an action potential in the postsynaptic neuron. As a result, the behavioral response (e.g., reflex) weakens over time. Short-Term Habituation: The changes described above (reduced neurotransmitter release) occur relatively quickly and are transient. They fade over time, and the response can be restored if the stimulus is presented after a break. Long-Term Habituation: With prolonged or repeated exposure over a longer period, more permanent changes can occur at the synapse, including a reduction in the number of synaptic connections (synaptic pruning). This can lead to more long-lasting habituation.  Sensitization Sensitization is an increase in the strength of a behavioral response following exposure to a strong stimulus. Sensitization makes the organism more responsive to subsequent stimuli, even if those stimuli are mild or neutral. Synaptic Mechanisms of Sensitization: Sensitization involves synaptic facilitation, where there is an increase in neurotransmitter release at the synapse, making the response stronger. 1.Serotonin Release: In sensitization, a strong or harmful stimulus activates interneurons that release serotonin onto the presynaptic terminals of sensory neurons. 2.Activation of Second Messengers: Serotonin binds to receptors on the presynaptic neuron, activating second messenger systems, particularly cyclic AMP (cAMP), which in turn activates protein kinase A (PKA). 3.Enhanced Neurotransmitter Release: PKA reduces the closing of potassium channels, prolonging the action potential in the presynaptic neuron. This allows more calcium to enter the neuron during the action potential, resulting in more neurotransmitter being released. 4.Stronger Postsynaptic Response: The increased release of neurotransmitter (such as glutamate) into the synaptic cleft causes a larger postsynaptic response, enhancing the organism’s reaction to the stimulus. Short-Term Sensitization: This process happens quickly and lasts for minutes to hours, depending on the intensity of the stimulus. The changes are temporary and involve the modulation of neurotransmitter release. Long-Term Sensitization: With repeated or prolonged sensitization, structural changes occur at the synapse, including the formation of new synaptic connections. This leads to a more permanent increase in the strength of the response, much like what happens in long- term potentiation (LTP).  Amnesia Anterograde Amnesia Inability to form new memories after the onset of amnesia. People with anterograde amnesia can remember events and knowledge from before the brain injury or trauma but struggle to retain new information. Causes: Damage to the hippocampus or nearby structures (e.g., medial temporal lobes), which are crucial for converting short-term memory into long-term memory. Conditions such as Korsakoff’s syndrome (often caused by chronic alcohol abuse and thiamine deficiency), Alzheimer's disease, or traumatic brain injury (TBI). Surgical interventions like removal of parts of the hippocampus to treat epilepsy (e.g., the famous case of Patient H.M.). Hippocampus: Critical for encoding new declarative (explicit) memories. Medial Temporal Lobe: Involved in memory consolidation. Mammillary Bodies and Thalamus: Damage here can also cause anterograde amnesia, often linked to Korsakoff’s syndrome. Retrograde Amnesia Loss of memory for events that occurred before the onset of amnesia. People with retrograde amnesia can form new memories, but they may be unable to recall personal experiences or knowledge from before their brain injury or trauma. Causes: Traumatic brain injury (TBI) due to accidents, falls, or blows to the head. Stroke, tumors, or brain infections. Progressive neurological conditions like Alzheimer's disease. Electroconvulsive therapy (ECT) can cause temporary retrograde amnesia in some patients. Cortex: Particularly the temporal and frontal lobes, where long-term memories are stored. Hippocampus: While retrograde amnesia often spares the hippocampus, its connections to other brain areas, like the prefrontal cortex, may be affected. Thalamus: Involved in memory retrieval. Type Definition Cause Example Damage to Inability to form new Forgetting events after Anterograde Amnesia hippocampus or medial memories a brain injury temporal lobes Head trauma, stroke, or Forgetting personal Retrograde Amnesia Loss of past memories neurodegenerative history after an diseases accident Both retrograde and Transient ischemic Temporary memory Global Amnesia anterograde memory attack (TIA) or mild confusion loss stroke Forgetting events Post-Traumatic Memory loss after Physical injury to the surrounding an Amnesia brain trauma brain accident Inability to recall Not remembering Normal developmental Infantile Amnesia memories from early events from before age process childhood 3 Forgetting a traumatic Memory loss due to Psychological stress or Dissociative Amnesia event, such as an psychological trauma trauma assault  Korsakoff’s Syndrome Brain damage caused by prolonged thiamine (vitamin B1) deficiency – Impedes brain’s ability to metabolize glucose – Leads to a loss of or shrinkage of neurons in the brain Often due to chronic alcoholism Distinctive symptom: confabulation (taking guesses to fill in gaps in memory) – Also apathy, confusion, and memory loss © 2019 Cengage. All rights reserved.  Alzheimer’s Disease Associated with a gradually progressive loss of memory, often occurring in old age – Affects 50 percent of people over 85 and 5 percent of people 65–74 – Early onset seems to be influenced by genes  99 percent of cases are late onset No drug is currently effective Alzheimer’s disease is associated with an accumulation and clumping of the following brain proteins: – Amyloid beta protein  Creates plaques from damaged axons and dendrites and decreases plasticity – An abnormal form of the tau protein  Creates tangles  Part of the intracellular support system of neurons © 2019 Cengage. All rights reserved. Brain Atrophy in Alzheimer’s Disease © 2019 Cengage. All rights reserved. Cerebral Cortex of an Alzheimer’s Patient © 2019 Cengage. All rights reserved. INTELLIGENCE © 2019 Cengage. All rights reserved.  Intelligence refers to the ability to acquire, process, and apply knowledge and skills to solve problems, adapt to new situations, and learn from experiences. In biopsychology, intelligence is explored through the interaction of biological structures (such as the brain and nervous system) and psychological processes (like cognition, memory, and problem- solving).  Types of Intelligence General Intelligence (g-factor): Proposed by Charles Spearman, the g-factor refers to a general cognitive ability that underlies performance in a variety of intellectual tasks. This theory suggests that individuals who perform well in one cognitive domain (e.g., mathematical reasoning) tend to perform well in others (e.g., verbal ability), suggesting a common underlying capacity. Multiple Intelligences: Howard Gardner’s Theory of Multiple Intelligences proposes that intelligence is not a single general ability but rather consists of distinct types: 1. Linguistic: Ability to use language effectively. 2. Logical-Mathematical: Ability to reason and solve mathematical problems. 3. Spatial: Ability to visualize and manipulate objects. 4. Musical: Sensitivity to sounds, rhythms, and music. 5. Bodily-Kinesthetic: Control of bodily motions and handling objects skillfully. 6. Interpersonal: Ability to understand and interact with others. 7. Intrapersonal: Self-awareness and self-regulation. 8. Naturalistic: Understanding of nature and the environment. Triarchic Theory of Intelligence: Proposed by Robert Sternberg, this theory breaks intelligence into three parts: 1. Analytical Intelligence: Problem-solving and logical reasoning (similar to the g- factor). 2. Creative Intelligence: Ability to generate novel ideas and think outside the box. 3. Practical Intelligence: "Street smarts" or the ability to adapt to everyday challenges. Prefrontal Cortex: PFC is crucial for executive functions, such as planning, decision- making, working memory, and problem-solving. It's often referred to as the "seat of intelligence" due to its involvement in integrating information and controlling complex behaviors. Dorsolateral Prefrontal Cortex: Associated with working memory, cognitive flexibility, and abstract thinking. Ventromedial Prefrontal Cortex: Involved in decision-making, especially in emotional and social contexts.Parietal Lobes: The parietal lobes play a key role in spatial reasoning and manipulating information. The parieto-frontal integration theory (P-FIT) suggests that intelligence results from efficient communication between the frontal and parietal regions, integrating sensory and cognitive information for problem-solving. Temporal Lobes: The temporal lobes, particularly the left hemisphere, are involved in verbal intelligence, language processing, and memory. The right hemisphere contributes to nonverbal, visual-spatial intelligence. Hippocampus: The hippocampus, important for forming and retrieving long-term memories, plays a critical role in learning and integrating new information, supporting the development of intellectual skills over time. Cerebellum: Although traditionally associated with motor functions, the cerebellum also contributes to cognitive processes, particularly attention, and the coordination of complex tasks. Recent research shows that it may play a role in various cognitive functions, including working memory and executive functioning. Neural Efficiency and Intelligence Neural efficiency hypothesis suggests that people with higher intelligence may use their brains more efficiently. Faster Neural Processing: People with higher IQ scores often show more efficient neural activity, especially in the frontal and parietal regions. They may use fewer neural resources to solve complex problems, indicating more efficient information processing. White Matter Integrity: White matter is composed of myelinated nerve fibers that facilitate communication between different brain regions. Higher intelligence has been linked to greater white matter integrity, which allows faster and more efficient neural signaling. Intelligence and Neurotransmitters Dopamine: Dopamine is essential for working memory, attention, and executive functioning. The dopaminergic system, particularly in the prefrontal cortex and striatum, is involved in the reward-based learning processes that underlie problem- solving and decision-making Glutamate: The primary excitatory neurotransmitter, glutamate is crucial for synaptic plasticity (the brain’s ability to form and strengthen connections) and learning. Long- term potentiation (LTP), a process involved in forming long-term memories, relies heavily on glutamatergic signaling. Acetylcholine: This neurotransmitter supports attention and memory, particularly in the hippocampus. It is essential for learning and neuroplasticity, playing a role in both cognitive development and maintaining cognitive function. https://forms.office.com/r/1j0TmDSHPn