Hippocampus Function and Memory Encoding

Part of the brain involved in spatial memory, learning, and novelty detection, commonly studied in rodents.

The most prominent layer in the hippocampus, characterized by its arrangement of pyramidal neurons.

The axons of the granule cells in the dentate gyrus, which project into the CA3 region of the hippocampus.

A region within the hippocampus that receives mossy fibers from the dentate gyrus.

A region within the hippocampus known for its smaller, less complex neurons.

The primary cell type within the dentate gyrus, characterized by their simple, monopolar structure.

The axons of granule cells in the dentate gyrus, extending perpendicular to the layer towards CA3 neurons.

A brain region highly susceptible to seizures due to its unique neuronal composition and activity patterns.

Neurons in a specific brain area fire together in a synchronized pattern, contributing to the spread of seizure activity.

The ability of neurons to fire action potentials more easily, contributing to the increased excitability seen in seizures.

A type of seizure confined to a specific area of the brain, often involving complex and unusual behaviors.

A type of seizure that starts in one area and spreads to other regions, often causing uncontrolled muscle contractions.

The brief, sharp waveforms observed in an EEG during the period between seizures, indicative of an increased likelihood of seizure occurrence.

A brief period of depolarization in a neuron that precedes the occurrence of a seizure, detected using intracellular recordings.

A brain region crucial for encoding new memories and consolidating existing ones.

A neurodegenerative disease that affects memory formation and retrieval, often with prominent involvement of the hippocampus and entorhinal cortex.

A mental disorder characterized by cognitive and emotional disturbances, with evidence suggesting a connection to hippocampal dysfunction.

A type of memory that encodes specific personal experiences and events, including the context in which they happened. These memories are often vivid and detailed, and they can be triggered by sensory cues like smells or sounds.

A brain structure critically involved in encoding new memories. These memories can include personal experiences, facts, and skills. It helps make connections between different parts of a memory to create a coherent whole.

This mechanism within the hippocampus allows for the strengthening of connections between neurons that represent different parts of the same memory. This process is essential for recalling the entire memory when only some parts are presented.

A mechanism used by the hippocampus to encode sequences of events, such as the order in which things happened. It establishes directional links between neurons that represent different events, preserving the chronology of experiences.

A structure in the hippocampus that plays a role in autoassociation by strengthening connections between neurons representing different parts of the same memory. This is useful for consolidating and retrieving memories.

The dendrites that extend longer than basal dendrites. They travel through the stratum radiatum, lucidum, and lacunosum-molecular.

Shorter dendrites that originate from the base of the pyramidal neuron. They project into the stratum oriens.

A type of neural pathway that connects the hippocampus to other brain structures. This pathway is responsible for the transmission of information between different areas of the brain.

The primary way in which information is received by pyramidal neurons. These are the inputs that influence the neuron's activity.

A type of inhibitory signal that follows an excitatory postsynaptic potential (EPSP). It's mediated by interneurons releasing GABA, which binds to GABA receptors on the post-synaptic neuron.

A type of inhibition where an interneuron is activated by the same input that excites the target neuron. This helps to reduce the effect of excitation and fine-tune neuronal activity.

A type of neuron that can respond specifically to stimuli that occur at the same time. This allows the neuron to selectively filter information and transmit only relevant signals.

The inherent electrical characteristics and behavior of a neuron, independent of external inputs. These properties determine how a neuron responds to stimuli.

The electrical activity recorded outside of a neuron. These signals reflect the collective activity of many neurons in a specific brain region.

CA3 neurons within the same septo-temporal level have reciprocal connections, leading to mutual excitation. This creates a positive feedback loop that can make CA3 neurons highly excitable, potentially leading to seizures.

Axons from CA3 pyramidal neurons project to CA1 neurons through a pathway known as the Schaffer Collateral Pathway. These synapses demonstrate remarkable plasticity, making them a key area of study in the brain.

CA3 has five main types of GABAergic interneurons: Basket Cells, Axo-Axonic Cells, Bistratified Cells, Oriens-Lacunosum Moleculare Cells, and Trilaminar Cells. These interneurons work to regulate the activity of CA3 pyramidal neurons, playing a crucial role in the hippocampal circuitry.

Some interneurons in CA3 are connected by dendritic gap junctions, which synchronize their activity. This synchronized activity allows for synchronized inhibition of pyramidal cells within CA3.

CA3 neurons also send reciprocal projections to CA3 neurons in the contralateral hemisphere, known as commissural projections. These projections link the two sides of the brain, allowing for communication between the hemispheres.

The hippocampus is particularly susceptible to neurological diseases like epilepsy, Alzheimer's disease, and Schizophrenia. This vulnerability is likely related to the hippocampus's high excitability and the role it plays in memory formation.

The hippocampus is highly excitable, meaning it can easily become overactive. This can lead to uncontrolled excitation that spreads to other brain regions, potentially triggering seizures. The CA3 region is particularly vulnerable to overexcitation due to its recurrent circuitry and tendency for neurons to fire in bursts.

Over-stimulation of NMDA receptors in the hippocampus can cause an excessive increase in intracellular calcium levels. This can trigger cell death through necrosis and apoptosis.

The hippocampus's ability to rapidly encode new information comes at a cost. Its high excitability and sensitivity make it prone to disease and dysfunction.

The hippocampus is involved in the formation of episodic memories, which are memories of specific events and experiences. It integrates information from different brain regions to create a coherent representation of an event.

A type of short-term synaptic plasticity where the strength of a synapse increases for a short time after high-frequency stimulation.

A long-lasting increase in the strength of a synapse, induced by high-frequency stimulation.

A long-lasting decrease in the strength of a synapse, induced by low-frequency stimulation.

A property of LTP where only the activated pathways are strengthened.

A property of LTP where coordinated activation of both the presynaptic and postsynaptic neurons is required for its induction.

The ability of the nervous system to change in response to experience, including learning and memory.

The cellular correlate of learning and memory, involving long-lasting changes in synaptic strength.

The activation of a previously inactive synapse, contributing to the early phases of LTP.

The process of maintaining LTP, involving changes in gene expression and protein synthesis.

A type of LTP that is specific to the activated synapses.

A type of LTP that affects nearby synapses on the same dendrite.

The coordinated activation of both synapses is required for this type of heterosynaptic LTP.

The process of increasing the sensitivity of the postsynaptic neuron to glutamate, often through increasing the number or sensitivity of glutamate receptors.

The insertion of new receptors into the postsynaptic membrane, contributing to the increased sensitivity of the postsynaptic neuron to glutamate.

The process of decreasing the number or sensitivity of AMPA receptors, contributing to LTD.

Two different inputs must be activated together, within a short time frame, to induce long-term potentiation (LTP). This means that the neurons involved must be firing simultaneously or in close succession.

A single, weak stimulus to a pathway is insufficient to induce LTP. The stimulus must be strong enough to surpass a threshold to trigger this long-lasting strengthening of the synapse.

LTP is specific to the pathway that has been stimulated. So if one pathway is activated, only that pathway will show changes in synaptic strength.

LTP requires simultaneous activation of the presynaptic and postsynaptic neuron. This means the neuron sending the signal (presynaptic) and the neuron receiving the signal (postsynaptic) must both be active at the same time.

LTP is thought to be the biological basis of learning and memory, particularly the process of associating separate events or stimuli.

LTD and LTP are complementary processes that reversibly affect synaptic strength at the same location. This means that they both act on the same synapse, one strengthening it (LTP), the other weakening it (LTD).

The mechanisms underlying LTP involve complex interactions between neurons and their receptors. Understanding these mechanisms can help explain why LTP exhibits characteristics like cooperativity.

NMDA receptors are critical for LTP induction. Drugs that block NMDA receptors prevent LTP, suggesting that these receptors play a key role in strengthening synapses.

A specific type of learning where animals learn to avoid a harmful environment or stimulus, often studied using a shock-avoidance paradigm. This learning process is known to rely on the strengthening of synapses in the hippocampus.

A type of experimental procedure where animals are trained to find a hidden platform in a pool of water, often using spatial cues. This task tests the animal's ability to form and retrieve memories about the platform's location. Lesions in the hippocampus impair performance on this task.

An antagonist of the NMDA receptor, a type of glutamate receptor crucial for LTP. Injecting AP5 into the brain blocks LTP induction, impairing the animal's ability to form new memories in the water maze.

A type of protein kinase that is essential for LTP induction. Genetic mutations in CaMKII disrupt LTP and impair memory formation in the water maze. However, these mice also have problems with swimming to a visible platform, indicating other impairments outside of hippocampal function.

A learning paradigm where rodents learn to avoid a specific chamber associated with an unpleasant experience, usually a foot shock. It's used to study memory formation and the role of synaptic plasticity.

A process where altering the strength of synaptic connections induced by a previous learning experience modifies the memory of that experience. It demonstrates that synaptic plasticity plays a crucial role in memory modulation.

The ability to detect changes in synaptic efficacy (LTP) after a memorable event occurs. It suggests that LTP should be detectable as a result of a learning experience.

The process of artificially inducing synaptic weight changes to create a memory for an event that did not actually happen. This suggests that changes in synaptic connections can directly contribute to memory formation.

The prevention of LTP before or during a learning experience, leading to impaired memory of that experience. This demonstrates the importance of LTP in the formation of memory.

A brain region with 6 layers involved in higher cognitive functions like perception, learning, and intelligence.

A surgical procedure used to treat epilepsy by destroying neurons in specific brain areas, but first stimulating them to test function and avoid vital areas.

Brain regions that process and integrate information from primary sensory and motor areas, responsible for complex cognitive functions like planning and decision making.

The most prominent layer in the neocortex, characterized by large pyramidal neurons, critical for long-range communication.

A region in the frontal lobe responsible for high-level cognitive functions like planning, working memory, and decision making.

A type of Nissl stain used to visualize neurons in the brain, enabling the identification of different areas based on their cellular architecture.

A method of mapping the brain's functional areas based on the unique arrangement of neuronal cell populations.

The prefrontal cortex, a brain region involved in complex cognitive functions, undergoes a gradual decline in size, volume, and cell density with age. This process contributes to age-related cognitive changes.

The orbitofrontal lobotomy, a surgical procedure that severs connections of the prefrontal cortex, can drastically alter personality and behavior. It was once used for treating severe mental illnesses, but is now considered unethical.

The prefrontal cortex plays a crucial role in working memory, the ability to hold information in mind for a short period of time. Different regions of the PFC may be specialized for different types of working memory.

The dorsolateral prefrontal cortex (dlPFC) is involved in spatial working memory, the ability to remember the location of objects in space. This region shows persistent activity during delays in spatial tasks.

The domain specificity theory suggests that different regions of the prefrontal cortex are specialized for different types of cognitive tasks, including working memory.

The ability of a neuron to maintain its activity over time during a delay period in a working memory task is influenced by its biophysical properties, including its ability to fire continuously and its synaptic connections.

Different parts of the prefrontal cortex are interconnected, forming complex neural circuits. These connections facilitate information flow and allow for coordinated activity between different regions.

Phineas Gage provided one of the first insights into prefrontal cortex function, demonstrating that damage to this region can significantly affect personality and behavior. The famous case of Phineas Gage showed that the prefrontal cortex plays a role in social behavior, emotional regulation, and decision-making.

The six distinct layers within the neocortex, each with a unique cell structure and function.

The principle cells of the neocortex, responsible for transmitting information.

Large, pyramid-shaped neurons, the major output cells of the neocortex.

The vertical columns of neurons within the neocortex, each processing a specific type of information.

The idea that the brain uses repeated, functional columns to process information. Each column is responsible for a small range of stimuli.

Areas such as face and object recognition, which process complex, related sensory information, may also have columnar organization.

Persistent neuronal activity refers to the ability of a neuron to maintain its activity over time, even after the stimulus has ceased.

Distinct areas within the prefrontal cortex (PFC) may have different "memory directions," explaining how PFC neurons can sustain stimulus-selective activity.

GABAergic neurons are a diverse group of inhibitory neurons found in the neocortex, making up about 20% of its local neurons. These neurons release GABA, a neurotransmitter that inhibits the activity of other neurons. They are important for regulating neuronal activity and maintaining a balance between excitation and inhibition in the cortex.

The neocortex has a consistent organizational pattern, with distinct layers and connections. This 'canonical organization' applies to all areas of the neocortex, with variations based on specific functions. It allows the neocortex to process information efficiently.

Inputs to the neocortex come from various sources, including sensory organs and other brain regions. These inputs arrive at specific layers, triggering neural activity that is further processed within the cortex.

Outputs from the neocortex, known as efferents, transmit processed information to other brain regions or even back to sensory organs. This communication allows for integration, control, and coordination of various brain functions.

Feedback and recurrent excitation between principal cells create a dynamic loop of activity in the neocortex. This loop allows the cortex to amplify and sustain information processing, enhancing learning and decision-making.

Inhibitory neurons in the neocortex play a crucial role in regulating the activity of principal cells, controlling the flow of information. They target different parts of the principal cells, influencing their activity and shaping the overall cortical response.

Inputs from various sources, not just principal cells, can activate both principal cells and interneurons, allowing for a more sophisticated level of information processing within the neocortex.

The thalamus plays a key role in relaying sensory information from the body to the neocortex. This information primarily arrives at layer 4 of the cortex, triggering a cascade of processing through different cortical layers.

The neocortex has a columnar structure, with distinct columns of neurons that process information related to a specific sensory input. This structure enhances the organization and efficiency of sensory processing.

Sensory information is processed hierarchically in the cortex, with simpler features being integrated into more complex representations at subsequent stages. This allows for the extraction of increasingly detailed and meaningful information.

The amygdala is a brain structure that plays a crucial role in processing and responding to emotions, particularly fear and threat. It's also involved in emotional learning and memory, assigning emotional value to sensory information and triggering adaptive responses.

The amygdala receives sensory information from all systems about the external world to assess potential threats. This information processing helps trigger appropriate responses to danger.

The central nucleus of the amygdala (CeA) plays a key role in mediating emotional responses and generating physiological reactions. These responses might include physical changes such as increased heart rate or trembling.

The amygdala is involved in assigning emotional significance to incoming sensory stimuli. It determines what stimuli should be considered important and what should be ignored, influencing our attention.

The amygdala can release hormones and neuromodulators that influence cognitive processes such as attention, perception, and memory. These chemical signals modify how we process information and shape our thoughts.

The basolateral amygdala (BLA) is a crucial region within the amygdala responsible for forming emotional memories and associating stimuli with emotions. Think of it as the 'memory bank' for emotional experiences.

The majority of neurons in the BLA are principal neurons, responsible for transmitting signals within the amygdala. They are characterized by their ability to fire action potentials, forming the basis of communication within the amygdala.

The BLA also contains interneurons, a type of neuron that inhibits other neurons. Interneurons help regulate the activity of other neurons in the BLA and fine-tune emotional responses.

The activity of neurons in the BLA can be influenced by their intrinsic properties, including their ability to fire action potentials and their connections with other neurons. These properties contribute to the BLA's ability to process information and generate emotional responses.

The amygdala plays a crucial role in the development of fear responses. When we encounter a threatening situation, the amygdala triggers physiological and behavioral responses designed to protect us.

A group of interconnected brain regions found in the temporal lobe, crucial for processing emotions, especially fear and anxiety.

A distinct set of neurons within the amygdala that is involved in the processing of fear and anxiety. It receives input from the basolateral complex and projects widely to other brain regions.

A complex of interconnected nuclei within the amygdala responsible for acquiring and processing emotional information.

Involved in the processing of information about fearful stimuli.

A region within the amygdala, it receives input from the lateral nucleus and projects to the central nucleus. It plays a role in fear conditioning and anxiety.

An experimental procedure where a specific brain structure is surgically removed to study its function.

A syndrome characterized by emotional blunting, hyperorality, and increased visual exploration, often resulting from bilateral temporal lobe lesions, including the amygdala.

A type of learning where an animal learns to associate a neutral stimulus with a negative outcome, such as a shock, and subsequently avoids the stimulus.

A rare condition where a person has severe bilateral damage to the amygdala, leading to a profound loss of fear.

A group of interconnected brain structures involved in various emotional processes, including fear, anxiety, motivation, and memory.

Two main types of interneurons in the amygdala, distinguished by the neurotransmitters they express: Parvalbumin (PV+) and Somatostatin (SOM+).

PV+ interneurons receive input from the basolateral amygdala (BLA) and provide feedback inhibition to principal neurons.

SOM+ interneurons receive input from outside the amygdala and provide feedforward inhibition to principal neurons.

The external capsule is a pathway that connects the thalamus to the amygdala.

Stimulating the external capsule evokes a depolarizing EPSP followed by an IPSP in BLA neurons.

Activation of principal neurons in the BLA triggers the release of neurotransmitters, including GABA, which activates local interneurons via axon collaterals.

This results in feedback inhibition, which helps to regulate the activity of principal neurons within the BLA.

CEA is the central nucleus of the amygdala. It is mainly composed of GABAergic neurons, which release GABA as a neurotransmitter.

LA is the lateral nucleus of the amygdala.
IT is the intercalated cells of the amygdala. BA is the basolateral amygdala.

The LA projects sparsely to the CeL (central lateral) and projects more heavily to the BA, which in turn projects to the CeM (central medial) and the IT.

This indirect pathway allows LA inputs to indirectly influence CEA outputs.

Intercalated cells (IT) are a group of small GABAergic neurons found in the amygdala.

They form connections depending on their location, generating feedforward inhibition.

ICM are masses of intercalated cells that are not organized into a compact nucleus but rather in small, densely packed clusters.

The majority of intercalated cells are GABAergic, meaning they release GABA as a neurotransmitter.

These neurons have a high density of µ-opioid receptors and dopamine D1 receptors, contributing to their potent responsiveness to rewarding stimuli.

Amygdala neurons exhibit a stable, consistent firing pattern known as regular spiking, making them reliable signal processors.

Their high input resistance allows them to easily reach threshold for firing an action potential, making them highly excitable. This sensitivity is further enhanced by weak spike frequency adaptation.

The amygdala receives sensory information about both the conditioned stimulus (CS) and the unconditioned stimulus (US), enabling the formation of associations between neutral stimuli and biologically significant events.

Damage to the amygdala can significantly impair or even abolish various fear responses, including both unconditioned and conditioned reactions.

Stimulating the amygdala, either electrically or chemically, can evoke fear-related responses that mimic conditioned responses, suggesting its direct role in fear behavior.

Blocking the amygdala's function before learning prevents the acquisition of fear conditioning, highlighting its importance in forming new fear memories.

Inactivating the amygdala after learning prevents the expression of conditioned fear responses, indicating its crucial role in retrieving and expressing fear memories.

The amygdala undergoes changes during learning that strengthen the connection between the conditioned stimulus (CS) and the fear response, making the CS capable of triggering fear on its own.

When a novel stimulus is presented repeatedly, the amygdala initially responds strongly, but its activity rapidly diminishes if the stimulus is irrelevant and safe, demonstrating habituation.

The internal biological clock responsible for regulating circadian rhythms and sleep-wake cycles.

A mechanism that keeps time without relying on external cues like clocks, found in all living organisms.

These are cycles in our biological processes, such as hormone levels, body temperature, and sleep, that repeat roughly every 24 hours.

This is the process that regulates the need for sleep based on the duration and intensity of prior wakefulness.

Light exposure directly influences the SCN, resetting the circadian clock, leading to adjustments in day and night perception.

These are genes that regulate the circadian rhythm, operating through a feedback loop that takes about 24 hours to complete one cycle.

This refers to the consistent and self-sustaining rhythm of electrical activity that central clock neurons produce, independent of external factors.

Poor sleep quality or lack of sleep can have significant impacts on various aspects of our health and well-being.

A state characterized by a distinct set of physiological and neurological changes, including diminished consciousness and reduced responsiveness.

Sleep-wake cycles are controlled by two major processes: circadian rhythms and sleep homeostasis. Circadian rhythms determine the timing of sleep, while sleep homeostasis regulates the need for sleep based on how long you have been awake.

A group of neurons in the lateral hypothalamus that release the neurotransmitter orexin. These neurons are important for promoting wakefulness and suppressing REM sleep.

The orexin neurons excite neurons in the cortex, thalamus, and other brain regions that promote wakefulness. This leads to increased arousal and alertness.

The loss of orexin neurons doesn't completely eliminate sleep, but it does increase transitions between sleep stages.

This brain region is involved in promoting NREM sleep by inhibiting neurons that promote wakefulness.

These neurons, also found in the basal forebrain, release GABA, a neurotransmitter that inhibits other neurons. They contribute to the promotion of sleep by calming down the brain.

This area of the brain is involved in generating REM sleep, a stage of sleep characterized by rapid eye movements, dreaming, and muscle paralysis.

During REM sleep, the SLD nucleus inhibits motor neurons in the spinal cord. This paralysis prevents us from acting out our dreams while we're asleep.

The 'sleep switch' is a theoretical model that explains how the brain transitions between sleep and wakefulness.

The 'REM-NREM sleep flip-flop' switch is similar to the sleep-wake switch. It involves mutually inhibitory neurons that control transitions between REM and NREM sleep stages.

The 'flip-flop' switches are thought to be stabilized by orexin neurons.

These substances are presumed to directly promote sleep states and inhibit wakefulness.

It's proposed that the accumulation of adenosine during wakefulness is a primary factor in the buildup of sleep pressure.

The electroencephalogram (EEG) is the primary tool used to measure brain activity during various states of sleep and wakefulness.

A hypnogram graphically represents the different stages of sleep (NREM and REM) over time, illustrating sleep "architecture."