Sensory Input and Neural Processing

Sensory Input and Processing

• Sensory systems mediate four attributes of sensory input: modality (type of stimulus), intensity (encoded by action potential rate), location (spatial arrangement of receptors), and duration (how long receptors respond).
• Lateral inhibition sharpens sensory perception by suppressing signals from neighboring neurons, enhancing contrast at stimulus boundaries.
• Slowly adapting receptors respond continuously to a sustained stimulus, unlike rapidly adapting receptors which respond only to stimulus changes.
• Rapidly adapting receptors detect motion or vibration, whereas slowly adapting receptors can respond to pressure sensitivity
• Pacinian corpuscles' layered, onion-like structure filters sustained pressure, responding only to rapid changes, making them mechanically sensitive to vibrations.
• Neural tuning curves based on spike frequency can be ambiguous because a single neuron's spike rate may respond similarly to different stimuli.
• Broad tuning curve describes a neuron responding to a wide range of stimuli, opposed to a narrow tuning curve which responds to a selected stimulus feature
• Temporal coding describes a stimulus, capturing spike timing, which conveys additional information about stimulus features like frequency and phase.
• Population coding reduces the ambiguity of a rate-coded signal, as multiple neurons encode a stimulus collectively, increasing precision.
• Color perception arises from three types of cone cells detecting different wavelengths (trichromatic theory) and opposing responses between cones (opponent process theory).
• Sparse coding involves activating a small subset of neurons to represent complex stimuli, as seen in the visual cortex with neurons responding to highly distinct features.

Central Pattern Generators (CPGs)

• Reciprocal reflexes depend on sensory feedback loops, unlike central pattern generators (CPGs) which can produce rhythmic activity without sensory input.
• Fictive motor pattern describes the recording of a motor pattern in isolated nervous systems, absent muscle contractions.
• Deinactivation of Na+ channels refers to the recovery of Na+ channels from an inactivated state, enabling future action potentials.
• Burst firing relies on persistent Na+ currents along with Ca2+-dependent K+ currents.
• AB-PD neurons of the pyloric circuit connectome of the stomatogastric ganglion (STG) are the pacemaker kernel because they generate the fundamental rhythm of the circuit.
• Inhibitory connections between neurons in a circuit can lead to rhythmic excitatory behavior through reciprocal inhibition, creating alternating phases of excitation and inhibition.
• AB-PD neurons set the pyloric rhythm, while LP and PY neurons follow with phase delays to maintain coordination.
• Rhythmic patterns parameters are period (time for one full cycle), burst duration (active phase length), delay (latency between bursts), duty cycle (burst duration/total period), and phase (timing of burst relative to the cycle).
• The delay between bursts must scale with the cycle period to maintain the same phase relationships between two neurons connected with inhibitory synapses.
• Synaptic plasticity and intrinsic conductance changes are the 2 cellular mechanisms that account for the maintenance of phase when the period changes in the pyloric circuit of the STG
• Alternating contractions of muscles on opposite sides of the body mediate lamprey swimming behavior
• I neurons inhibit contralateral motor output, while E neurons excite ipsilateral motor neurons, sustaining bursts during rhythmic lamprey swimming
• Conductances that underlie the oscillatory behavior of excitatory interneurons in lamprey swimming are persistent Na+ and Ca2+ currents driving depolarization, and Ca2+-dependent K+ channels contributing to hyperpolarization.
• Removing sensory input alters the rhythmic pattern of motor pattern generation in leech swimming and locust flight.
• Neuromodulators influence CPG activity by modifying ion channel conductance, which alters neuronal excitability and network dynamics.
• Neuromodulation can reconfigure CPG circuits by altering the frequency and phase of rhythmic patterns, changing swimming frequency, or shifting in response to neuromodulatory inputs.
• Electrical synapses provide fast coupling between neurons, ensuring synchronized activity, unlike chemical synapses which rely on neurotransmitter release.

Synaptic Plasticity and Learning

• Synaptic plasticity involves changes in synaptic strength, underlying learning and memory by strengthening or weakening neural connections based on experience.
• The two main types of synaptic plasticity are short-term (temporary changes) and long-term (persistent changes).
• Long-term potentiation (LTP) involves a lasting increase in synaptic strength following high-frequency stimulation, requiring NMDA receptor activation and Ca²⁺ influx, which increases AMPA receptor insertion.
• Long-term depression (LTD) describes a lasting decrease in synaptic strength after low-frequency stimulation, also involving NMDA receptors but with a lower Ca²⁺ influx, leading to AMPA receptor removal.
• Blocking NMDA receptors prevents LTP and impairs learning, while mutant mice with enhanced LTP show improved memory performance, supporting its role in memory formation.
• Strong stimulation leads to spine enlargement and stabilization, while weak activity causes spine shrinkage or elimination.
• Homeostatic plasticity refers to a mechanism that maintains network stability by adjusting synaptic strength, preventing runaway excitation or excessive inhibition.

Neural Circuits of Learning and Memory

• The hippocampus helps to organize and consolidate episodic and spatial memories before transferring them to the cortex,
• Declarative memory involves facts and events, and relies on the hippocampus whereas procedural memory relies on the striatum and cerebellum, and entails skills and habits.
• The striatum plays a key role in procedural learning and habit formation, whereas the prefrontal cortex contributes to goal-directed behavior.
• The amygdala is critical for emotional learning, especially fear conditioning, and modulates memory consolidation based on emotional significance.
• The prefrontal cortex influences working memory by maintaining and manipulating information over short timescales, supporting executive functions.

Neuromodulation and Behavior

• Neuromodulators regulate neuronal excitability and synaptic strength, with widespread and long-lasting effects, unlike fast synaptic transmission.
• Dopamine release in the ventral striatum helps to reinforce rewarding behaviors, while dopaminergic prediction error signals help update expectations in reward learning.
• Serotonin regulates mood, impulsivity, and appetite; deficits are linked to depression and anxiety disorders.
• The noradrenergic system enhances arousal, attention, and stress responses, releasing norepinephrine in response to novel or threatening stimuli.
• Acetylcholine facilitates cortical plasticity and sensory processing, enhancing focus and information encoding

Sleep and Neural Rhythms

• NREM sleep is important for memory consolidation and synaptic homeostasis, while REM sleep is involved in emotional memory processing and creativity.
• The suprachiasmatic nucleus (SCN) acts as the brain’s circadian clock, whereas the reticular activating system modulates transitions between sleep and wakefulness.
• Sleep deprivation impairs attention, working memory, and emotional regulation, and reduces LTP and neuroplasticity.

Disorders of the Nervous System

• Alzheimer’s disease is characterized by amyloid-beta plaques and tau tangles, Parkinson’s disease is caused by dopaminergic neuron loss, and ALS involves motor neuron degeneration leading to paralysis.
• Depression is linked to dysregulated monoamine neurotransmitters, and treatments include SSRIs, cognitive-behavioral therapy, and deep brain stimulation.
• Epilepsy results from hyperexcitable neuronal networks and excessive synchronized firing, and treatments involve anticonvulsants and surgical intervention.
• Microglia act as immune cells in the CNS, and their chronic activation is implicated in neurodegenerative diseases.

Synaptic Changes in LTP and LTD

• Activity dependent potentiation (ADP) and persistent firing sustains neural activity in the prefrontal cortex.
• Voltage-Gated Ca2+ and calcium-activated nonselective cation (CAN) channels are essential for persistent neural activity.
• Disinhibition in persistent activity removes inhibition to sustain activity.
• The hippocampus contains CA1, CA3, and dentate gyrus neurons.
• Both direct and indirect inputs to CA1 contribute to memory formation.
• Pathway lesions disrupt different memory types.
• Different mechanisms exist in hippocampal synapses, in relation to forms of long-term potentiation (LTP).
• Experimental studies support different long-term potentiation (LTP) mechanisms.
• Mossy Fiber long-term potentiation (LTP) is nonassociative and independent of presynaptic coincidence.
• Mossy Fiber long-term potentiation (LTP) in Aplysia exhibits similarities in synaptic plasticity.
• Schaffer Collateral LTP is associative and requires presynaptic and postsynaptic activity.
• Long-term potentiation (LTP) Induction differs from expression due to different molecular mechanisms.
• NMDA, Mg2+, CA2+, CaMKII, PKC, and Fyn contribute to LTP.
• Silent synapses can be activated via long-term potentiation (LTP).
• Long-term potentiation (LTP) in CA1 shows cooperativity, associativity, and specificity.
• Late long-term potentiation (LTP) phases are necessary for long-term maintenance, and are governed by different mechanisms.
• Protein synthesis is required in Late long-term potentiation (LTP) for the long-term maintenance.
• Quantal Analysis of long-term potentiation (LTP) reveals presynaptic and postsynaptic changes.
• Ca2+/calmodulin, cAMP, PKA, MAP kinase, and CREB-1, are signaling pathways involved in long-term potentiation (LTP).
• The Morris Water Maze is a test of hippocampal-dependent spatial memory.
• Long-term potentiation (LTP) and learning is enhanced by NR2B Subunit Overexpression.
• The hippocampus, amygdala, and synaptic plasticity play key roles in neural pathways involved in fear learning.

Spatial Navigation and Neural Representation

• Direct entorhinal cortex input is the likely source of place cell information.
• Grid cells encode spatial locations in a regular pattern, whereas place cells encode spatial locations.
• Grid cell firing patterns feature hexagonal spatial tuning.
• Dead reckoning and tessellation refers to path integration mechanisms.
• Grid cells of function irrespective of environmental limits, in their boundary independence.
• Allothetic and idiothetic cues refer to external and self-motion cues, respectively.
• Distributed grid cell phases describes Spatial encoding across neurons.
• Grid Cell Organization in medial entorhinal cortex (MEC) offers different spatial scales in relation to MEC position.
• Integrating grid cell inputs is the mechanism of Place Cell Formation.
• Head direction cells represent orientation.
• Conditional grid cells encode orientation-direction conjunctions.
• Border cells encode environmental boundaries.
• Input from grid cells to place cell modulate grid activity.
• The default Role of medial entorhinal cortex (MEC) cells is head direction tuning.
• Grid cells in humans have been demonstrated via fMRI (functional magnetic resonance imaging) and single-unit recordings.
• Synaptic Modifications enable complex representations, during memory storage.

Active Sensing and Reafference

• Active senses require motor control, whereas passive senses do not.
• Active sensing refers to actively generating sensory input.
• Reafference refers to self-generated stimuli, whereas exafference refers to external stimuli.
• Efference copy refers to internal motor predictions, whereas corollary discharge refers to sensory gating.
• Efference copy arises from motor commands.
• Corollary Discharge suppresses self-generated sensory noise.
• Saccadic Suppression of Blur happens via preventing motion blur during eye movements.
• Neural Circuit of Saccadic Suppression involves the superior colliculus and thalamic inhibition.
• Curare works by blocking neuromuscular transmission.
• Curarization in Electric Fish isolates motor command effects.
• Electric fish possess two electroreceptive cell types.
• Reafference Comparator is for function of differentiating self-generated and external signals.
• Electric fish possess a Reafference Comparator.
• Efference Copy Plasticity Timescales adjust over different periods.
• Plasticity in Electric Fish adapts as they respond to motor output changes.
• Efference Copy depends more on motor patterns than afferent feedback.