Nervous System Physiology PDF

—Module 1 ​ Describe the subdivisions of the nervous system ​ Central Nervous System: -​ Structurally consists if the brain and spinal cord -​ Integrates and processes nervous information -​ the brain and spinal cord are covered by protective layers called the men...

—Module 1 ​ Describe the subdivisions of the nervous system ​ Central Nervous System: -​ Structurally consists if the brain and spinal cord -​ Integrates and processes nervous information -​ the brain and spinal cord are covered by protective layers called the meninges ​ Peripheral Nervous System: -​ Structurally consists of all neural tissue found outside of the CNS -​ Carries information from the body to the CNS -​ Receives information from the CNS to cause a response in the body -​ Everything outside of the meninges is part of the PNS ​ Both the central and peripheral nervous systems have the same basic parts (neurons and glial cells) ​ Functional Divisions: -​ Two functional divisions: Motor & Sensory nervous system– both systems work together to do the following: -​ Collect information (stimuli) about the internal and external environments -​ Process information to determine a response (if needed) -​ Initiate a response based on the collected information ​ Motor (Efferent) Nervous System -​ Responsible for carrying motor information away from the CNS towards the PNS -​ Carries motor impulses from the brain or spinal cord → through nerves → muscle tissue throughout the body -​ Impulses that contribute to a movement are carried by nerves in the PNS -​ Efferent: causes muscle tissue to contract -​ Carries Somatic and Visceral information ​ Sensory (Afferent) Nervous System: -​ Responsible for collecting sensory information (called stimuli, e.g., pain) because it carries info from peripheral to central NS -​ Receptors sense stimuli, e.g., temperature or pain → stimuli is transmitted to the CNS -​ Initiates different movements (not the actual movement) -​ Afferent: Pain, touch, temperature -​ Carries Somatic and Visceral information ​ Discuss the function of neurons & explain the importance of myelination Somatic motor fibres -  ​ carry nerve impulses to skeletal muscle which controls voluntary movements, allowing us to do things like walk, type, or move our eyes. We consciously control these muscles. Visceral motor fibres or autonomic motor fibres - ​ carry nerve impulses to both smooth and cardiac muscles, and glands which control involuntary actions, like how our stomach digests food or how our heart beats. We don't have conscious control over these functions. This system is further divided into two parts: the sympathetic and parasympathetic systems, which help regulate different organs and body functions. Excitable cells - ​ Definition: Cells capable of generating electrical activity due to ion concentration differences across the plasma membrane. ​ Examples: ○​ Nerve cells (neurons) ○​ Muscle cells: Skeletal, smooth, and cardiac ○​ Pancreatic β cells Ion Concentration Differences - ​ Ions: Charged particles (positive or negative) that create a membrane potential across the plasma membrane. ​ Key Gradients: ○​ Sodium (Na+): Higher concentration outside the cell → Wants to move into the cell. ​ Both concentration and electrical gradients attract Na+ inward. ○​ Potassium (K+): Higher concentration inside the cell → Wants to move out of the cell. ​ Concentration gradient pushes K+ out, but the electrical gradient pulls it inward. ​ At rest, the concentration gradient of K+ is stronger than the electrical gradient. Depolarization - ​ The inside of the neuron becomes less negative (or more positive) compared to its resting potential. ​ Triggered by the opening of sodium (Na+) channels → Na+ flows into the cell. Result: ​ If depolarization reaches a threshold, an action potential is generated. ​ The action potential travels down the axon, sending an electrical signal. Purpose: ​ Excitatory signals increase the likelihood of the neuron firing and transmitting a signal to other neurons. Hyperpolarization - ​ The inside of the neuron becomes more negative than its resting potential.= ​ Caused by: ○​ Opening potassium (K+) channels → K+ flows out of the cell. ○​ Opening chloride (Cl−) channels → Cl− flows into the cell. Result: ​ Neuron becomes less likely to reach the threshold for an action potential. Purpose: ​ Inhibitory signals reduce the chance of a neuron firing, helping control and limit neural activity. Key Points to Remember - ​ Both concentration gradients and electrical gradients influence ion movement: ○​ Na+ wants to enter the cell due to both gradients. ○​ K+ wants to leave the cell due to the concentration gradient but is partially held back by the electrical gradient. Importance of Myelination - ​ The process of wrapping axons in a fatty, insulating layer called the myelin sheath. ​ Formed by Schwann cells (PNS) and oligodendrocytes (CNS). Functions of Myelination: 1.​ Increases Speed of Signal Transmission: ○​ Facilitates saltatory conduction, where electrical signals "jump" between gaps in the myelin (called nodes of Ranvier). ○​ This speeds up action potentials compared to unmyelinated fibers. 2.​ Conserves Energy: ○​ Reduces the need for ion channels to work continuously along the entire axon length. 3.​ Supports Communication: ○​ Ensures rapid and efficient communication between neurons, vital for complex processes like motor control, learning, and cognition. Clinical Significance: ​ Diseases like Multiple Sclerosis (MS) involve damage to the myelin sheath, leading to slower signal transmission, muscle weakness, and impaired coordination ​ Describe the basic types of ion channels involved in neuron function Ion Channels - ​ Definition: Specialized channels in cell membranes that allow charged ions (e.g., Na+, K+) to move across the membrane. ​ Key Feature: Movement of charged ions generates an electrical current, essential for neuron signaling. ​ Ions of Interest: Sodium (Na+) and Potassium (K+) Types of Ion Channels - 1. Leak Channels ​ Function: ○​ These channels randomly alternate between open and closed positions, allowing a steady flow of ions. ​ Purpose: ○​ Maintain the resting membrane potential by permitting passive ion movement. 2. Ligand-Gated Channels ​ Function: ○​ Open or close in response to a specific chemical stimulus (ligand), such as a neurotransmitter. ​ Example: ○​ Acetylcholine binding to a receptor, causing Na+ channels to open. ​ Importance: ○​ Involved in synaptic transmission and communication between neurons.  3. Mechanically-Gated Channels ​ Function: ○​ Open or close in response to mechanical stimulation, such as: ​ Touch ​ Pressure ​ Tissue stretching ​ Vibration ​ Example: ○​ Channels in sensory receptors like those in the skin or inner ear. 4. Voltage-Gated Channels Function: ​ Open or close in response to changes in membrane potential (voltage). Example: ​ Sodium (Na+) and potassium (K+) channels involved in the generation and propagation of action potentials. Importance: ​ Critical for initiating and conducting electrical signals in neurons. ​ Discuss the importance of graded potentials & outline the events that occur in an action potential How Neurons Use Ion Flow to Transmit Information - Ion flow across the plasma membrane generates electrical currents, which neurons use to communicate information: 1.​ Graded Potentials: Communicate over short distances. 2.​ Action Potentials (APs): Communicate over long distances. ***Both processes depend on the opening and closing of gated ion channels Graded Potentials - ​ Small, localized changes in membrane potential. ​ Can be either: ○​ Depolarizing: Makes the membrane potential less negative (closer to zero). ○​ Hyperpolarizing: Makes the membrane potential more negative (further from zero). How They Work: ​ Result from the opening of ligand-gated or mechanically-gated ion channels. ​ Cause localized currents that weaken over distance. Key Characteristics - ​ Not all-or-none: Strength depends on the size of the stimulus. ​ If strong enough, they can trigger an action potential. ​ Generated by receptors responding to stimuli: ○​ Thermal (temperature changes) ○​ Chemical (e.g., neurotransmitters) ○​ Pressure (mechanical force) Importance of Graded Potentials:  ​ Initiate Action Potentials: Graded potentials provide the depolarization needed to reach the threshold for an AP. ​ Neuronal Communication: Allow neurons to pass electrical signals via neurotransmitters, starting feedback cycles for processes like homeostasis. ​ Without graded potentials, action potentials cannot occur. Action Potentials (APs) - ​ Large, rapid changes in membrane potential that communicate over long distances. ​ All-or-None: ○​ APs either occur fully (if the threshold is reached) or not at all. ○​ The amplitude (size) of the AP is always the same, regardless of the stimulus strength. Threshold - ​ To generate an AP, the membrane potential must hit a specific threshold voltage, usually around -55 mV in human nerve cells. How It’s Achieved: ○​ A graded potential depolarizes the neuron’s membrane to reach or exceed the threshold. ○​ If the threshold is reached, voltage-gated Na+ and K+ channels open, triggering the AP. What Happens During an Action Potential - 1.​ Depolarization: ○​ Voltage-gated Na+ channels open, allowing Na+ ions to flow into the cell. ○​ The membrane potential becomes more positive. 2.​ Repolarization: ○​ Voltage-gated K+ channels open, allowing K+ ions to flow out of the cell. ○​ The membrane potential returns to resting levels. 3.​ After-Hyperpolarization: ○​ The membrane potential may briefly become more negative than the resting potential before stabilizing. Propagation of Action Potentials - ​ Local Current Flow: The depolarization at one section of the axon triggers the threshold in adjacent sections, causing the AP to propagate along the axon. ​ Unidirectional Flow: The AP moves in one direction due to the refractory period of previously depolarized regions. Factors Influencing AP Velocity - Fiber Diameter: Larger diameter fibers conduct APs faster because they have lower resistance to ion flow. Myelination: Myelinated fibers are faster due to saltatory conduction (APs jump between gaps in the myelin sheath called Nodes of Ranvier).  ​ Explain the events of signal transmission at a synapse Neurons - ​ Cell Body (Soma): ○​ The control center of the neuron. ○​ Processes incoming signals and sends outgoing signals. ​ Dendrites: ○​ Branch-like projections from the cell body. ○​ Receive signals from other neurons and send them to the soma. ​ Axon: ○​ A long projection extending from the soma. ○​ Carries signals away from the cell body to other neurons, muscles, or glands. ​ Axon Hillock: ○​ The trigger zone where action potentials (APs) begin before traveling down the axon. ○​ Acts as a decision-making point: if the threshold is reached, the signal is sent. ​ Axon Terminals: ○​ The branched ends of the axon. ○​ Form connections (synapses) with other cells. The Synapse - The synapse is the functional connection between: ​ A neuron and another neuron, or ​ A neuron and an effector organ (muscle or gland). Parts of a Synapse - 1.​ Presynaptic Neuron: ○​ The neuron sending the signal. ○​ Releases neurotransmitters from its axon terminals. 2.​ Synaptic Cleft: ○​ The small gap between the presynaptic and postsynaptic cells. ○​ Neurotransmitters travel across this gap. 3.​ Postsynaptic Cell: ○​ The cell receives the signal. ○​ Contains receptors that bind to neurotransmitters. Postsynaptic Activation - ​ Signals received by the postsynaptic cell create a graded potential, which can be either:  ○​ Excitatory (EPSP): Increases the likelihood of triggering an action potential. ○​ Inhibitory (IPSP): Decreases the likelihood of triggering an action potential. How It Works: 1.​ Neurotransmitter (ligand) binds to ligand-gated ion channels on the postsynaptic cell. 2.​ Ion channels open, causing a graded potential: ○​ EPSP: Positive ions (e.g., Na⁺) flow into the cell, depolarizing the membrane. ○​ IPSP: Negative ions (e.g., Cl⁻) flow in, or positive ions (e.g., K⁺) flow out, hyperpolarizing or stabilizing the membrane. ​ Describe the action of excitatory and inhibitory neurotransmitters Excitatory (EPSP): Depolarizes the membrane, moving closer to action potential. Inhibitory (IPSP): Hyperpolarizes or stabilizes the membrane, moving away from action potential. Mechanism of Inhibitory Synapses - Ion Channel Activation: ○​ K+ Channels Open: K+ moves out → Results in IPSP. ○​ Cl⁻ Channels Open: ​ Cl⁻ moves in → IPSP. ​ Cl⁻ stabilizes the membrane potential. Purpose of Inhibitory Neurotransmitters: ○​ Regulate information flow ("volume control"). ○​ Prevent overstimulation of the nervous system Importance of Inhibitory Synapses ​ Regulatory Function: Essential for balanced neuronal activity and preventing uncontrolled excitation. Examples of Dysfunction: ○​ Tetanus Toxin: ​ Blocks release of GABA and glycine (inhibitory neurotransmitters). ​ Result: Uncontrolled muscle spasms. ○​ Strychnine: ​ Competes with glycine at postsynaptic receptor sites. ​ Blocks inhibitory signals → Overactivation of motor nerves. ​ Consequences: Convulsions, muscle spasticity, and potentially death ​ Explain the importance of presynaptic modulation Presynaptic modulation is like adjusting the volume on a speaker before the sound reaches your ears. It controls how much signal (neurotransmitter) is sent from one neuron to the next across a synapse. Why important: ​ Fine-tunes communication: It ensures the right amount of signal is sent—neither too much nor too little—so the next neuron responds appropriately. ​ Prevents overstimulation: By regulating the signal, it avoids overwhelming the nervous system with too much information.  ​ Adjusts based on needs: Factors like calcium levels, certain drugs, or diseases can influence this process, making it adaptable to the body’s needs ​ List the different ways neurotransmitters can be removed from a synapse Reuptake: ​ Neurotransmitters are taken back into the presynaptic neuron for reuse or recycling. ​ Example: Serotonin reuptake by specific transport proteins. Enzymatic Degradation: ​ Enzymes break down neurotransmitters into inactive components. ​ Example: Acetylcholine is broken down by acetylcholinesterase. Diffusion: ​ Neurotransmitters diffuse away from the synaptic cleft into surrounding areas. Uptake by Glial Cells: ​ Glial cells (e.g., astrocytes) absorb neurotransmitters to regulate their levels in the synaptic cleft. Desensitization of Receptor Endocytosis: ​ Although not directly removing neurotransmitters, receptors may become less responsive (desensitized) or internalized, reducing the effect of the neurotransmitter ​ Describe the functions of the different types of neurotransmitters General Neurotransmitter Information - ​ Definition: Neurotransmitters are chemical messengers that transmit signals across synapses from one neuron to another or to a target cell (e.g., muscle, gland). ​ Classification: ○​ Excitatory: Promote action potentials (e.g., glutamate, aspartate). ○​ Inhibitory: Suppress action potentials (e.g., GABA, glycine). ○​ Modulatory: Adjust the strength of synaptic communication (e.g., serotonin, dopamine). Neurotransmitter Systems - 1.​ Cholinergic System (Acetylcholine): ○​ Major Roles: Present in both CNS and PNS, involved in attention, learning, memory, and neuromuscular function. ○​ Synthesis: From acetyl CoA and choline, stored in vesicles. Receptors: ​ Nicotinic: Agonist is nicotine. ​ Muscarinic: Agonist is muscarine. Breakdown: ​ Short-lived response, degraded by acetylcholinesterase. Cholinergic System: ​ Releases Ach, essential for cognitive functions. ​ Alzheimer's disease: Linked to the degeneration of cholinergic neurons, leading to confusion, memory loss, and language decline. ○​ 2.​ Adrenergic System (Catecholamines):  ○​ Receptor Details: ​ Alpha Receptors (α): Vasoconstriction, pupil dilation. ​ Beta Receptors (β): Heart rate regulation, bronchodilation. ○​ Clinical Relevance: Beta-blockers target β-receptors to treat hypertension and anxiety. 3.​ Serotonergic System (Serotonin): ○​ Clinical Relevance: ​ Depression: Often treated with selective serotonin reuptake inhibitors (SSRIs) like fluoxetine. ​ Serotonin Syndrome: Overactivation of serotonin receptors, causing agitation, confusion, and sweating. 4.​ Dopaminergic System (Dopamine): ○​ Pathways: ​ Mesolimbic Pathway: Reward and addiction. ​ Nigrostriatal Pathway: Motor control (degeneration here leads to Parkinson’s). ​ Mesocortical Pathway: Cognitive functions, linked to schizophrenia. 5.​ Histaminergic System (Histamine): ○​ Clinical Relevance: ​ Antihistamines (e.g., diphenhydramine) block histamine to reduce allergies but may cause drowsiness by crossing the blood-brain barrier. 6.​ Glutamatergic System (Glutamate): ○​ Receptor Details: ​ AMPA Receptors: Fast synaptic transmission. ​ NMDA Receptors: Involved in synaptic plasticity and learning. ○​ Clinical Relevance: ​ NMDA receptor antagonists (e.g., ketamine) used in anesthesia and depression treatment. 7.​ GABAergic System (GABA): ○​ Clinical Relevance: ​ Epilepsy: Treated with GABA-enhancing drugs like benzodiazepines. ​ Alcohol withdrawal: GABA agonists may be used to prevent seizures. More on Removal of Neurotransmitters - ​ Enzymes for Breakdown: ○​ Monoamine Oxidase (MAO): Breaks down dopamine, serotonin, and norepinephrine. ○​ Catechol-O-Methyltransferase (COMT): Degrades catecholamines like dopamine and norepinephrine. ​ Reuptake Inhibitors: ○​ Drugs like SSRIs and norepinephrine reuptake inhibitors (NRIs) prevent reuptake, prolonging neurotransmitter action. Clinical Disorders Linked to Neurotransmitter Imbalances - ​ Parkinson’s Disease: Dopamine deficiency in the substantia nigra. ​ Schizophrenia: Excess dopamine in certain brain regions. ​ Anxiety Disorders: Reduced GABA activity. ​ Epilepsy: Overactivation of glutamate or underactivity of GABA. ​ Identify the regions of the brain (and their roles) involved in sleep and awakening 1. Hypothalamus ​ Key Structure: Suprachiasmatic Nucleus (SCN) ○​ Receives light exposure information from the eyes. ○​ Regulates the behavioral rhythm of the sleep/wake cycle. ○​ Damage to SCN: Leads to the inability to regulate the sleep/wake cycle. ○​ Visual Impairment: Most individuals with visual impairment can still sense light and adjust their sleep cycles to some degree. 2. Brainstem ​ Communicates with the hypothalamus to transition between wakefulness and sleep. ​ Sleep-Promoting Cells: ○​ Found in the hypothalamus and brainstem. ○​ Release GABA to reduce activity in arousal centers, promoting sleep. ​ Role in REM Sleep: ○​ The pons and medulla signal muscle relaxation, preventing the body from acting out dreams. 3. Thalamus ​ Acts as a relay station for sensory information to the cerebral cortex. ​ Activity During Sleep: ○​ Quiet during most sleep stages. ○​ Becomes active during REM sleep, sending sensory information (sights, sounds, and images) to the cortex, contributing to dreams. 4. Amygdala ​ Processes emotions and becomes highly active during REM sleep. 5. Pineal Gland ​ Receives signals from the SCN. ​ Increases melatonin production to facilitate sleep. 6. Basal Forebrain ​ Releases adenosine, which promotes the sleep drive. ​ Caffeine's Effect: ○​ Blocks adenosine receptors, reducing the sleep drive and promoting wakefulness. Key Concepts: ​ GABA: A neurotransmitter that reduces arousal and promotes sleep. ​ Melatonin: A hormone that helps regulate sleep by signaling the body to rest. ​ Adenosine: Builds up throughout the day, increasing sleep pressure; caffeine inhibits its effects. ​ REM Sleep: Critical for muscle relaxation, emotional processing, and dream activity ​ Define circadian rhythms and identify which neurotransmitters and genes play a role in regulating them Biological processes that follow a 24-hour cycle, regulating daily fluctuations in body temperature, metabolism, hormone release, and sleep/wake cycles. ○​ Control sleep timing—promote sleepiness at night and wakefulness in the morning. ○​ Synchronize with environmental cues such as light and temperature. ○​ Can persist without external cues (e.g., in darkness). Sleep-Wake Homeostasis -  ​ Function: ○​ Reminds the body to sleep after being awake for an extended period. ○​ Regulates sleep intensity. ​ Regulation: ○​ Primarily influenced by adenosine, which builds throughout the day. ​ Factors Affecting Sleep-Wake Homeostasis: ○​ Medical conditions, medications, stress, sleep environment, diet, and light exposure. Neurotransmitters and Their Roles in Sleep - ​ GABA: ○​ Released by neurons in the SCN and basal forebrain. ○​ Inhibits wakefulness-promoting cells, promoting sleep. ​ Histamine: ○​ Known as the "master wakefulness neurotransmitter." ○​ Highest levels during wakefulness, lowest during REM sleep. ○​ Antihistamines block histamine, inducing drowsiness. ​ Serotonin: ○​ Modulates SCN response to light signals from the retina. ○​ Disruptions in this pathway can contribute to Seasonal Affective Disorder (SAD). ○​ Precursor to melatonin, which promotes sleep ​ Other Key Neurotransmitters: ○​ Norepinephrine (NE): Promotes arousal and alertness. ○​ Hypocretin (Orexin): Regulates wakefulness and appetite. ○​ Acetylcholine (ACH): Active during REM sleep, supporting dreams. ○​ Glutamate: Facilitates neural communication during wakefulness. Genes Involved in Sleep and Circadian Rhythms - ​ "Clock" Genes: ○​ Examples: Per, Tim, Cry. ○​ Influence circadian rhythms and sleep timing. ​ Sleep Disorders Linked to Genes: ○​ Familial Advanced Sleep-Phase Disorder: Causes early sleep and wake times. ○​ Narcolepsy: Linked to genetic mutations affecting hypocretin. ○​ Restless Legs Syndrome: Associated with specific gene variations. ​ DEC2 Mutation: ○​ Found in "short sleepers" who function well on 4-6 hours of sleep. ○​ Enhances orexin production, promoting wakefulness ​ What genes are upregulated by sleep deprivation? ​ What genes are down regulated by sleep deprivation? ​ What causes a global 24% increase in heart attacks on one day each year? ​ How much does sleep deprivation impair the ability to learn? ​ Discuss the physiological injuries that can happen with concussion  Cause: ○​ Mechanical “shake” of the brain due to acceleration and deceleration forces. ○​ Leads to pathophysiological changes, including ionic shifts, neuronal architecture damage, increased neuroinflammation, and impaired cerebral blood flow. Ionic Shifts - ​ Initial Impact: ○​ Stretching of neuronal/axonal membranes causes unregulated ion flux. ○​ Key Ionic Changes: ​ Potassium (K⁺) exits neurons. ​ Sodium (Na⁺) and Calcium (Ca²⁺) enter neurons. ○​ Triggers voltage- and ligand-gated ion channels, leading to: ​ Widespread neuronal depression ​ Impaired debris clearance, inflammation resolution, and neuronal repair. ​ Energy Crisis: ○​ Neurons attempt to restore ionic balance via membrane ionic pumps, requiring ATP. ○​ Concussion reduces ATP production due to: ​ Mitochondrial dysfunction from excess intracellular calcium. ​ Decreased cerebral blood flow. ○​ Duration: Mismatched energy demands can persist up to 10 days or more (exact duration in humans unknown). Neuronal Architecture Damage - ​ Structural Effects: ○​ Axonal stretch and calcium influx cause: ​ Collapse of axons and microtubules. ​ Axonal swelling and disrupted cellular transport. ​ Impact on Children and Teens: ○​ Developing brains are more vulnerable due to ongoing myelination and weaker axonal microstructures. Increased Neuroinflammation - ​ Microglia Activation: ○​ Microglia (CNS immune cells) respond within 6 hours post-concussion. ○​ Release of damage-associated molecular patterns (DAMPs) elevates neuroinflammation. ​ Prolonged Elevations: ○​ Elevated levels of glutamate, glutamine, Na⁺, K⁺, and Ca²⁺: ​ Alter neuronal function. ​ Increase inflammation and damage. Excitatory Neurotransmitter Release - ​ Acute Changes Post-Concussion: ○​ Increased glutamate release affects ion channels and NMDA receptor function. ○​ Contributes to altered neuronal signaling and function. Behavioral and Functional Impairments - ​ Physical Symptoms: ○​ Headache, dizziness, nausea, vomiting, balance issues, sensitivity to light (photophobia) and sound (phonophobia).  ​ Cognitive Effects: ○​ Slowed mental processing, concentration deficits, memory impairments. ​ Emotional Changes: ○​ Irritability, anxiety, depression. ​ Fatigue and Sleep Disturbances: ○​ Increased fatigue and trouble focusing ​ Identify the possible causes of post-concussion syndrome Causes and Risk Factors of PCS - 1.​ Post-Concussive Brain Vulnerability ○​ Brain remains more vulnerable to further injury after a concussion. ○​ Second Impact Syndrome: Occurs when a second concussion is sustained before the brain has healed from the first, often leading to severe outcomes. ○​ Increased Risk: Athletes with a history of concussions are 3 times more likely to experience subsequent concussions. ○​ Symptom Severity: Increases with each additional concussion. ○​ Multiple Concussions: Raises the likelihood of developing PCS. 2.​ Autonomic Nervous System Damage ○​ Affects both sympathetic and parasympathetic systems. ○​ White matter tracts between cortical control centers and vagal nerve control are damaged. 3.​ Demographic Factors ○​ PCS occurs in 10-15% of concussive cases. ○​ More common in women, possibly due to hormonal differences or reporting patterns. Symptoms of PCS - 1.​ Cognitive and Emotional ○​ Depression. ○​ Confusion. ○​ Difficulty concentrating. 2.​ Autonomic Dysregulation ○​ Issues with cerebral blood flow regulation. ○​ Difficulty controlling blood pressure and heart rate. ○​ Orthostatic intolerance (dizziness upon standing). 3.​ Physical ○​ Headaches. ○​ Dizziness. Treatment of Concussion and PCS - 1.​ Initial Phase (24-48 hours) ○​ Physical and cognitive rest to minimize symptom exacerbation. ○​ Avoid lying in a dark room without stimulation (outdated practice). 2.​ Gradual Return to Function ○​ Light exercises like yoga or aerobic activities that do not worsen symptoms. ○​ Cognitive activities that are manageable without symptom flare-ups. ○​ Minimize screen time and avoid fluorescent lights. 3.​ Criteria for Physiological Recovery ○​ Ability to achieve maximum age-predicted heart rate.  ○​ Exercise for 20 minutes over 2-3 consecutive days without symptoms. Additional information on PCS - ​ Potential Mechanisms for PCS Symptoms ○​ Structural: Damage to axonal pathways disrupts neural communication. ○​ Biochemical: Neuroinflammation and imbalance of neurotransmitters like glutamate. ○​ Vascular: Impaired cerebral blood flow and oxygen delivery ​ Identify the two key endocannabinoids found in the body Key Endocannabinoids - 1.​ Anandamide (AEA) ○​ Known as the "bliss molecule" (from Sanskrit word ananda, meaning joy or bliss). ○​ Functions: ​ Binds primarily to CB1 receptors in the brain. ​ Involved in regulating mood, memory, appetite, and pain. ○​ Breakdown: ​ Metabolized by the enzyme FAAH (fatty acid amide hydrolase). 2.​ 2-Arachidonoylglycerol (2-AG) ○​ Most abundant endocannabinoid in the body. ○​ Functions: ​ Binds to both CB1 and CB2 receptors, with slightly greater activity at CB2. ​ Plays a critical role in regulating inflammation, pain, immune responses, and emotional balance. ○​ Breakdown: ​ Degraded by the enzyme MAGL (monoacylglycerol lipase). ​ Describe how CB1 and CB2 receptors work Endocannabinoid Receptors - ​ CB1 Receptors ○​ Location: ​ Primarily in the central nervous system (CNS), particularly in the brain regions such as the hippocampus, cerebellum, and basal ganglia. ○​ Functions: ​ Regulate cognitive processes, emotional regulation, pain perception, and motor control. ​ Involved in the psychoactive effects of THC (from cannabis). Mechanism - ​ Endocannabinoids are released by the postsynaptic cell. ​ They travel backwards (retrograde) to bind to the presynaptic cell’s CB1 receptors. ​ This suppresses the release of neurotransmitters like glutamate or GABA ​ CB2 Receptors ○​ Location: ​ Predominantly in the peripheral immune system (e.g., spleen, tonsils) and tissues involved in immune responses.  ​ Also present in smaller amounts in the brain and other tissues. ○​ Functions: ​ Modulate inflammation and immune responses. ​ Contribute to pain management. Mechanism - ​ Binds with endocannabinoids to regulate immune signaling and reduce excessive inflammation How the Endocannabinoid System Works - 1.​ Production and Release of Endocannabinoids ○​ On-Demand Production: Endocannabinoids like anandamide (AEA) and 2-AG are synthesized as needed rather than stored in vesicles (unlike other neurotransmitters). ○​ Retrograde Signaling: ​ Released by the postsynaptic neuron. ​ Travel backward to the presynaptic neuron, where they bind to CB1 or CB2 receptors. 2.​ Control of Neurotransmitter Activity ○​ Endocannabinoids act like "traffic cops," controlling the release of most neurotransmitters. ○​ Suppress excessive neurotransmitter activity, maintaining balance in the brain and body. 3.​ Breakdown of Endocannabinoids ○​ FAAH: Breaks down anandamide (AEA). ○​ MAGL: Breaks down 2-AG. ○​ Endocannabinoids are rapidly degraded after completing their function, making it challenging to determine typical concentrations in the body. Interactions with Cannabis Products - 1.​ THC (Tetrahydrocannabinol) ○​ Binding: ​ Binds to CB1 receptors in the brain, producing psychoactive effects (e.g., euphoria, altered memory, and judgment). ​ Also binds to CB2 receptors, contributing to anti-inflammatory and pain-relief effects. ○​ Persistence: FAAH cannot break down THC, leading to prolonged effects. ○​ Potential Effects: ​ Slow reaction times. ​ Memory disruption. ​ Anxiety. ​ Impaired judgment. 2.​ CBD (Cannabidiol) ○​ Binding: Does not directly bind to CB1 or CB2 receptors. ○​ Mechanism: ​ Inhibits FAAH and MAGL, increasing levels of anandamide and 2-AG. ​ Modulates the endocannabinoid system indirectly, providing anti-inflammatory and calming effects. ○​ Properties: Non-psychoactive, meaning it does not produce a "high."  ​ Explain the functional significance of the autonomic nervous system / Compare the major responses of the body to stimulation of the parasympathetic and sympathetic branches of the ANS Overview of the Autonomic Nervous System (ANS) - ​ The ANS is responsible for involuntary physiological functions, influencing smooth muscle, glands, and the heart. ​ It plays a critical role in maintaining homeostasis by regulating internal organs without conscious effort. ​ The ANS is divided into two primary subdivisions: 1.​ Sympathetic Nervous System (SNS) – "Fight or Flight" response. 2.​ Parasympathetic Nervous System (PNS) – "Rest and Digest" response. Functions of the ANS - The ANS regulates vital physiological functions, including: ​ Homeostasis: Balances bodily functions to maintain a stable internal environment. ​ Stress Response: SNS activation increases heart rate, dilates pupils, and redirects blood flow to muscles during emergencies. ​ Reproduction: Controls sexual arousal and other reproductive processes. ​ Thermoregulation: Regulates sweating and blood vessel dilation/constriction to control body temperature. ​ Enteric System (Digestion): Regulates peristalsis, enzyme secretion, and nutrient absorption in the gastrointestinal tract. Dysautonomia: Dysfunction of the ANS - ​ Definition: Dysautonomia refers to an abnormal function of the ANS, leading to inappropriate SNS or PNS responses based on environmental or bodily conditions. ​ Causes: ○​ Neurological conditions: Multiple Sclerosis (MS), Parkinson’s disease, Guillain-Barré syndrome. ○​ Chronic illnesses: Diabetes, HIV, Lyme disease. ○​ Trauma: Concussions, spinal cord injury, stroke. ○​ Substance-related: Alcoholism. Signs and Symptoms of Dysautonomia - Individuals with dysautonomia may experience a wide range of symptoms, including: ​ Neurological & Cognitive Issues: Brain fog, double vision, tunnel vision. ​ Cardiovascular Dysregulation: Low or high blood pressure, tachycardia (rapid heart rate), dizziness, vertigo. ​ Gastrointestinal Dysfunction: Constipation, bowel incontinence. ​ Fatigue & Weakness: Chronic fatigue, muscle weakness, exercise intolerance. ​ Other Autonomic Disturbances: Insomnia, anxiety, temperature regulation issues ​ Outline the components of an autonomic pathway The ANS controls involuntary body functions, including heart rate, digestion, and respiratory rate. It consists of a two-neuron chain that connects the central nervous system (CNS) to an effector organ. Autonomic Nerve Pathway Structure - 1.​ Preganglionic Neurons ○​ Cell body is located inside the CNS (brainstem or spinal cord).  ○​ Sends signals to postganglionic neurons through autonomic ganglia. 2.​ Postganglionic Neurons ○​ Located in ganglia (clusters of neuron cell bodies outside the CNS). ○​ Directly innervates the effector organ (smooth muscle, cardiac muscle, or glands). Anatomy of the Parasympathetic Nervous System (PNS) - ​ Preganglionic neurons originate in the: ○​ Brainstem (cranial nerves) ○​ Sacral spinal cord (S2-S4) ​ Neuronal Structure: ○​ Long preganglionic neurons extend to terminal ganglia, which are located near or within the effector organ. ○​ Short postganglionic neurons travel from the ganglia to the effector organs. ​ Function: ○​ "Rest and Digest" – conserves energy, promotes digestion, lowers heart rate, and increases glandular secretions. Anatomy of the Sympathetic Nervous System (SNS) - ​ Preganglionic neurons originate in the: ○​ Lateral gray horns of spinal segments T1-L2 (thoracolumbar region). ​ Neuronal Structure: ○​ Short preganglionic neurons synapse in ganglia near the spinal cord. ​ Paravertebral (sympathetic chain) ganglia – located along the spinal column. ​ Prevertebral (collateral) ganglia – found closer to target organs (e.g., celiac, superior mesenteric ganglia). ○​ Long postganglionic neurons extend from the ganglia to the effector organ. ​ Function: ○​ "Fight or Flight" – increases heart rate, dilates pupils, decreases digestion, and redirects blood flow to muscles ​ Describe the neurotransmitters and receptors of the ANS Neurotransmitters of the ANS - Neurotransmitters are chemical messengers that transmit signals across synapses between neurons or from neurons to effector organs (muscles or glands). The type of neurotransmitter released determines the physiological response. 1. Preganglionic Neurons (Both Sympathetic & Parasympathetic) ​ Release acetylcholine (ACh) → classified as cholinergic neurons. ​ ACh binds to nicotinic receptors on postganglionic neurons in autonomic ganglia. 2. Parasympathetic Postganglionic Neurons ​ Release ACh → also cholinergic. ​ ACh binds to muscarinic receptors on target organs (smooth muscle, cardiac muscle, glands). 3. Sympathetic Postganglionic Neurons ​ Release norepinephrine (NE) → classified as adrenergic neurons. ​ NE binds to alpha (α) or beta (β) adrenergic receptors on target organs. 4. Hormones of the Adrenal Medulla ​ 80% epinephrine (E) ​ 20% norepinephrine (NE)  ​ Released into the bloodstream to enhance and prolong sympathetic responses. Effect of Neurotransmitters - ​ Can either stimulate or inhibit target tissues depending on the receptor type present in the effector organ. ​ Effector organs express specialized receptors that determine their response. Cholinergic Receptors (Bind ACh) - Two types of receptors respond to acetylcholine: 1. Nicotinic Cholinergic Receptors - ​ Activated by nicotine (agonist). ​ Found on postganglionic neurons in all autonomic ganglia (both sympathetic and parasympathetic). ​ ACh binding causes depolarization → excitatory response in postganglionic neurons. ​ Two subtypes: ○​ N1 – Found in autonomic ganglia. ○​ N2 – Found in neuromuscular junctions of skeletal muscles. 2. Muscarinic Cholinergic Receptors - ​ Activated by muscarine (a mushroom poison). ​ Found on effector cell membranes (smooth muscle, cardiac muscle, glands). ​ Bind ACh released by parasympathetic postganglionic fibers. ​ Five subtypes (M1-M5), each with different effects depending on the target tissue. Adrenergic Receptors (Bind Epinephrine & Norepinephrine) Adrenergic receptors are divided into two main classes, alpha (α) and beta (β), each with subclasses that determine their specific effects. Alpha (α) Adrenergic Receptors ​ Located on effector organs of the sympathetic nervous system. ​ Most common adrenergic receptors. ​ Typically excitatory. ​ Have a greater affinity for norepinephrine than epinephrine. Beta (β) Adrenergic Receptors ​ Bind both norepinephrine and epinephrine, but some subtypes have a greater affinity for one over the other. ​ Located in different organs with varied effects.  ​ Explain the events that take place in order for sensation to occur Sensation is the process of detecting and interpreting stimuli from the environment and the body. It involves specialized receptors, signal transduction, and processing by the nervous system. 1. Afferent Branch of the Peripheral Nervous System - ​ Function: Carries sensory information from the periphery to the CNS. ​ Divisions: ○​ External Environment (Sensory Afferent) → Vision, hearing, touch, taste, smell. ○​ Internal Environment (Visceral Afferent) → Signals from internal organs (e.g., blood pressure, pH levels). 2. Sensory Receptors & Receptor Physiology - ​ Sensory Receptors: Specialized nerve endings or separate cells that detect stimuli and generate a graded potential. ​ Key Processes: ○​ Transduction: Converts stimulus energy into electrical energy. ○​ Adaptation: Decrease in receptor sensitivity over time with continued stimulus exposure. 3. Sensory Modality & The Law of Specific Nerve Energies - ​ Modality: The type of stimulus energy detected by a receptor (e.g., light, sound, pressure). ​ Law of Specific Nerve Energies: ○​ Each receptor is most sensitive to one type of stimulus. ○​ This is called the adequate stimulus. ○​ However, if another stimulus is strong enough, it may also activate the receptor (e.g., a strong blow to the head can activate photoreceptors, causing "seeing stars"). 4. Steps in Sensory Processing - 1.​ Stimulation of a Sensory Receptor ​ A stimulus (e.g., light, sound, pressure) activates a receptor. 2.​ Transduction (Conversion to Electrical Signal) ​ The receptor converts the stimulus energy into an electrical signal. ​ This graded potential may trigger an action potential if strong enough. 3.​ Transmission (Propagation of the Signal) ​ If the graded potential reaches threshold, it triggers an action potential in the afferent neuron.  ​ The signal travels toward the CNS via the spinal cord or cranial nerves. 4.​ Integration & Processing in the CNS ​ The signal reaches the spinal cord or brainstem, where some processing occurs. ​ It is then relayed to the thalamus (except for smell). 5.​ Perception (Interpretation in the Brain) ​ The cerebral cortex interprets the signal, allowing conscious awareness of the stimulus. ​ Compare the receptive fields of different types of sensory neurons ​ Discuss how the following attributes of a stimulus are encoded: modality, location, intensity & duration The nervous system encodes sensory stimuli through four key attributes: modality, location, intensity, and duration. Sensory receptors convert physical stimuli into neural signals, which are then processed by the brain. 1. Modality (Type of Stimulus) - Definition: The specific type of stimulus detected (e.g., touch, temperature, pain, sound, light).​ How it’s encoded: ​ Labeled-line principle – Each sensory receptor is specialized for a particular modality and connects to specific brain regions (e.g., photoreceptors → visual cortex, mechanoreceptors → somatosensory cortex). ​ Types of receptors by modality: ○​ Mechanoreceptors (touch, pressure) ○​ Thermoreceptors (temperature) ○​ Nociceptors (pain) ○​ Chemoreceptors (taste, smell) ○​ Photoreceptors (light) Example: Light is detected by photoreceptors in the retina, which send signals through the optic nerve to the visual cortex. 2. Location (Where the Stimulus Occurs) - Definition: The ability to determine where a stimulus is coming from.​ How it’s encoded: ​ Receptive fields – Each sensory neuron responds to a specific region. ○​ Small receptive fields (fingertips) → High spatial resolution. ○​ Large receptive fields (back) → Low spatial resolution. ​ Somatotopic, Retinotopic, and Tonotopic Mapping – The brain maintains maps of sensory input (e.g., the homunculus in the somatosensory cortex). ​ Lateral Inhibition (detailed below) – Enhances stimulus contrast and localization. Example: In touch sensation, the fingertips have small receptive fields, allowing for precise object identification. 3. Intensity (Strength of the Stimulus) - Definition: How strong the stimulus is perceived.​ How it’s encoded: ​ Frequency coding – The stronger the stimulus, the higher the firing rate of neurons. ​ Population coding – Intense stimuli activate more neurons (recruitment of neighboring receptors). Example: A light touch produces a low firing rate, while a firm press leads to high-frequency firing and more neurons being recruited. 4. Duration (How Long the Stimulus Lasts) - Definition: The length of time a stimulus is detected.​ How it’s encoded: ​ Slow-adapting (tonic) receptors – Continue to fire as long as the stimulus is present (e.g., Merkel cells for pressure). ​ Fast-adapting (phasic) receptors – Fire at the onset and offset of a stimulus but stop responding if it persists (e.g., Pacinian corpuscles for vibration). Example: When you put on a watch, you initially feel it (fast-adapting response), but after a while, you stop noticing it (due to adaptation). Lateral Inhibition: Enhancing Stimulus Contrast - Definition: A process where strongly activated neurons inhibit their neighboring neurons, improving contrast and sharpening perception.​ How it works: 1.​ A stimulus activates multiple sensory neurons. 2.​ The most strongly stimulated neuron inhibits neighboring neurons, reducing their response. 3.​ This increases contrast between the stimulated area and its surroundings, allowing for more precise localization. Example: ​ When you press on your skin, the center of the contact feels sharp, while the edges fade out due to lateral inhibition. ​ In vision, lateral inhibition enhances edge detection, making objects appear clearer. Key Definitions: ​ Modality: Determined by receptor type (mechanoreceptors, photoreceptors, etc.). ​ Location: Encoded by receptive fields, brain mapping, and lateral inhibition. ​ Intensity: Encoded by firing rate (frequency coding) and neuron recruitment (population coding). ​ Duration: Encoded by slow-adapting (tonic) or fast-adapting (phasic) receptors. ​ Lateral Inhibition: Enhances contrast and sharpens perception