Nervous System Physiology

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Nervous System Subdivisions

• The central nervous system (CNS) includes the brain and spinal cord
• The CNS integrates and processes nervous information
• The brain and spinal cord are covered by protective layers called the meninges
• The peripheral nervous system (PNS) consists of all neural tissue outside the CNS
• The PNS carries information to the CNS, receives information from the CNS, and causes a response in the body
• Everything outside the meninges is part of the PNS
• Neurons and glial cells are the same basic parts in both the central and peripheral nervous systems

Functional and Motor Divisions

• Motor and sensory nervous systems work together to collect information about internal/external environments
• There are two functional divisions; motor and sensory
• Information is processed to determine a response; the responses are initiated based on collected information
• The motor (efferent) nervous system carries motor information away from the CNS towards the PNS
• Motor impulses are carried from the brain or spinal cord through nerves to muscle tissue throughout the body
• Nerves in the PNS carry impulses which contribute to a movement
• "Efferent" means causing muscle tissue to contract
• The motor (efferent) nervous system carries somatic and visceral information

Sensory and Motor Fibers

• The sensory (afferent) nervous system is responsible for collecting sensory information or stimuli, like pain, and carries info from peripheral to central NS
• Receptors sense stimuli (e.g., temperature or pain)
• Stimuli is transmitted to the CNS
• The sensory nervous system initiates different movements (not the actual movement)
• The sensory (afferent) nervous system carries somatic and visceral information related to pain, touch, and temperature
• Somatic motor fibers carry nerve impulses to skeletal muscle which controls voluntary movements, allowing movement like walking/typing
• Visceral or autonomic motor fibers carry nerve impulses to smooth and cardiac muscles, and glands which control involuntary actions, with further division into sympathetic and parasympathetic systems

Excitable Cells and Ion Concentration

• Excitable cells can generate electrical activity using ion concentration differences across their plasma membrane (e.g. nerve cells/neurons, muscle cells, pancreatic B cells)
• Ions are charged particles (positive or negative) that create a membrane potential across the plasma membrane, creating key sodium and potassium gradients
• Higher sodium concentration outside the cell wants to move sodium into the cell, attracting sodium inward through concentration and electrical gradients
• Higher potassium concentration inside the cell wants to move potassium out of the cell
• Concentration gradient pushes potassium out, but the electrical gradient pulls it inward
• Potassium has a stronger concentration gradient than electrical gradient

Polarization

• A polarized neuron's inside becomes less negative (or more positive) compared to its resting potential, known as depolarization
• Depolarization is triggered by the opening of sodium channels, causing sodium to flow into the cell
• If depolarization hits a threshold; an action potential is generated and travels down the axon to send an electrical signal
• Excitatory signals increase likelihood of transmission to other neurons
• Hyperpolarization is becoming more negative than its resting potential, caused by opening potassium channels to allow potassium to flow out of the cell or opening chloride channels for chloride to flow into the cell
• Hyperpolarization makes it less likely to reach action potential threshold
• Inhibitory signals reduce the chance of firing, helping control and limit neural activity.
• Concentration and electrical gradients influence ion movement
  • Sodium wants to enter the cell due to both gradients
  • Potassium wants to leave the cell due to concentration gradient but held back by the electrical gradient

Myelination

• Myelination is the process of wrapping axons in a fatty, insulating myelin sheath, formed by Schwann cells (PNS) and oligodendrocytes (CNS)
• Myelination increases signal transmission speed due to saltatory conduction, conserving energy by reducing the need for continuous ion channel work along the axon
• Diseases like Multiple Sclerosis (MS) damage the sheath, leading to slower signal transmission, muscle weakness, and impaired coordination

Ion Channels

• Ion channels are specialized channels in cell membranes that allow charged ions to move across, generating electrical current essential for neuron signaling
• Ions of Interest: Sodium (Na+) and Potassium (K+)

Types of Ion Channels

• Leak channels randomly alternate between open and closed positions, allowing a steady flow of ions to maintain resting membrane potential through passive ion movement
• Ligand-gated channels open or close in response to a specific chemical stimulus (ligand)
• Acetylcholine binding to a receptor, causing Na+ channels to open, involved in synaptic transmission and communication
• Mechanically-gated channels open or close in response to mechanical stimulation like touch, pressure, tissue stretching, or vibration
• Ex. channels in sensory receptors in the skin or inner ear
• Voltage-gated channels open or close in response to changes in membrane potential (voltage) like Sodium and potassium channels involved in the generation of action potentials
• Voltage-gated channels are critical for initiating and conducting electrical signals in neurons

Graded and Action Potentials

• Ion flow across the plasma membrane generates electrical currents, which neurons use to communicate information over short and long distances using graded and action Potentials
• Both processes depend on the opening and closing of gated ion channels
• Graded potentials are small, localized changes in membrane potential that can be either depolarizing to become less negative or hyperpolarizing to become more negative
• Arise from opening ligand-gated or mechanically-gated ion channels, causing currents that weaken over distances
• Are not all-or-none - strength depends on the size of the stimulus but can trigger an action potential if strong enough
• Generated by receptors responding to thermal changes, chemicals, or mechanical force
• Initiate action potentials by providing the depolarization needed to reach the threshold and allow neuronal communication via neurotransmitters and feedback cycles
• Without graded potentials, action potentials cannot occur

Action Potentials

• Action Potentials (APs) are large, rapid changes in membrane potential that communicates over long distances (all-or-none)
• APs either occur fully (hits threshold) or not at all; the amplitude is always the same regardless of stimulus strength
• A specific threshold voltage must be met at typically around -55 mV in human nerve cells, requiring a polarized neuron's membrane to reach/exceed with voltage-gated Na+ and K+ channels opening to trigger the AP

Steps of Action Potential

1. Voltage-gated Na+ channels open, allowing Na+ ions to flow into the cell, and the membrane potential becomes more positive: Depolarization
2. Voltage-gated K+ channels open, allowing K+ ions to flow out of the cell and returns membrane potential to its resting levels: Repolarization
3. The membrane potential briefly becomes more negative than the resting potential before stabilizing: After-Hyperpolarization

• Depolarization at one section of the axon triggers the threshold in adjacent sections, propagating the AP in local current flow
• APs move one direction due to the refractory period
• Larger fibers conduct APs faster because of lower resistance to ion flow
• Myelinated fibers are faster due to saltatory conduction where APs jump between Nodes of Ranvier

Signal Transmission at a Synapse

• The cell body or soma is the control center that processes incoming signals and sends outgoing ones
• Branch-like projections from the cell body to receive signals from other neurons and send to the soma: Dendrites
• A long projection extending from the soma to carry signals away from the cell body to other neurons, muscles, or glands: Axon
• The trigger zone where APs begin before traveling down the axon, acting as a decision-making point: Axon Hillock
• Branched ends of the axon to form connections with other cells: Axon Terminals
• The synapse is the functional connection between a neuron and another neuron, or with an a muscle/gland, including presynaptic neuron, synaptic cleft, and postsynaptic cell
• The presynaptic neuron is the sending cell, neurotransmitters are released from its axon terminals
• The synaptic cleft the small gap between cells where neurotransmitters travel, and the postsynaptic cell receives the signal with receptors to bind them

Potentials

• Graded potentials are created by signals from the postsynaptic cell
• Increasing likelihood of action potential/excitatory: Excitatory Postsynaptic Potential (EPSP)
• Decreasing likelihood of action potential/inhibitory: Inhibitory Postsynaptic Potential (IPSP)
• Neurotransmitter binds to ligand-gated ion channels on the postsynaptic cell, opening channels causing a graded potential by positive ions (e.g., Na+) flowing into the cell, depolarizing it, or negative ions (e.g., Cl-) flowing in, or positive ions (e.g., K⁺) flowing out, hyperpolarizes/stabilizes membrane

Neurotransmitters

• Excitatory neurotransmitters depolarize membrane, Inhibitory neurotransmitters hyperpolarize/stabilize membrane
• Ion Channel Activation causes the following: Mechanism of Inhibitory Synapses, Potassium Channels Open with Potassium moving out or Chloride Channels Open with Chloride moving in and stabilizes the membrane potential
• The purpose of Inhibitory Neurotransmitters is to regulate information flow while preventing overstimulation
• Inhibitory Synapses Regulatory Function prevent uncontrolled excitation
• Tetanus Toxin dysfunction stops GABA/glycene release for uncontrolled muscle spasms, and Strychnine competes with glycine and blocks inhibitory signals, which over activates motor nerves

Presynaptic Modulation

• Presynaptic modulation adjust the neurotransmitter (signal) being sent to the next neuron across a synapse
• This fine-tunes communication, prevents overstimulation and ensures an appropriate neuron response
• It adjusts to needs base on calcium/drugs

Neurotransmitter Removal

• Reuptake: Transmitters are taken back into the presynaptic neuron that will be reused
  • Ex: Serotonin reuptake by specific transport proteins.
• Enzymes degrade neurotransmitters: Enzymatic Degradation, Acetylcholine is broken down by acetylcholinesterase.
• Diffusion: Diffuses from the membrane, and dilutes into the synaptic cleft
• Glial cells: (e.g., astrocytes) regulate them by absorbing the synaptic cleft

Neurotransmitter Types

• Neurotransmitters are messengers that signal across a synapse for a target cell: Gland/Muscle
• Can promote action potentials or inhibit actions:
  • Action promoter or excitatory neurotransmitter is glutamate and aspartate
  • Action suppressor or inhibitory neurotransmitter is GABA and glycine
  • Modulatory adjusts synaptic communication which are serotonin and dopamine
• Cholinergic: muscle function, memory, and learning
  • Made from acetyl CoA and choline
  • Regulated by acetylcholinesterase
  • Nicotinic receptor agonist is nicotine
  • Muscarinic receptor agonist is muscarine

Neurotransmitter Breakdown, Imbalances, and More

Symptoms

• Alzheimer's disease causes degeneration of cholinergic neurons and confuses cognitive function.
• Adrenergic - Catecholamines system helps with receptor sensitivity Dopamine is broken down MAO and COMT
• Parkinson's, or Dopamine deficiency in the brain, can cause motor deficiencies
• Serotonin's selective regulates SSRIs and balance reuptake.
• Anxiety is caused by underactivity of GABA and reduced activity
• Epilepsy overactivates glutamate with more excitability More neurotransmitter cleaning enzymes MAO breaks down dopamine, serotonin and norepinephrine

Brain Regions

• Key structure the suprachiasmatic nucleus, which light gather from the eyes, and which regulates behavioural circadian cycles
  • SCN damage disrupts the cycles - People with visual harm can sense degrees of cycling
• Brainstem communicates transitions, and contains sleep promoter cells, releases GABA in arousal centres
  • PONS and medulla signal muscles in sleep to relax
• Thalamus is a relay/receiver for sensory cortex information
  • Shuts down during sleep stages
  • Cortex active during REM sleep (sight, sound, and imaging)
• Amgydala highly active emotion processor with REM sleep
• Pineal gland receives sleep signals increasing melatonin, that are produced
• Basal brain release adenosines to increase sleeping pressure for the mind wants to rest Helps to remove arousal factors for wakefulness
• Arousal reliever that blocks adenosine receptors reducing sleep drive and promotes wakefulness (like caffeine to regulate these factors).

Rhythms

• Circadian rhythms control daily fluctuations: body temp, hormone release, sleeping Homeostasis causes control and sleeping timing by: Causes sleeping cues and to maximize sleep.
• Can not be prevented without external cues:
• The sleep deprivation the body adjusts and intensifies its needs, to regulate hormone factors. Sleep increases and homeostasis The increased sleep pressure that the body develops influenced by building adenosine causes regulations with stressors.

Transmitters

Released by:

• The release of GABA inhibits wakefulness and promotes sleep Histamine
• Is a wakefulness neurotransmitter for REM and lowers blockages and drowsiness Serotonin
  • Regulate retina and disrupt what can contribute to SAD Helps body and mind to release sleeping neurotransmitters: NE - arousal and alert Orexin regulates appetite AC helps REM state Glutamate neural communication for mental clarity Genes Per, Tim, Cry influence cycles and timing Linked disorders Genetic mutations for sleeping, restless legs There are DEC2 mutations as well.

Concussion Injuries

• The Mechanical shake of the brain from the impact of acceleration causes ionic shifts of:
  • Potassium leaks
  • Calcium or sodium enter. Causes widespread depression with inflammation resulting from energy requirements Inhibits ATP production, disrupts, reduces, and mismatches metabolic activity Causes collapsing, axonal/disturbed flow and weaker structures; Microglia CNS activates and elevates Inflammation Nerve damage Due to:
• Glutamate affecting functions to disrupt signalling by:
• Headache, balance, and dizziness

Concussion Causes and Syndromes

• The mind stays vulnerable from impact and is often a reoccurring syndrome
  • Causes increased symptoms

2. Autonomic imbalance that hurts motor skills with demographic factors that impact hormonal differences

• Dysregulation and with mental well being
• Causes mental symptoms
• The exercise and recovery

Treatment

• Initial phase with physical mental rest
• Symptoms reset by exercise and diet
• Lights minimized during exercise, for longer term reset
• Potential and long term issues and mechaisms Disruptions can have long term issues.

Cannabinoids

• AEA, is a signalling molecule, and modulator
• Food, mood memory regulatory Functions and metabolism, and controls
• FAAH in the brain: metabolism:

Functions between receptor systems 1/2 balance and control functions Involved in balances in the brain

• CB 1
• CB 2 tissue activation

Retrograde signals Receptor stimulators CBD1 hippo compus link Suppresses inflammation and binds for muscle activity via ACH

• CB 2 aids inflammation
• And release via FAAH/MAGL
• Aids balances and activity Aids in inhibition or binding depending how they need to work THD long slow reactions Creates effects Psycho activity. Slows reaction functions by memory disruption, anxeiety etc.

Non psycho activity Inhibition balanced by both Effects balancing

Test your knowledge on concussion recovery, endocannabinoid signaling, and neuronal communication. Questions cover graded potentials, action potentials, and mechanisms of post-concussion syndrome (PCS). Evaluate understanding of neurophysiology and recovery processes.