Nervous System Research Notes
I. Introduction
Overview of mission: Research brain development to understand cognitive, emotional, and behavioral changes across the lifespan; create an organized informational site using platforms like Google Sites or Canva to disseminate findings.
Recommended resources for study:
The Nervous System - Crash Course Biology #26: Provides a broad overview of the fundamental components and functions of the nervous system.
Central Nervous System: Crash Course A&P #11: Focuses on the brain and spinal cord, detailing their structures and critical roles in processing information.
Peripheral Nervous System: Crash Course A&P #12: Explores the nerves extending outside the CNS, including sensory and motor neurons.
Autonomic Nervous System: Crash Course A&P #13: Differentiates between the sympathetic and parasympathetic divisions and their involuntary control over body functions.
Scanning the Brain: Introduces various neuroimaging techniques used to study brain structure and activity.
II. Brain Structural Functionality
A. Scanning Technique
EEG (Electroencephalography)
Definition: A non-invasive method that measures the electrical activity of the brain (brainwaves) using electrodes placed on the scalp. These electrical signals result from synaptic activity in the brain's outer layers.
Usage: Typically used for diagnosing epilepsy (identifying abnormal brain activity), sleep disorders (monitoring sleep stages through wave patterns like alpha, beta, theta, delta), evaluating head injuries, strokes, and other neurological disorders. It provides excellent temporal resolution.
CAT Scan (Computerized Axial Tomography)
Definition: An imaging method that uses a series of X-ray images taken from different angles around the body and uses computer processing to create cross-sectional images (slices) of the brain or other body parts. It can create 3D images.
Usage: Used to detect tumors, hemorrhages (bleeding), brain injuries, bone damage, and to guide certain neurological treatment plans or biopsies. Sometimes a contrast dye is used to enhance visibility of structures.
PET Scan (Positron Emission Tomography)
Definition: An imaging test that uses a small amount of a short-lived radioactive tracer (often a glucose analog like FDG) injected into the bloodstream to visualize metabolic activity in the brain. Areas with higher metabolic rates (e.g., active neurons) accumulate more tracer and show up brighter.
Usage: Often used in cancer diagnosis (identifying metabolically active tumors), to assess brain function in conditions like Alzheimer's (showing areas of decreased glucose metabolism), identifying areas of decreased blood flow in stroke, and researching neurological and psychiatric disorders.
MRI (Magnetic Resonance Imaging)
Definition: A non-invasive medical imaging technique that uses strong magnetic fields and radio waves to create high-resolution images of soft tissues, including brain structures, by detecting the activity of hydrogen atoms in water molecules within the body.
Usage: Valuable for identifying structural abnormalities like tumors, lesions, multiple sclerosis plaques, and assessing brain disorders without using ionizing radiation. It provides superior soft-tissue contrast compared to CAT scans.
fMRI (Functional Magnetic Resonance Imaging)
Definition: A specialized MRI technique that measures brain activity by detecting changes associated with blood flow. It relies on the principle that active brain areas require more oxygenated blood (known as the BOLD - Blood-Oxygen-Level Dependent - signal).
Usage: Utilized for understanding brain function by showing which brain regions are active during specific cognitive tasks (e.g., language, memory), assessing neurological conditions, and pre-surgical planning to map critical functional areas.
B. The Infant/Child Brain
Development of the Infant's Brain
The infant's brain undergoes rapid development within the first years of life, characterized by processes like synaptogenesis (formation of new synapses), synaptic pruning (elimination of unused synapses), and myelination (insulation of neuronal axons for faster signal transmission). These processes shape the brain's architecture based on experiences.
Visual Perception: Initially, an infant's visual perception is limited. Their vision is blurry, and they have limited color differentiation. Over the first few months, visual acuity significantly improves, depth perception begins to develop, and they become adept at facial recognition, essential for social bonding.
Language Acquisition in Children
Neurological changes that occur as children learn to speak and understand language involve the rapid development and specialization of brain regions such as Broca's area (speech production) and Wernicke's area (language comprehension). This period often involves a critical window for language learning, with early exposure being key.
Connections between comprehension and brain maturation levels directly influence a child's ability to process complex sentences, understand nuances of language, and develop narrative skills, often linked to cognitive and social development.
Learning to Read
Neurophysiological processes involved in reading development include phonemic awareness (the ability to hear, identify, and manipulate individual sounds in spoken words), grapheme-phoneme mapping (connecting letters to sounds), and visual processing of letters. Key brain areas activated include the visual word form area (VWFA) in the left fusiform gyrus, angular gyrus, and areas involved in phonological processing.
Discussing typical brain areas activated during reading tasks involves the coordinated effort of regions in the temporal, parietal, and frontal lobes, with specific pathways strengthening as reading proficiency increases. Challenges like dyslexia involve different patterns of brain activation during reading.
C. The Teenage Brain
Developmental Changes
Neurological transformations happening during adolescence involve continued synaptic pruning, particularly in the prefrontal cortex, leading to more efficient brain circuits. Myelination also continues, enhancing the speed of neural communication. These changes impact executive functions like planning, decision-making, and impulse control.
Explore the role of hormones (e.g., surges in estrogen and testosterone affecting mood and risk-taking) and environmental influences (such as peer pressure, stress, and access to education) which profoundly shape the developing adolescent brain and behavior.
Sleep Patterns
Changes in sleep requirements and patterns in teenagers include a natural shift in their circadian rhythm, often leading to a later release of melatonin. This results in teenagers typically wanting to go to bed later and wake up later, needing around 8-10 hours of sleep nightly.
Discussion on whether the adolescent brain actually enters a deep sleep state (such as REM sleep) reveals that teenagers experience typical sleep stages, but the timing and duration of these stages can be affected by lifestyle, leading to chronic sleep deprivation and its impact on cognitive function, mood, and academic performance.
Memory Formation
Memory functions are established and refined in the teenage brain, with significant development in working memory and long-term memory capabilities. The prefrontal cortex, involved in executive functions, and the hippocampus, crucial for declarative memory formation, undergo maturation, allowing for more complex learning and memory consolidation.
III. Schizophrenia Overview
Definition
Schizophrenia is a chronic, severe, and often debilitating mental disorder that affects how a person thinks, feels, and behaves. It is characterized by a disintegration of thought processes and emotional responsiveness, typically emerging in late adolescence or early adulthood.
Causes
Schizophrenia has mixed contributions from a complex interplay of genetic factors (high heritability, though no single gene is responsible), environmental factors (such as prenatal complications, exposure to viruses, childhood trauma, and cannabis use), and neurobiological factors (including abnormalities in brain structure, reduced grey matter volume, and dysregulation of neurotransmitter systems, especially dopamine, but also glutamate and serotonin).
Symptoms
Symptoms are typically categorized into positive, negative, and cognitive symptoms. Positive symptoms include delusions (false beliefs), hallucinations (seeing or hearing things that aren't there), and disorganized thinking and speech. Negative symptoms involve a lack of motivation (avolition), reduced pleasure (anhedonia), and diminished emotional expression (affective flattening). Cognitive symptoms include difficulties with attention, memory, and executive function.
Types of Treatments
Treatments typically involve a multifaceted approach. Medications (primarily antipsychotics, which can be first-generation or atypical/second-generation, targeting dopamine receptors) are crucial for managing positive symptoms. Psychotherapy (such as cognitive behavioral therapy - CBT - and social skills training) helps individuals manage symptoms and improve daily functioning. Community support programs, family therapy, and vocational training are also vital for recovery and integration, though challenges like medication adherence and side effects remain.
IV. The Adult Brain
A. Developmental Characteristics
Understanding Emotion
Definition: Emotion is a complex biopsychosocial state involving three components: a subjective experience (what we feel), a physiological response (e.g., heart rate, sweating), and a behavioral or expressive response (e.g., facial expressions, body language).
Exploration of the limbic system as the "emotional brain" highlights its key structures: the amygdala (involved in fear and emotional memory), the hippocampus (integrating emotion with memory), and the hypothalamus (regulating physiological responses to emotion). This system's influence on cognitive processes means emotions can significantly impact decision-making, memory, and perception.
Emotional Control
Mechanisms of emotional regulation involve both automatic and conscious processes. The prefrontal cortex plays a critical role in executive functions, allowing for cognitive reappraisal (reinterpreting an emotional situation), suppression (inhibiting emotional expression), and other strategies to modulate emotional responses. These mechanisms are intricately linked with rational thought, allowing individuals to adapt their behavior to social contexts.
Stroke Impact
Examination of how strokes, which can be ischemic (due to a clot) or hemorrhagic (due to bleeding), can profoundly change emotional responses and overall brain function depends heavily on the affected brain region. Damage to areas involved in emotional processing (e.g., frontal lobe, limbic system) can lead to significant emotional dysregulation.
Discussion of emotional lability post-stroke, also known as Pseudobulbar Affect (PBA), involves involuntary, inappropriate, and often intense episodes of crying or laughing. Other neuropsychiatric consequences can include depression, anxiety, apathy, and irritability, often requiring tailored therapeutic interventions.
Role of Laughter
Explore the physiological and psychological benefits of laughter on mental health. Physiologically, laughter releases endorphins (natural pain-killers), reduces stress hormones like cortisol, improves immune function, and relaxes muscles. Psychologically, it enhances mood, reduces anxiety, strengthens social bonds, and can even increase the pain threshold.
Mention studies providing insights into how laughter therapy and humor can enhance mood, reduce stress, improve coping mechanisms, and foster resilience in various populations, from healthy individuals to those with chronic illnesses.
B. Aging of the Adult Brain
Brain Aging Process
Discuss how aging is a complex process affecting neuronal function (e.g., reduced neurotransmitter synthesis, slower synaptic transmission), synaptic plasticity (reduced capacity for long-term potentiation - LTP), and leading to cognitive decline associated with memory pathways. This can manifest as reduced processing speed, decreased fluid intelligence, and challenges in memory retrieval. Brain volume also typically decreases with age, particularly in the frontal lobes and hippocampus.
Alzheimer's Disease
Symptoms: Beyond memory loss (especially short-term), symptoms include difficulty with problem-solving, planning, and performing familiar tasks (apraxia), impaired language (aphasia), confusion regarding time or place, poor judgment, spatial disorientation, and significant changes in mood or behavior (e.g., apathy, depression, agitation).
Causes: Alzheimer's is believed to result from a complex combination of genetic factors (e.g., APOE-e4 allele being a risk factor), lifestyle choices (e.g., diet, exercise, cardiovascular health), and environmental factors that lead to progressive neurodegeneration. Key pathological hallmarks are the accumulation of beta-amyloid plaques outside neurons and neurofibrillary tangles (composed of tau protein) inside neurons, disrupting neural communication and causing cell death.
Treatments: Overview of current medications includes cholinesterase inhibitors (e.g., donepezil) which boost acetylcholine levels to improve cognitive function, and memantine, which regulates glutamate activity. Research on possible future cures focuses on disease-modifying therapies targeting amyloid and tau pathologies, as well as neuroinflammation and genetic approaches.
V. Addiction in the Adult Brain
Definition of Addiction
A chronic, relapsing brain disorder characterized by compulsive drug seeking irrespective of harmful consequences, continued use despite adverse outcomes, and long-lasting functional and structural changes in the brain's reward, motivation, memory, and related circuitry. It is recognized as a complex brain disease rather than a moral failing.
Manifestations of Addiction
Discuss physiological dimensions of addiction, primarily involving the brain's dopamine reward pathways (mesolimbic pathway, connecting the ventral tegmental area to the nucleus accumbens and prefrontal cortex). Addictive substances hijack this system, leading to exaggerated dopamine release and subsequent adaptations that diminish the brain's natural reward responses. Behavioral dimensions include intense cravings, loss of control over use, and continued engagement in substance use despite severe negative consequences. The role of stress and trauma in addiction tendencies is significant, as these can alter neural circuits, making individuals more vulnerable to seeking substances as coping mechanisms.
Discussion on Treatment
Overview of various treatment strategies encompasses behavioral therapies (e.g., Cognitive Behavioral Therapy - CBT for coping skills; Motivational Interviewing for increasing desire for change; Contingency Management for positive reinforcement), pharmacotherapy (e.g., naltrexone for opioid/alcohol cravings; buprenorphine/methadone for opioid dependence), and integrated care models addressing co-occurring mental health disorders. Effectiveness varies based on addiction type, individual circumstances, and treatment adherence, often requiring long-term support and relapse prevention strategies.
VI. Neurotransmitters and Degenerative Disorders
A. Neurotransmitters: Overview and Key Functions
Dopamine
Function: Primarily involved in motivation, reward, pleasure, motor control, and executive functions.
Associated Disorders (deficiency/dysregulation): Parkinson's disease (due to significant loss of dopamine-producing neurons); Schizophrenia (associated with excessive dopamine activity in certain brain areas and deficiencies in others); Restless Legs Syndrome.
Serotonin (5-HT)
Function: Regulates mood, sleep, appetite, digestion, learning, memory, and social behavior.
Associated Disorders (deficiency/dysregulation): Major Depressive Disorder, Anxiety Disorders, Obsessive-Compulsive Disorder (OCD), eating disorders (many antidepressant medications target serotonin pathways).
Acetylcholine (ACh)
Function: In the Peripheral Nervous System (PNS), it triggers muscle contraction. In the Central Nervous System (CNS), it plays a crucial role in learning, memory, attention, and arousal.
Associated Disorders (deficiency): Alzheimer's disease (characterized by significant degeneration of cholinergic neurons in the basal forebrain); Myasthenia Gravis (autoimmune disorder affecting ACh receptors at the neuromuscular junction).
Norepinephrine (Noradrenaline)
Function: Acts as both a neurotransmitter and a hormone. Involved in alertness, arousal, vigilance, mood regulation, and the fight-or-flight response.
Associated Disorders (deficiency/dysregulation): Major Depressive Disorder, Anxiety Disorders, Attention-Deficit/Hyperactivity Disorder (ADHD).
GABA (Gamma-Aminobutyric Acid)
Function: The primary inhibitory neurotransmitter in the CNS. It reduces neuronal excitability, calming nervous activity and promoting relaxation.
Associated Disorders (deficiency): Anxiety disorders, epilepsy (low GABA levels can lead to increased neuronal firing and seizures), insomnia.
Glutamate
Function: The primary excitatory neurotransmitter in the CNS. Crucial for learning, memory formation (via long-term potentiation - LTP), and synaptic plasticity.
Associated Disorders (dysregulation): Excitotoxicity (excessive glutamate leading to neuronal damage) is implicated in stroke, traumatic brain injury, and neurodegenerative diseases like Alzheimer's and Huntington's. Dysregulation also thought to play a role in Schizophrenia.
B. Degenerative Disorders Associated with Neurotransmitter Deficiencies
Parkinson's Disease (PD)
Neurotransmitter Deficiency: Primarily dopamine. This is due to the progressive degeneration of dopaminergic neurons in the substantia nigra, a region of the midbrain essential for motor control. The loss of these neurons leads to an imbalance in the basal ganglia pathways, resulting in characteristic motor symptoms.
Symptoms: Predominantly motor symptoms include resting tremor, bradykinesia (slowed movement), rigidity (stiffness of limbs and trunk), and postural instability (impaired balance and coordination). Non-motor symptoms are also common, such as depression, anxiety, sleep disturbances, cognitive impairment, and loss of smell.
Brain Regions Involved: Substantia nigra, basal ganglia.
Treatments: Focus on managing symptoms by increasing dopamine levels or mimicking its effects. Medications include Levodopa (a precursor to dopamine that crosses the blood-brain barrier) and dopamine agonists (which activate dopamine receptors). Deep brain stimulation (DBS) is a surgical option for advanced cases.
Alzheimer's Disease (AD)
Neurotransmitter Deficiency: A significant deficiency in acetylcholine is observed due to the widespread degeneration of cholinergic neurons, particularly in the basal forebrain, which projects to the cerebral cortex and hippocampus. While primarily cholinergic, AD also involves dysregulation of glutamate, serotonin, and norepinephrine systems.
Symptoms: Characterized by progressive cognitive decline, starting with memory loss (especially short-term or episodic memory). Other symptoms include difficulty with problem-solving, planning (executive dysfunction), language problems (aphasia), confusion regarding time or place, impaired judgment, spatial disorientation, and significant behavioral and mood changes (e.g., apathy, agitation, depression).
Brain Regions Involved: Primarily affects the hippocampus (critical for memory), cerebral cortex (responsible for language, perception, reasoning), and basal forebrain.
Treatments: Current treatments aim to enhance neurotransmitter function and manage symptoms. Cholinesterase inhibitors (e.g., donepezil, rivastigmine, galantamine) boost acetylcholine levels by preventing its breakdown. Memantine is used to regulate glutamate activity by blocking NMDA receptors. Research continues into disease-modifying therapies targeting amyloid plaques and tau tangles.
Huntington's Disease (HD)
Neurotransmitter Impact: While not a simple deficiency, HD involves a profound loss of medium spiny neurons in the striatum, which are primarily GABAergic (inhibitory). This loss leads to an imbalance in the basal ganglia circuits, creating a relative excess of dopamine activity and often involving glutamate receptor changes.
Symptoms: A progressive neurodegenerative disorder characterized by involuntary movements (chorea, a jerky, dance-like movement), cognitive decline (executive function, memory, judgment), and psychiatric problems (depression, irritability, anxiety, psychosis). Symptoms typically begin in mid-adulthood.
Brain Regions Involved: Primarily the striatum (caudate and putamen).
Treatments: Symptomatic treatments are available, but there is no cure. Medications like tetrabenazine or deutetrabenazine help reduce chorea by depleting dopamine. Antipsychotics and antidepressants may be used to manage psychiatric symptoms.
Amyotrophic Lateral Sclerosis (ALS) / Lou Gehrig's Disease
Neurotransmitter Implication: ALS is characterized by the degeneration of motor neurons. While the primary pathology is motor neuron death, the mechanism is complex, with glutamate excitotoxicity being a significant implicated factor. Overstimulation of motor neurons by glutamate receptors may contribute to their demise.
Symptoms: Progressive muscle weakness, atrophy, twitching (fasciculations), and spasticity (stiffness), leading to difficulty speaking, swallowing, and eventually breathing. Sensory and cognitive functions are generally preserved, though a subset of patients may develop frontotemporal dementia.
Brain Regions Involved: Motor cortex, brainstem, and spinal cord (specifically upper and lower motor neurons).
Treatments: Riluzole is a medication approved for ALS that is believed to reduce glutamate activity. Edaravone is another drug that may slow functional decline. Treatment primarily focuses on supportive care to manage symptoms and improve quality of life.
VII. Fundamental Concepts of the Nervous System
A. The Divisions of the Nervous System
The nervous system is broadly divided into two main parts:
Central Nervous System (CNS): Consists of the brain and spinal cord. It is the integration and command center.
Peripheral Nervous System (PNS): Consists of all the nerves extending outside the CNS. It acts as a communication highway between the CNS and the rest of the body.
The PNS is further subdivided into:
Somatic Nervous System: Controls voluntary movements of skeletal muscles and transmits sensory information from the skin, muscles, and sensory organs to the CNS.
Autonomic Nervous System (ANS): Regulates involuntary functions such as heart rate, digestion, breathing, and glandular activity. It operates mostly unconsciously and is further divided into the sympathetic and parasympathetic divisions.
B. The Central Nervous System: The Brain and Spinal Cord
The Brain
The brain is the primary control center of the body, responsible for thought, emotion, memory, movement, and the interpretation of sensory information.
Major Parts:
Cerebrum: The largest part of the brain, divided into two hemispheres (left and right) and four major lobes:
Frontal Lobe: Involved in planning, decision-making, problem-solving, voluntary movement, and personality.
Parietal Lobe: Processes sensory information such as touch, temperature, pain, and pressure; spatial awareness.
Temporal Lobe: Responsible for processing auditory information, memory formation, and language comprehension (Wernicke's area).
Occipital Lobe: Processes visual information.
Cerebellum: Located beneath the cerebrum, it coordinates voluntary movements, balance, posture, and motor learning.
Brainstem: Connects the cerebrum and cerebellum to the spinal cord. It controls vital involuntary functions such as breathing, heart rate, blood pressure, sleep, and consciousness. It consists of the midbrain, pons, and medulla oblongata.
The Spinal Cord
A long, thin, tubular bundle of nervous tissue extending from the brainstem down to the lower back.
Functions:
Communication Pathway: Serves as the main pathway for nerve signals traveling between the brain and the rest of the body.
Reflex Center: Acts as a minor reflex center, enabling rapid, involuntary responses to stimuli without direct input from the brain (e.g., knee-jerk reflex).
Structure: Composed of gray matter (nerve cell bodies, dendrites) in the center, shaped like a butterfly, and white matter (myelinated axons) surrounding it.
C. The Peripheral Nervous System: The Spinal and Cranial Nerves
The PNS acts as the messenger, carrying signals to and from the CNS.
Somatic Nervous System
Voluntary Control: Controls skeletal muscle movements.
Sensory Input: Transmits sensory information (touch, pain, temperature, sight, sound, taste, smell) from sensory receptors to the CNS.
Nerves:
Spinal Nerves: 31 pairs of nerves that branch off the spinal cord, responsible for sensation and motor control of the trunk and limbs.
Cranial Nerves: 12 pairs of nerves that originate directly from the brain, primarily serving the head and neck region (e.g., optic nerve for vision, vagus nerve for internal organs).
Autonomic Nervous System (ANS)
Involuntary Control: Regulates internal organs and glands, controlling functions like heart rate, digestion, respiration, salivation, perspiration, pupil dilation, and sexual arousal.
Divisions:
Sympathetic Division: Often referred to as the "fight or flight" system. It prepares the body for stressful situations by increasing heart rate, dilating pupils, inhibiting digestion, and releasing adrenaline. Utilizes primarily norepinephrine as a neurotransmitter at target organs.
Parasympathetic Division: Often referred to as the "rest and digest" system. It calms the body down after stress, promoting functions essential for maintenance, such as slowing heart rate, constricting pupils, and stimulating digestion. It primarily uses acetylcholine as a neurotransmitter at target organs.
D. The Functions of the Nervous System
The nervous system performs three overarching and fundamental functions:
Sensory Input (Afferent Function):
Gathers information from sensory receptors located throughout the body, detecting changes (stimuli) both inside and outside the body.
This information is then converted into electrical signals (nerve impulses) and transmitted to the CNS by afferent (sensory) neurons.
Integration:
Involves processing and interpreting the sensory input received by the CNS.
Interneurons within the CNS analyze the information, compare it to past experiences, and determine appropriate responses.
This function is crucial for higher cognitive processes like learning, memory, and decision-making.
Motor Output (Efferent Function):
Sends signals from the CNS to effector organs (muscles and glands) in response to the integrated sensory input.
Efferent (motor) neurons transmit these commands, leading to muscle contraction (movement) or glandular secretion.
Additional Functions:
Homeostasis: Maintaining stable internal conditions by continually monitoring and adjusting physiological processes.
Cognition, Emotion, and Memory: Enables complex thought, emotional experience, and the storage and retrieval of information.
E. Classification of Nervous System Cells
The nervous system is composed of two main types of cells:
Neurons (Nerve Cells)
The fundamental units that transmit electrical and chemical signals throughout the body.
Structure:
Soma (Cell Body): Contains the nucleus and most of the cell's organelles; responsible for the neuron's metabolic maintenance.
Dendrites: Branch-like extensions that receive chemical signals from other neurons and transmit them toward the cell body.
Axon: A long, slender projection that transmits electrical impulses (action potentials) away from the cell body to other neurons or effector cells.
Axon Terminals (Synaptic Boutons): The very end of the axon, where neurotransmitters are released into the synaptic cleft.
Myelin Sheath: A fatty layer that insulates many axons, speeding up nerve impulse transmission. Formed by oligodendrocytes in the CNS and Schwann cells in the PNS.
Functional Types of Neurons:
Sensory (Afferent) Neurons: Transmit impulses from sensory receptors (e.g., skin, eyes, nose) towards the CNS.
Motor (Efferent) Neurons: Transmit impulses away from the CNS to muscles and glands (effectors).
Interneurons (Association Neurons): Lie entirely within the CNS, forming connections between sensory and motor neurons and playing a crucial role in integration and complex neural circuits.
Structural Classification:
Multipolar Neurons: Have one axon and multiple dendrites; most common type in the CNS (e.g., motor neurons, interneurons).
Bipolar Neurons: Have one axon and one dendrite extending from opposite sides of the cell body; found in special sensory organs (e.g., retina, olfactory bulb).
Unipolar (Pseudounipolar) Neurons: Have a single process extending from the cell body that then divides into an axon and a dendrite; primarily sensory neurons.
Glia (Neuroglia)
Non-neuronal cells that provide support, nourishment, and protection for neurons, but do not transmit nerve impulses themselves. They outnumber neurons significantly.
Types of Glia in the Central Nervous System (CNS):
Astrocytes: Star-shaped cells that are the most abundant glia. They support neurons, regulate the chemical environment (e.g., regulate ion concentrations, neurotransmitter uptake), form the blood-brain barrier, and assist in synaptic formation and function.
Oligodendrocytes: Form myelin sheaths around axons in the CNS, increasing the speed of nerve impulse transmission. One oligodendrocyte can myelinate multiple axons.
Microglia: Small, mobile cells that act as the immune cells of the CNS. They phagocytize cellular debris, pathogens, and damaged neurons, playing a role in inflammation.
Ependymal Cells: Line the ventricles of the brain and the central canal of the spinal cord. They produce cerebrospinal fluid (CSF) and help circulate it.
Types of Glia in the Peripheral Nervous System (PNS):
Schwann Cells: Form myelin sheaths around axons in the PNS. Unlike oligodendrocytes, one Schwann cell typically myelinates a single segment of an axon. They also aid in axon regeneration.
Satellite Cells: Surround neuron cell bodies in PNS ganglia, providing structural support and regulating the chemical environment.
F. The Synapse and Nerve Impulse Transmission
Communication between neurons occurs at specialized junctions called synapses.
Nerve Impulse Transmission (Action Potential)
Resting Membrane Potential: A neuron at rest maintains an electrical potential difference across its membrane, typically around -70 millivolts (mV), with the inside being more negative than the outside. This is maintained by the sodium-potassium pump (pumping 3 Na+ out for every 2 K+ in) and differing membrane permeability to ions.
Threshold: When a neuron receives sufficient stimulation, its membrane potential depolarizes to a critical level, usually around -55 mV, known as the threshold.
Depolarization: Upon reaching the threshold, voltage-gated sodium (Na+) channels open rapidly, causing a massive influx of Na+ ions into the cell. This makes the inside of the membrane briefly positive, reaching about +30 mV.
Repolarization: Immediately after depolarization, voltage-gated sodium channels inactivate, and voltage-gated potassium (K+) channels open, allowing K+ ions to flow out of the cell. This restores the negative charge inside the membrane.
Hyperpolarization: K+ channels close slowly, leading to a brief period where the membrane potential becomes even more negative than the resting potential (e.g., -90 mV). The sodium-potassium pump then quickly restores the resting potential.
All-or-None Principle: An action potential either fires completely once the threshold is reached, or it doesn't fire at all. The strength of the stimulus does not affect the amplitude of the action potential, only its frequency.
Propagation: The depolarization at one point on the axon triggers the opening of voltage-gated channels in adjacent regions, propagating the action potential along the axon.
Myelination and Saltatory Conduction: In myelinated axons, action potentials "jump" from one Node of Ranvier (gaps in the myelin sheath) to the next. This "saltatory conduction" significantly increases the speed of nerve impulse transmission compared to unmyelinated axons.
The Synapse
The junction where an action potential is transmitted from one neuron (presynaptic neuron) to another neuron or an effector cell (postsynaptic cell).
Components:
Presynaptic Neuron: The neuron sending the signal. Its axon terminal contains synaptic vesicles filled with neurotransmitters.
Synaptic Cleft: The small gap between the presynaptic and postsynaptic membranes.
Postsynaptic Neuron/Cell: The cell receiving the signal. Its membrane contains receptors for neurotransmitters.
Steps in Synaptic Transmission:
An action potential arrives at the axon terminal of the presynaptic neuron.
This depolarization opens voltage-gated calcium (Ca2+) channels in the presynaptic membrane.
Ca2+ ions rush into the presynaptic terminal.
The influx of Ca2+ causes synaptic vesicles to fuse with the presynaptic membrane, releasing neurotransmitters into the synaptic cleft via exocytosis.
Neurotransmitters diffuse across the synaptic cleft and bind to specific receptors on the postsynaptic membrane.
This binding causes ion channels on the postsynaptic membrane to open, leading to a change in its membrane potential:
Excitatory Postsynaptic Potential (EPSP): Causes a depolarization, making the postsynaptic neuron more likely to fire an action potential.
Inhibitory Postsynaptic Potential (IPSP): Causes a hyperpolarization, making the postsynaptic neuron less likely to fire an action potential.
The effect of neurotransmitters is terminated by:
Reuptake: Neurotransmitters are reabsorbed by the presynaptic neuron or glial cells.
Enzymatic Degradation: Enzymes in the synaptic cleft break down neurotransmitters.
Diffusion: Neurotransmitters diffuse away from the synaptic cleft.
Neurotransmitters: Chemical messengers that transmit signals across synapses (e.g., Acetylcholine, Dopamine, Serotonin, GABA, Glutamate, Norepinephrine).