Study Notes on the Efferent Division of the Peripheral Nervous System
THE PERIPHERAL NERVOUS SYSTEM: EFFERENT DIVISION
LECTURE OBJECTIVES
Understanding the organization and significance of the efferent division of PNS.
Exploring the autonomic nervous system (ANS), its organization, and the roles of the sympathetic and parasympathetic nervous systems.
Understanding the somatic nervous system and the mechanism of message transfer to skeletal muscles.
OVERVIEW OF THE PNS
Input to CNS from periphery:
Peripheral nervous system (PNS) receives sensory stimuli.
Divided into two main divisions:
Afferent Division: Collects sensory data and transmits it to the Central Nervous System (CNS).
Efferent Division: Sends motor commands from the CNS to the periphery.
CNS Composition:
Consists of the brain and spinal cord.
Integrates information and coordinates responses.
Efferent Division:
Comprises motor neurons that target effector organs including:
Skeletal muscles (somatic nervous system) - voluntary control. Parts we can control.
Smooth muscles, cardiac muscles, exocrine glands, and some endocrine glands (autonomic nervous system - involuntary control).
Key Components of the Autonomic Nervous System
Sympathetic Nervous System: Mediates involuntary responses to stimuli. Fight or Flight mode.
Parasympathetic Nervous System: Facilitates bodily functions during restful states. Rest and Digest
Enteric Nervous System: Specifically controls digestive organs only.
STRUCTURE OF EFFERENT PNS
Efferent Division of PNS:
Functions as a communication link enabling CNS to control effector organs. The cell body located in the CNS gets the message from the Interneuron after it has been sent from the afferent neuron and then sends it to the target effector organ.
Composed of:
Autonomic nervous system (involuntary):
Controls cardiac muscles, smooth muscles, exocrine glands, and some endocrine glands.
Somatic nervous system (voluntary):
Directly controls skeletal muscles.
AUTONOMIC NERVOUS SYSTEM
Sympathetic and Parasympathetic
A GANGLION IS A CONNECTION OF THE NEURON CELL BODIES OUTSIDE THE CNS
Composed of two types of neurons
Preganglionic Fiber: This comes before from the CNS. The cell body is in the CNS which receives the message and the axon extends to the ganglion, where it synapses with the second type of neuron.
Emerges from CNS and releases acetylcholine (ACh).
Postganglionic Fiber: This is wha works on the effector organs. The cell body of the postganglionic fiber is located in the ganglion, and its axon extends to the effector organs, where it can release either norepinephrine or acetylcholine, depending on the specific function of the autonomic nervous system.
Extends to effector organ, releasing either ACh or norepinephrine (NE).
Ganglion: A cluster of neuronal cell bodies outside the CNS that connects CNS to organs.
Varicosity: Allows autonomic nerves to affect all effector organs simultaneously and rapidly. It affects all of the effector organs at once and quickly.
SUBDIVISIONS OF ANS
Sympathetic Nervous System
Origins: Nerve fibers emerge from thoracic and lumbar regions of the spinal cord.
Preganglionic Fibers:
Short in length and release acetylcholine (ACh).
Postganglionic Fibers:
Long fibers that primarily release norepinephrine and are termed adrenergic.
Synapse: Takes place at sympathetic ganglion chains or collateral ganglia.
Parasympathetic Nervous System
Origins: Nerve fibers stem from cranial and sacral levels of CNS.
Preganglionic Fibers:
Long, release acetylcholine (ACh).
Postganglionic Fibers:
Short, also release ACh (cholinergic).
Synapse: Most occur at terminal ganglia located near effector organs.
Key Components of ANS
Includes a variety of receptors like nicotinic and muscarinic for parasympathetic and adrenergic receptors for sympathetic.
Nicotinic Receptors: Located at postganglionic cell bodies and act as ion channels, causing depolarization upon activation. Parasympathetic.
Muscarinic Receptors: Found on effector organs; G-protein coupled receptors. Parasympathetic
Adrenergic Receptors: Bind to Norepinepherine and epinephrine; categorized into alpha and beta subtypes, with specific pathways and responses (e.g., excitatory or inhibitory).
CONTROL OF ANS
Involuntary Responses: Manage functions such as circulation, digestion, sweating, and urination.
Dual Innervation: Most visceral organs receive signals from both sympathetic and parasympathetic subdivisions, allowing for dynamic control: They all work together though sometimes one has more control over things than the other depending on what state the boy is in at that particular time. This balance between the two systems is essential for maintaining homeostasis and responding to changes in the internal and external environment.
Sympathetic Tone: Predominates during stress (flight or fight responses).
Parasympathetic Tone: Dominates under restful conditions (rest and digest).
SYMPATHETIC DOMINANCE
Prepares the body for emergency situations:
Dilates blood vessels supplying skeletal muscles.
Increases heart and respiratory rates. More blood and oxygen in and CO2 out.
Stimulates the conversion of glycogen to glucose in the liver.
Promotes sweating and dilates pupils and bronchioles. EX. Need to see when running.
Inhibits digestive processes and urination. Not really needed when in fight or flight mood. Who wants to stop running and pee in an emergency.
PARASYMPATHETIC DOMINANCE
Dominates in calm situations to facilitate:
When sitting ad resting body needs to relax
Decreased heart and respiratory rates.
Enhanced digestion and urination.
Overall conserves energy and maintains homeostasis, characterized by housekeeping activities. Look around and do some work essentially.
DUAL/RECIPROCAL INNERVATION
Advantages: Allows for precise control over effector organs.
Exceptions: Certain organs respond primarily to either the sympathetic or parasympathetic system, such as blood vessels (sympathetic only) and salivary glands (both but distinct responses).
Think of this as a brake and accelerator. Where the brakes and parasympathetic and the accelerator is sympathetic. Parasympathetic causes you to make more enzymes watery mouth where as sympathetic causes thick mucus think dry mouth when running.
TARGET SPECIFICITY
Involves receptor types that selectively bind neurotransmitters such as ACh and NE, affecting signaling specificity.
Cholinergic Receptors:
Nicotinic Receptors: Fast response via ion channels.
Muscarinic Receptors: Slower response via G-proteins.
Adrenergic Receptors: Subtypes exhibit varied sensitivity to neurotransmitters:
Alpha Receptors: More sensitive primarily to NE.
Beta Receptors: Primarily respond to E and NE, differing pathways that influence organ responses.
There are multiple receptors present for NE AND ACh. They are present in different locations. They are couple to different signaling pathways. Different kinds of receptors may have different sensitivity to the NT
SOMATIC NERVOUS SYSTEM
Function: Direct control of skeletal muscle through somatic motor neurons.
Anatomy:
Efferent neurons originate in the ventral horn of the spinal cord; axons project directly to muscles.
Distinguishing Features:
No synapsing in ganglia as in ANS; stimulation of skeletal muscle is direct. They have no preganglion or postganglions
Diseases: Associated motor neuron diseases such as Polio and Lou Gehrig’s disease (ALS).
Effector motor neurons are NOT also composed of two neuron chains. These features highlight the unique functioning of the efferent division, where a single motor neuron directly innervates skeletal muscles, thereby allowing for swift and voluntary motor control.
IMPORTANT!!!
Dorsal Horn, CELL BODIES OF INTERNEURONS ON WHICH AFFERENT NEURONS TERMINATE. As name suggests they are in the back.
Lateral Horn, CELL BODIES OF AUTONOMIC EFFERENT NERVE FIBERS.
Ventral Horn, CELL BODIES OF SOMATIC EFFERENT NEURONS. As name suggests in the front.
NEUROMUSCULAR JUNCTION
Structure:
Efferent neuron: Myelinated axon branching into terminal buttons which connect to muscle fibers. The axons are myelinated coming from the ventral horn and as they get closer to the muscle they slowly become unmyelinated.
ACh: Acts as the neurotransmitter released at the neuromuscular junction (NMJ). Only skeletal muscles have neuromuscular junctions. This is the connection between neuron and muscle skeletal.
Process: AP arrival at terminal button triggers exocytosis of ACh, leading to muscle fiber contraction. The terminal button is a knob-like terminal at the muscle fiber. The ACh binds to receptors on the muscle fiber's membrane, resulting in depolarization and the initiation of an action potential in the muscle, which ultimately leads to contraction.
Motor end plate is a muscle membrane below the terminal button.
ACh is the chemical messenger or neurotransmitter released when action potential reaches the terminal button. Leading to the generation of end plate potential
GENERATION OF END PLATE POTENTIAL
Mechanism: AP reaches the terminal button of the motor neuron which then causes or triggers the opening of voltage-gated calcium channels, allowing calcium influx which triggers ACh release.
All the calcium rushing in starts or intiates the exocytosis of ACh from the synaptic vesicles which are stored at the terminal button.
Once ACh has been released it binds to specific receptors that are located on the muscle fiber’s motor end plate, which is a specialized region of the muscle cell membrane.
This binding then leds to the influx of NA+ into the muscles causing depolarization of the muscles and this generates an action potential causing the muscle to contract.
After contraction, the muscle fiber relaxes as ACh is broken down by the enzyme acetylcholinesterase, which prevents continuous stimulation of the muscle. This process is crucial for the proper functioning of the neuromuscular junction and highlights the importance of neurotransmitter regulation in muscle physiology.
Termination: Acetylcholinesterase (AChE) breaks down ACh, ceasing the muscle activation signal. AChE is an enzyme present in the synaptic cleft. The regulation of ACh levels ensures that muscle contractions are precise and controlled, preventing issues such as muscle spasms or fatigue.
THEY ARE LIGAND-GATED CHANNELS BECAUSE THEY ARE BINDING TO ACh AND OPENING AND ALLOWING MOVEMENT OF IONS.
CHEMICAL AGENTS AND DISEASES AFFECTING NMJ
Toxins: Affect normal function of ACh release, potentially causing respiratory failure:
Black Widow Venom: Causes explosive ACh release.
Botulinum Toxin: Prevents ACh release at NMJ.
Curare: Blocks receptors at the motor end plate.
Organophosphates: Irreversible inhibit AChE activity.
Myasthenia Gravis: Autoimmune disorder leading to loss of ACh receptors, resulting in muscle weakness.