Exam 4 - Lecture 33, Intro to ANS Flashcards by Patryk Lasiuk

Central Nervous system

Main control centers for conscious thought and all body activities

Brain: located in cranial cavity

Spinal Cord: located in vertebral cavity

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Peripheral nervous system

connects CNS with organs and glands

12 pairs of cranial nerves
31 pairs of spinal nerves

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Miosis of pupil

Parasympathetic stimulation

Caused by activation of M3-R leads to constriction of the circular muscle

Acetylcholine, opiates and opioids cause

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Mydriasis

Sympathatic stimulation

Caused by activation of a1-R leads to constriction of radial muscle

Adrenaline, Anticholinergics, Cocaine, Amphetamine, Hallucinogens cause

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PNS subdivided into

Sensory (afferent) nerves and motor (efferent) nerves

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Two types of motor nerves

Somatic NS for voluntary contraction of skeletal muscles

Autonomic NS regulate involuntary control of smooth, cardiac muscles and glands

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Autonomic NS has two branches

Sympathetic and parasympathetic

Sympathetic stimulates tissues
Parasympathetic inhibit tissues

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Simplified scheme of ANS organization

CNS (Preganglionic neuron, almost always ACh, released onto nicotinic receptors)

Peripheral ganglion (Postganglionic neuron, AChi, NE released onto M/a,b receptors…onto target cell)

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Somatic system

Typically monosynaptic, ACh to N1 receptors

Heavily myelinated axon

Effect: Stimulatory

Effector organs: Skeletal muscle

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Sympathetic system

Preganglionic neuron releases ACh onto N2-Rs

Lightly myelinated

Most neurons release NE onto adrenergic GPCRs (alpha and beta)

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Parasympathetic system

Preganglionic neuron release ACh onto N2-Rs

Lightly myelinated

Most neurons release ACh onto muscarinic GPCRs (M1 - M5)

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Function of ANS

with endocrine system, regulates activity of most internal organs by innervating smooth muscle, cardiac muscle and glands

Independent of thought

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Characteristics of ANS

controls involuntary or reflex activities

Typically 2 neuron chain, Preganglionic neurons originate in brain or spinal cord, postganglionic neurons originate in ganglion located outside the CNS

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Gross Anatomy of ANS - Parasympathetic

Preganglionic fibers are long

Postganglionic fibers are short

Fibers originate in brain stem (cranial) or Sacral

Ganglia are within or near visceral effector organs

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Gross Anatomy of ANS - Sympathetic

Preganglionic fibers are short

Postganglionic fibers are long

Fibers originate in thoracic and lumbar spinal cord

Ganglia are close to spinal cord

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Sympathetic Nervous system

Generally stimulates the effector organ

Can be activated in emergencies, fight or flight reaction

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Key facts Sympathetic nervous system

Preganglionic fibers produce ACh (cholinergic fiber), and Postganglionic produce NE (adrenergic fiber)

Short pre-, long post-ganglionic fibers

Key facts Parasympathetic nervous system

Most pre- and post-ganglionic fibers produce ACh (cholinergic)

Long pre-, short post-ganglionic fibers

Generalized noradrenergic junction

tyrosine enters via Na+ dependent carrier
tyrosine converted to dopamine
Dopamine and related amines enter vesicles via VMAT
Dopamine converted to NE by DBH
Vesicles with NE (and other signaling molecules) released into synaptic cleft
NE activated postsynaptic adrenoreceptors
NE diffuses away and is taken back up into presynaptic neuron by NET

Alpha GPCR

Alpha-1 receptors (Gaq coupled)

Alpha-2 receptors (Gai coupled

Alpha-1 receptors

Gaq coupled

Mediate fight or flight response
cause constriction of blood vessels (control BP)

inhibit motility in gut by contracting sphincter muscles and relaxing non-sphincter tissue

Mobilize energy by breaking down liver glycogen to glucose

Alpha-2 receptors

Gai coupled

Presynaptic, provide feedback control for neurotransmitter release (decrease Ca2+ influx to decrease release of transmitter)

Beta GPCR

Beta-1 receptors (Gas coupled)

Beta-2 receptors (Gas coupled0

Beta-1 receptors

Cardiac, inotropic, chronotropic

Smooth muscle relaxation in the gut

Beta-2 receptors

Induce bronchodilaton Induce smooth muscle relaxation in the gut Induce conversion glycogen to glucose Stimulate secretion of insulin from the pancreas

Generalized cholinergic junction

1. Choline transported into presynaptic nerve terminal by Na dependent CHT 2. ACh synthesized from choline and acetly Co-A by ChAT 3. ACh enters vesicles via VAT 4. Release of vesicles requires increased intracellular Ca2+ flux through Nav channels in response to depolarization 5. ACh and other signaling molecules interact with postsynaptic receptors 6. ACh diffuses to presynaptic auto receptors and is metabolized by aceylcholinesterase

Nicotinic Receptors

Excitatory cation channels, cause membrane depolarization Respond in milisec, not as fast as Na

Muscarinic receptors

All GPCRs Effect depends on subtype and target organ M1,M3,M5, coupled to Gaq M2,M4 coupled to Gai

Two important points

some postganglionic neurons (sympathetic and parasympathetic) have both nicotinic and muscarinic receptors Some neurons are neither cholinergic or adrenergic

Sympathetic neurons signaling via NE, ATP and Neuropeptide Y

3 Phases of contraction in vascular smooth muscle 1. ATP binds P2X purinoceptor (cation channel) Depolarization opens CaV -> Up [Ca2+] -> contraction, calcium is from outside (Rapid response) 2. Ne -> a1-Rs -> Gaq -> PLC -> Up IP3 -> [Ca2+] -> contraction. Calcium is form internal store (Moderately fast response) 3. Neuropeptide Y acts at the Y1 receptor to cause slow contraction; mechanism is unclear (Slowest response)

Parasympathetic neuron signaling using ACh, VIP and NO

two phases of relaxation in vascular smooth muscle 1. Neuron releases NO, which diffuses to muscle cell. ACh binds to M3-R on endothelial cells, leading to more NO production from eNOS (endothelial nitric oxide synthase). The NO activates guanylate cyclase in the muscle cell, generating cGMP and promoting relaxation. 2. Neuropeptide VIP binds the VIP receptor which activates Gas -> Increase Adenylyl Cyclase (AC) -> Increase cAMP -> Increase PKA -> Decrease [Ca2+] -> decrease contraction

M2-R pathway

Gai -> Up GaB -> Up K+ current via GIRK/Kir3 channels (hyper polarization) Gai -> Down Adenylyl Cyclase -> Down cAMP -> Down PKA

Exception 1: some postganglionic neurons (sympathetic and parasympathetic) have both nicotinic and (multiple) muscarinic receptors

Activating M1 slower than M2, N causes Spike EPSP.....M1 responsible for slow EPSP, Peptides can cause Later, slow EPSP. M2 cause IPSP

Exception 1: some postganglionic neurons (sympathetic and parasympathetic) have both nicotinic and (multiple) muscarinic receptors

Activating M1 slower than M2, N causes Spike EPSP.....M1 responsible for slow EPSP, Peptides can cause Later, slow EPSP. M2 cause IPSP

Reflexes in ANS

Stimulus 1. Receptor in Viscera 2. Visceral sensory neuron 3. Integration center 4. Motor neuron 5. Visceral effector Response

Eye Example

Lens focuses light onto Fovea in the back of eye Myopia - Focal point in front of Fovea Hyperopia - Focal point behind Fovea

Astigmatism

Light ends up off of the Focal point

slow EPSP

IPSP

Peptides

Late, slow EPSP