Exam 4 - Lecture 33, Intro to ANS Flashcards
Central Nervous system
Main control centers for conscious thought and all body activities
Brain: located in cranial cavity
Spinal Cord: located in vertebral cavity
Peripheral nervous system
connects CNS with organs and glands
12 pairs of cranial nerves
31 pairs of spinal nerves
Miosis of pupil
Parasympathetic stimulation
Caused by activation of M3-R leads to constriction of the circular muscle
Acetylcholine, opiates and opioids cause
Mydriasis
Sympathatic stimulation
Caused by activation of a1-R leads to constriction of radial muscle
Adrenaline, Anticholinergics, Cocaine, Amphetamine, Hallucinogens cause
PNS subdivided into
Sensory (afferent) nerves and motor (efferent) nerves
Two types of motor nerves
Somatic NS for voluntary contraction of skeletal muscles
Autonomic NS regulate involuntary control of smooth, cardiac muscles and glands
Autonomic NS has two branches
Sympathetic and parasympathetic
Sympathetic stimulates tissues
Parasympathetic inhibit tissues
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)
Somatic system
Typically monosynaptic, ACh to N1 receptors
Heavily myelinated axon
Effect: Stimulatory
Effector organs: Skeletal muscle
Sympathetic system
Preganglionic neuron releases ACh onto N2-Rs
Lightly myelinated
Most neurons release NE onto adrenergic GPCRs (alpha and beta)
Parasympathetic system
Preganglionic neuron release ACh onto N2-Rs
Lightly myelinated
Most neurons release ACh onto muscarinic GPCRs (M1 - M5)
Function of ANS
with endocrine system, regulates activity of most internal organs by innervating smooth muscle, cardiac muscle and glands
Independent of thought
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
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
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
Sympathetic Nervous system
Generally stimulates the effector organ
Can be activated in emergencies, fight or flight reaction
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
- Choline transported into presynaptic nerve terminal by Na dependent CHT
- ACh synthesized from choline and acetly Co-A by ChAT
- ACh enters vesicles via VAT
- Release of vesicles requires increased intracellular Ca2+ flux through Nav channels in response to depolarization
- ACh and other signaling molecules interact with postsynaptic receptors
- 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
- ATP binds P2X purinoceptor (cation channel)
Depolarization opens CaV -> Up [Ca2+] -> contraction, calcium is from outside (Rapid response) - Ne -> a1-Rs -> Gaq -> PLC -> Up IP3 -> [Ca2+] -> contraction. Calcium is form internal store (Moderately fast response)
- 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
- 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.
- 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
- Receptor in Viscera
- Visceral sensory neuron
- Integration center
- Motor neuron
- 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
M1
slow EPSP
M2
IPSP
Peptides
Late, slow EPSP
