Peripheral Nervous System - Efferent Div (230 #7) Flashcards Preview

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autonomic nervous system

originates: brain or lateral horn of SC
# of neurons: two-neuron chain (preganglionic and postganglionic)
organs: cardiac muscle, smooth muscle, exocrine glands and some endocrine glands
type: dually innervated by sympathetic and parasympathetic (antagonistic)
neuroTx: para = acetylcholine, symp = norepinephrine
effects: either stimulation or inhibition
control: involuntary
higher: SC, medulla, hypothalamus, prefrontal association cortex


somatic nervous system

originates: ventral horn of SC, muscles in head are in brain
# of neurons: single neuron
organs: skeletal muscle
type: only by motor neurons
neuroTx: only acetylcholine
effects: stimulation only (inhibition through IPSPs on dendrites and cell bodies of motor neurons)
control: voluntary, much activity subconciously coordinated
higher: SC, motor cortex, basal nuclei, cerebellum, brain stem


preganglionic fibre

the cell body in the first neuron in the two-neuron chain is in the CNS. The axon (preganglionic fibre) synapses with the cell body of the second neuron, inside a ganglion.


postganglionic fibre

the axon of the second neuron in the two-neuron chain - innervates the effector organ.


sympathetic system

origin of PRE: thoracic and lumbar region of SC
origin of POST: sympathetic ganglion chain (near SC) or collateral ganglia (halfway btwn SC and organ)
length: short cholinergic pre, long adrenergic post
organs: cardiac muscle, almost all smooth muscle, most exocrine, some endocrine
types of neuroTx receptors: pre = nicotinic, post = alpha 1 & 2, beta 1 & 2
dominance: 'fight or flight', prep for strenuous physical activity


parasympathetic system

origin of PRE: sacral and cranial region of SC
origin of POST: terminal ganglia
length: long cholinergic pre, short cholinergic post
organs: cardiac muscle, most smooth muscle, most exocrine, some endocrine
types of neuroTx receptors: pre = nicotinic, post = muscarinic
dominance: 'rest & digest', relaxed situations, housekeeping


adrenal medulla

modified sympathetic ganglion which releases epinephrine and norepinephrine into the blood. Is the inner portion of the two adrenal glands next to the kidneys. Does not give rise to postganglia. About 20% of neuroTx is NE, and 80% is epinephrine - both reinforce sympathetic.


acetylcholine (ACh)

neurotransmitter released by:
1) autonomic preganglia
2) parasympathetic postganglia
3) sympathetic postganglionic at sweat glands and some blood vessels in skeletal muscle
4) terminals of efferent motor neurons
5) CNS



neuroTx released by:
1) most sympathetic postganglia
2) adrenal medulla
3) CNS


tonic activity

when both sympathetic and parasympathetic systems are partially active - some level of action potential activity is in both fibres to the organ. DOMINANCE is when one is increased and the other is decreased simulataneously. Sympathetic dominance is more common.


dual reciprocal innervation

dual control exerted by autonomic system provides more precise control. i.e. hear rate can be reduced more rapidly by simultaneously decreasing the firing rate in the cardiac sympathetic nerve (letting up on the accelerator) AND increasing activity in the parasympathetic activity to the heart (applying the brake).


exceptions to dual innervation

1) innervated blood vessels receive only sympathetic nerve fibres (except for those in penis & clitoris)
2) sweat glands only have sympathetic (post fibres secrete ACh instead of NE)
3) salivary glands have both, but action is not antagonistic


Cholinergic Receptors

1) nicotinic - opens Na+ and K+ channels in autonomic postganglionic cells, Na+ movement brings depolarization that leads to AP in postganglionic cell.
2) muscarinic - 5 different subtypes, found on effector cell membranes where parasympathetic postganglionic fibres innervate. Linked to G proteins that activate 2nd messenger.


Adrenergic Receptors

catecholamine receptors, two types:
1) alpha (1 & 2) - greater sensitivity to norephinephrine. Stimulation of A1 elicits desired response to Ca2+ 2nd messenger (excitatory), while binding to A2 blocks cAMP in target cell (inhibitory)
2) beta (1,2,3) - target cell response by cAMP 2nd messenger.
B1 - bind primarily with epinephrine, excitatory, in the heart
B2 - bind with NE and E equally, inhibitory, resp, cardiac, etc
B3 - least common, found in adipose tissue, excitatory for fat breakdown.



short-lived bronchiodialator that activates B2-adrenergic receptor sites to provide relief from bronchiospasms, but has implications for aerobic sports as an ergogenic aid. Selectively activates B2 to dialate the bronchioles at low doses without undesirably stimulating the heart (mostly B1 receptors in heart)



bind to the same receptor as the neuroTx and elicit an effect that mimics the neuroTx



bind with the receptor and block the neuroTx response



blocks the effect of ACh at muscarinic receptors (site of parasympathetic postganglia), but does not affect nicotinic receptors (sympathetic activity). Used to suppress salivary and bronchial secretions before surgery.


Control of Autonomic Activities

1) reflexes (urination, defecation, erection) are integrated at SC level
2) medulla in brain stem - cardio, resp, digestion
3) hypothalamus - integrates auto, somatic and endo responses for emotional & behavioural (anger, fear)
4) prefrontal association cortex - personality (blushing) mediated through hypothalamic-medullary pathways


motor neurons

innervate skeletal muscles - axons of which constitute the somatic nervous system. Cell bodies are in ventral horn, while those supplying cranial nerves are in the brain stem. Continuous ofrom its origin in the CNS to the ending on skeletal muscle - release ACh for excitation/contraction. Can only stimulate, not inhibit. Inhibition can only be accomplished in the CNS through inhibitory synaptic input to the dendrites.


Control of Somatic Activities

1) motor regions of the cortex
2) basal nuclei
3) cerebellum
4) brain stem
Considered FINAL COMMON PATHWAY since only influence of skeletal muscle is by the motor neurons.



cell bodies of crucial motor neurons are selectively destroyed resulting in paralysis of the muscles innervated by the affected neurons


Amyotrophic Lateral Sclerosis (ALS)

Lou Gehrig's disease - most common motor neuron disease. Pathological changes in neurofilaments that block axonal transport of crucial materials, extracellular accumulation of toxic levels of excitatory neuroTx glutamate, aggregation of misfolded intracellular proteins, or mitochondrial dysfunction leading to reduced energy production.


neuromuscular junctions

as the axon approaches a muscle, it divides into many terminal branches and loses its myelin sheath - forms a special junction with one of the many muscle cells that compose the whole muscle. TERMINAL BUTTON fits into a shallow depression (cleft) of the underlying muscle fibre, but does not come into direct contact. TB contains vesicles of ACh.


Release of ACh at Neuromuscular Junction

1) AP triggers opening of voltage-gated Ca2+
2) triggers influx of Ca2+ into TB, causes exocytosis of ACh
3) receptors pick up ACh at motor end-plate of muscle fibres (nicotinic type)
4) triggers chemically-gated Na+ into muscle fibre - depolarization is END PLATE POTENTIAL (EPP)


End Plate Potential -> AP

EPP is graded potential, but much larger than EPSP
1) more neuroTx is released from terminal button than from a presynaptic knob
2) motor end plate has higher surface area with higher density of receptors.
3) more ion channels open in response, greater change in potential.

EPP intiates AP because it reduces the adjacent area to threshold and the AP propagates along the fibre by contiguous conduction.


Acetylcholinesterase (AChE)

muscle cell's electrical response is turned off by an enzyme in the motor end-plate membrane. It binds with ACh (which only binds with receptors in the muscle cell briefly), inactivating it - process repeats until all of the ACh is deactivated.


Black Widow Spider Venom

triggers explosive release of ACh from the storage vesicles at ALL cholinergic sites. They all undergo prolonged depolarization - respiratory paralysis results from the diaphragm - during 'depolarization block', Na+ channels are trapped in inactivated state and cannot initiate new APs to contract the diaphragm.



blocks the release of ACh from the terminal button in response to motor neuron AP. Respiratory failure since the diaphragm cannot contract.



antagonist - reversibly binds to the ACh receptor sites on the motor end plate, but does not alter membrane permeability and is not deactivated by AChE. Blocks ACh from combining on blocked receptors - Respiratory failure since the diaphragm cannot contract.



group of chemicals that modify neuromuscular junction activity - irreversibly inhibits AChE, which blocks deactivation of ACh. Diaphragm is in 'polarization block' and cannot repolarize to have another AP (contraction) - resp failure. Used in military nerve gases and insecticides.


Myasthenia Gravis

disease involving neuronmuscular junctions - characterized by extreme muscular weakness. Autoimmune condition produces antibodies against its own motor end plate receptors - reduces chances for ACh to bind. Treatment includes 'neostigmine' - inhibits AChE temporarily to prolong the action of the ACh and give it a better chance of finding a receptor.