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Autonomic Synapses

Physiology and Pharmacology

QuestionAnswer
Sympathetic NS Fight or flight Prepares body to face crisis, stress or physical activity Facilitation of motor responses Increases heart rate and blood pressure
Parasympathetic NS Rest and digest Body's housekeeping system Active during calm and rest Opposes SNS Leads to vasoconstriction - pale skin, fainting, cold, nausea
Double autonomic activation When both sympathetic and parasympathetic systems are activated Only during fainting and REM sleep
Organisation of neural pathways Afferents - petrosal ganglia to carotid sinus and nodose ganglia to aortic arch Efferents - paraSNA and SNA to heart, SNA to blood vessels and sympathetic ganglia to kidneys
Neurotransmitters used in sympathetic Ach in preganglionic neurons - nicotinic receptors Noradrenaline in postganglionic neurons - adrenergic receptors In adrenal gland Adrenaline is produced and secreted into blood - not a primary hormone
Neurotransmitters in parasympathetic Ach in both pre and post ganglionic neurons Pre - nicotinic receptors Post - muscarinic receptors Slower conduction velocity
Evidence for Vagus nerve action Loewi, Cannon found the vagus nerve stimulation decreases heart rate Took fluid from the heart after vagus stimulation and applied to another heart - decreased heart rate Proves it used chemical transmission - Ach
Cotransmission theory Both neuropeptides and gaseous transmitters used These can act as neuromodulators e.g. NPY in sympathetic
Features on NTs Presynaptic neuron must contain compound and synthesise it Compound released by presynaptic neuron on stimulation Micro application of compound to postsynaptic membrane mimics effects of stimulation of presynaptic neuron Can be altered by drugs
Somatic NS Effector - skeletal muscle Effect - excitation Innervation - single No. of neurons to effector - one Peripheral ganglia - no Transmitters - Ach with nicotinic receptors
Autonomic NS Effector - cardiac/smooth muscle, blood vessels Effect - excitation/inhibition Innervation - dual no. of neurons to effector - two Peripheral ganglia - yes Transmitters - Ach and noradrenaline
Ach synthesis and breakdown Acetyl CoA and choline joined by choline acetyltransferase to form acetylcholine Acetylcholine broken down by acetylcholinesterase to acetic acid and choline
Catecholamine synthesis Tyrosine converted to L dopa (Tyrosine hydroxylase) L-dopa converted to dopamine (DOPA Decarboxylase) Dopamine converted to Noradrenaline (Dopamine Beta-hydroxylase) Noradrenaline converted to adrenaline (Phenylethanolamine N-methyl Transferase)
Autoinhibition Neurotransmitters can bind to the presynaptic neuron Creates a negative feedback system, limiting release of the NT E.g. to prevent a massive blood pressure increase
Receptors in Autonomic NS - sympathetic Adrenergic receptors All are G protein linked Ligands - adrenaline, noradrenaline B1 and B2 blocked by propanol used to treat high blood pressure - but does cause airway constriction
Types of adrenergic receptor Alpha 1 - smooth muscle contraction Alpha 2 - nerve terminals - inhibits release Beta 1 - increases rate and force of heart contraction Beta 2 - relaxes smooth muscle Beta 3 - lipolysis in brown fat
Receptors in Autonomic NS - parasympathetic Muscarinic and nicotinic receptors Muscarinic - G protein linked Nicotinic - channel Ligands - Ach
Subtypes of muscarinic receptors Neuronal - excites neurons M1 - acid secretion in stomach M2 - slows rate of heart contraction M3 - contracts smooth muscle
End organ responses Shows that vagus nerve slows heart rate - vagal stimulation leads to missed beat on excitation measuring Shows neurotransmitters are used - on addition of a NT in an organ bath tension reduces and AP duration increases (NA) or decreases (Ach)
Sympathetic intracellular signalling NA binds to Beta receptor Activates adenylyl cyclase Converts ATP to cAMP Activated PKA Activated CA channels in membrane and SR - calcium influx
Parasympathetic intracellular signalling ACh binds to M2 receptor Inhibits adenylyl cyclase Inhibits ATP conversion to cAMP Reduces PKA activation Inhibits calcium influx
Nitric oxidase synthases NO is a gaseous messenger that diffuses across cell membranes Catalytic conversion of L-arginine and oxygen to No, H2O and l-citrulline occurs by a nitric oxidase synthase complex This uses calmodulin dependent electron flow
Nitric oxide action A free radical that forms stable covalent bonds with haem groups e.g. haemoglobin and myoglobin This activates cGMP, which activates PKG, activates phosphoglycerates and cyclin dependent channels This inhibits Ca release
Hypertensive patients There is an important relationship between pressure and flow High pressure = high flow rate Risks blowing plaques off arterioles Leads to strokes and myocardial infarction
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