Autonomic Nervous System

Structure and Function of the Autonomic Nervous System Organization of the Nervous System Functionally Target Systems): Two divisions: • Afferent (sensory). • Efferent (motor). • • Somatic (conscious movement and sensation). Visceral (autonomic). Afferent = toward the point of reference (CNS) Efferent = away from the point of reference (CNS) Elements of Motor System Effectors MOTOR SYSTEM Skeletal Muscle Smooth Muscle, Cardiac Muscle,& SYSTEM Glands SOMATIC MOTOR SYSTEM AUTONOMIC MOTOR (Sympathetic and Parasympathetic) CNS versus PNS The autonomic nervous system • Operates without conscious control • Receives information from enteroreceptors, special senses and somatic senses • Output (motor) pathways contain two neurons (preganglionic and postganglionic) innervating cardiac muscle, smooth muscle and glands • Output pathways have two divisions sympathetic and parasympathetic • Most organs receive dual innervation one causing excitation and the other causing inhibition The autonomic nervous system together with the endocrine system regulate the internal environment of the body – maintain homeostasis “the equilibrium of the body’s internal environment”. Changes from equilibrium are sensed by receptors and relayed to brain centers which send output responses (perhaps increased sympathetic output and decreased parasympathetic output) that restore homeostasis. ANS consists of both afferent (sensory) and efferent (motor) fibers. Autonomic two neurons ganglia Efferent (motor) Somatic ventral horn one neuron no synapse heavily myelinated excitatory lateral horns (intermediaolateral) Preganglionic: slightly myelinated. Postganglionic: non-myelinated. inhibitory or excitatory Craniosacral versus thoracolumbar output Sympathetic ANS A.Sympathetic ganglia: large and visible. B.Parasympathetic ganglia: Small and microscopic. Parasympathetic ANS • Hind gut. • Bladder and urethra. • Internal (and external) genitalia (except the body and the fundus of the uterus). Parasympathetic: Erection Sympathetic: Ejaculation Afferent (sensory) ANS 1. They come from body wall, limbs, and viscera. 2. Either follow (run with) somatic nerves or the incoming efferent autonomic fibers to the viscera. 3. Their cell bodies are either in the DRG or in the corresponding sensory ganglia of the cranial nerve. 1. Sensations like hunger, nausea, and sexual sensations. 2. Information necessary for the initiation of the visceral reflexes. 3. Visceral pain (stretch or lack of oxygen ). Visceral Pain • Special receptors sensitive to : • ischemia, stretching (tension of distension), • spasm of smooth muscles, irritation due to • inflammation, and chemical damage. • poorly localized. • Referred pain : e.g. Cardiac pain is referred to the upper • part of the chest and to the medial side of the left arm. FUNCTION OF THE ANS • The sympathetic responses prepare the body for emergency situations (the fight-or-flight responses). • The parasympathetic division regulates activities that conserve and restore body energy (energy conservation-restorative system). Function This complementary innervation by the parasympathetic and sympathetic systems pertains to glands and visceral vasculature but not skin or systemic vasculature. Sympathetic Preganglionic neuron in thoracic spinal cord, long ganglionic axon Adrenal gland a cluster of postganglionic cell bodies that release epinephrine & norepinephrine into blood Parasympathetic Preganglionic neuron in brainstem (cranial) or sacrum, short ganglionic axon Autonomic or Visceral Reflexes • A visceral autonomic reflex adjusts the activity of a visceral effector, often unconsciously. – changes in blood pressure, digestive functions etc – filling & emptying of bladder or defecation • Autonomic reflexes occur over autonomic reflex arcs. Components of that reflex arc: – – – – – sensory receptor sensory neuron integrating center pre & postganglionic motor neurons visceral effectors O. Loewi 1921Vagusstoff Adrenaline release by cocaine The autonomic nervous system together with the endocrine system regulate the internal environment of the body – maintain homeostasis “the equilibrium of the body’s internal environment”. Changes from equilibrium are sensed by receptors and relayed to brain centers which send output responses (perhaps increased sympathetic output and decreased parasympathetic output) that restore homeostasis. Mechanisms of indirect-acting and direct-acting adrenergic receptor agonists. Some indirect-acting agonists (e.g., cocaine) block norepinephrine reuptake, whereas other indirect-acting agonists (e.g., amphetamine) indirectly increase norepinephrine release from storage vesicles in sympathetic neurons. Direct-acting agonists bind to and activate adrenergic receptors. NE = norepinephrine a = a-adrenergic receptor b = b-adrenergic receptor. Downloaded from: StudentConsult (on 10 October 2006 01:45 AM) © 2005 Elsevier Sympathetic Cardiovascular system blood vessels to skeletal muscle to skin and viscera Heart rate, force of contraction Respiratory system diameter of air passages respiratory rate Eye accommodation Sweat gland Adrenal gland Parasympathetic none vasodilatation vasoconstriction increases increases increases dilate pupil distance vision increased secretion secretes E, NE decreases decreases decreases constrict pupil near vision none none Receptor Agonists and Antagonists • An agonist is a substance that binds to and activates a receptor, mimicking the effect of a natural neurotransmitter or hormone. • An antagonist is a substance that binds to and blocks a receptor, preventing a natural neurotransmitter or hormone from exerting its effect. • Drugs can serve as agonists or antagonists to selectively activate or block ANS receptors. Adrenergic Neurons and Receptors • The main types of adrenergic receptors are alpha and beta receptors. These receptors are further classified into subtypes. – Alpha1 and Beta1 receptors produce excitation – Alpha2 and Beta2 receptors cause inhibition – Beta3 receptors (brown fat) increase thermogenesis • Effects triggered by adrenergic neurons typically are longer lasting than those triggered by cholinergic neurons. Autonomic nervous system effects on organs. All parasympathetic effects are mediated by muscarinic receptors. Sympathetic effects are mediated by a-adrenergic receptors (a), b-adrenergic receptors (b), or muscarinic receptors (M). Downloaded from: StudentConsult (on 10 October 2006 01:45 AM) © 2005 Elsevier Primary tissue locations of a -adrenergic and a -adrenergic receptors. Whereas a 1- and b2adrenergic receptors are primarily located in smooth muscle, b1-adrenergic receptors are predominantly found in cardiac tissue. Some a2-adrenergic receptors are located on sympathetic neurons, where they produce feedback inhibition of neurotransmitter release. Other a2- and b2adrenergic receptors are located in blood platelets and a variety of organ tissues. The a - and badrenergic receptors are also found in the central nervous system. Downloaded from: StudentConsult (on 10 October 2006 01:45 AM) © 2005 Elsevier A comparison of the effects of norepinephrine, phentolamine, and prazosin on heart rate. (A) Norepinephrine (NE) activates presynaptic a 2-adrenergic receptors (a 2), and this inhibits the formation of cyclic adenosine monophosphate (cAMP) and decreases the release of NE. (B) Phentolamine blocks a 2 receptormediated inhibition of NE release. This increases the stimulation of cardiac b 1-adrenergic receptors (b 1) and results in tachycardia. (C) Prazosin, a selective a 1-blocker, does not block a 2 receptormediated inhibition of norepinephrine release. Therefore, prazosin causes less tachycardia than does phentolamine. a 1 = a 1adrenergic receptors. Downloaded from: StudentConsult (on 10 October 2006 01:46 AM) © 2005 Elsevier Cholinergic Neurons and Receptors • Cholinergic neurons release acetylcholine – all preganglionic neurons – all parasympathetic postganglionic neurons – few sympathetic postganglionic neurons (to most sweat glands) • Excitation or inhibition depending upon receptor subtype and organ involved. Cholinergic and adrenergic neurotransmission and sites of drug action. (A) Acetylcholine (ACh) is synthesized from choline and acetate, stored in neuronal vesicles, and released into the synapse by nerve stimulation. Hemicholinium blocks choline uptake by the neuron and inhibits ACh synthesis. Vesamicol blocks ACh storage, and botulinum toxin blocks ACh release. ACh breakdown is inhibited by cholinesterase inhibitors. Postjunctional cholinergic receptors are activated or blocked by cholinergic receptor agonists or antagonists, respectively. (B) Norepinephrine (NE) is synthesized from tyrosine in a three-step reaction: tyrosine to dopa (dihydroxyphenylalanine), dopa to dopamine (DA), and dopamine to NE. The conversion of tyrosine to dopa is inhibited by metyrosine. The vesicular storage of DA and NE is blocked by reserpine, and the release of NE in response to nerve stimulation is blocked by bretylium. After activating postsynaptic receptors, NE is sequestered by neuronal reuptake, a process blocked by cocaine. Amphetamine indirectly increases the release of NE into the synapse. Postsynaptic adrenergic receptors are activated or blocked by adrenergic receptor agonists or antagonists, respectively. M = muscarinic receptors N = nicotinic receptors a = a -adrenergic receptors b = b -adrenergic receptors Downloaded from: StudentConsult (on 10 October 2006 01:45 AM) MAO = monoamine oxidase COMT = catechol-O-methyltransferase (-) = inhibits and (+) = stimulates. © 2005 Elsevier Adrenergic Neurons and Receptors • Adrenergic neurons release norepinephrine (NE) ) – from postganglionic sympathetic neurons only • Excites or inhibits organs depending on receptors • NE lingers at the synapse until enzymatically inactivated by monoamine oxidase (MAO) or catechol-Omethyltransferase (COMT) Physiological Effects of the ANS • Most body organs receive dual innervation – innervation by both sympathetic & parasympathetic • Hypothalamus regulates balance (tone) between sympathetic and parasympathetic activity levels • Some organs have only sympathetic innervation – sweat glands, adrenal medulla, arrector pili mm & many blood vessels – controlled by regulation of the “tone” of the sympathetic system Autonomic versus Somatic NS - Review • Somatic nervous system – consciously perceived sensations – excitation of skeletal muscle – one neuron connects CNS to organ • Autonomic nervous system – unconsciously perceived visceral sensations – involuntary inhibition or excitation of smooth muscle, cardiac muscle or glandular secretion – two neurons needed to connect CNS to organ • preganglionic and postganglionic neurons Sympathetic Responses • Dominance by the sympathetic system is caused by physical or emotional stress -- “E situations” – emergency, embarrassment, excitement, exercise • Alarm reaction = flight or fight response – dilation of pupils – increase of heart rate, force of contraction & BP – decrease in blood flow to nonessential organs – increase in blood flow to skeletal & cardiac muscle – airways dilate & respiratory rate increases – blood glucose level increase • Long lasting due to lingering of NE in synaptic gap and release of norepinephrine by the adrenal gland Parasympathetic Responses • Enhance “rest-and-digest” activities • Mechanisms that help conserve and restore body energy during times of rest • Normally dominate over sympathetic impulses • SLUDD type responses = salivation, lacrimation, urination, digestion & defecation and 3 “decreases”--decreased HR, diameter of airways and diameter of pupil • Paradoxical fear when there is no escape route or no way to win – causes massive activation of parasympathetic division – loss of control over urination and defecation The baroreceptor reflex. (1) Increased arterial pressure activates stretch receptors in the aortic arch and carotid sinus. (2) Receptor activation initiates afferent impulses to the brain stem vasomotor center (VMC). (3) Via solitary tract fibers, the VMC activates the vagal motor nucleus, which increases vagal (parasympathetic) outflow and slows the heart. At the same time, the VMC reduces stimulation of spinal intermediolateral neurons that activate sympathetic preganglionic fibers, and this decreases sympathetic stimulation of the heart and blood vessels. By this mechanism, drugs that increase blood pressure produce reflex bradycardia. Drugs that reduce blood pressure attenuate this response and cause reflex tachycardia. Downloaded from: StudentConsult (on 10 October 2006 01:45 AM) © 2005 Elsevier