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Autonomic NS
PPT 3
| Term | Definition |
|---|---|
| Somatic system | -associated with Ach NTs -Nicotinic receptors |
| Parasympathetic Nervous System | "rest & digest" associated with Ach NTs -Muscarinic receptors |
| Sympathetic Nervous System | "fight or flight" associated with NE NTs -Adrenergic and Dopamine receptors (a, b, D) *exception=sweat glands (Ach NT and M receptor) |
| Structure of the SNS - location of preganglionic cell bodies | Thoraco-lumbar |
| Structure of the PNS - location of preganglionic cell bodies | Cranio-sacral |
| Structure of the SNS - location of ganglia, length of fibers | 1) sympathetic chain ganglia 2) collateral ganglia short preganglionic & long post-ganglionic |
| Structure of the PNS - location of ganglia, length of fibers | near effector organ (terminal) long preganglionic & short post-ganglionic |
| Structure of SNS vs PNS - divergence of neurons | more divergence in the SNS vs PNS |
| CN lll | Oculomotor Nerve type-motor function-eye movement |
| CN Vll | Facial Nerve type-mixed function-sensory for taste |
| CN IX | Glossopharyngeal Nerve type-mixed function-sensory from oral cavity, baro- and chemoreceptors from blood vessels |
| CN X | Vagus Nerve type-mixed function-sensory and efferent neurons from many organs |
| important PNS cranial nerves | CN 3,7,9,10 |
| activation of Vagus nerve | associated with the PNS "rest & digest" functions ex) slows heart rate |
| SNS and Adrenal Medulla | releases NE 20% and EPI 80% |
| PNMT | converts NE to EPI |
| storage of EPI | stored in chromaffin granules until released |
| PNS dominates in: | heart, bronchi, GI tract, bladder |
| SNS dominates in: | adrenal medulla, blood vessels, skeletal muscles |
| inhibition of one division leads to ____activity of the other division | increased activity |
| blood vessel diameter is regulated solely by the ___ | SNS |
| exceptions to vasoconstriction & vasodilation | "fight or flight" -BV in skeletal muscle dilate -BV in GI constrict to limit flow |
| CNS regulation of ANS | reflex activity is highly regulated by the CNS -limbic lobe sends info to frontal lobe & hypothalamus |
| reflex activity of ANS is mediated by: | the spinal cord and brain stem centers (medulla oblongata, pons, midbrain) |
| medulla oblongata | contains the cardiac center & the vasomotor center -oversees GI activities |
| pons | contains the respiratory center |
| midbrain | contains oculomotor nerve |
| Baroreceptors | stretch-sensitive nerve endings -maintains stable mean arterial pressure (MAP) |
| Carotid baroreceptors | maintain blood flow to the brain |
| Aortic arch baroreceptors | maintain peripheral BP |
| Autoreceptors | presynaptic receptors that mediate the release of the SAME Neurotransmitter |
| Heteroreceptors | presynaptic receptors that mediate the release of a DIFFERENT neurotransmitter |
| Receptor regulations | -auto/hetero -receptors -desensitization -down/up regulation |
| Receptor Desensitization | prolonged stimulation by agonist decreases ABILITY of receptor's response to stimulation -leads to drug tolerance |
| Receptor downregulation | prolonged stimulation by agonist reduces NUMBER of receptors available for binding -leads to drug tolerance |
| Receptor upregulation | long-term blockade of receptors increases the number of receptors ex) effect of an antagonist |
| Biosynthesis of Ach at the Cholinergic Synapse (2) (PNS) | in the pre-synapse Choline + Acetyl-CoA combine by enzyme ChAT |
| Biosynthesis of Ach at the Cholinergic Synapse (1) (PNS) | Choline is transported in the pre-synapse by Na+ dependent choline transporter (CHT) -transporter can be blocked by drug Hemicholinium |
| Biosynthesis of Ach at the Cholinergic Synapse (3) (PNS) | Ach is transported from cytoplasm into vesicles by transporter VAT, along with peptides and ATP -transporter blocked by drug Vesamicol |
| Release of Ach at the Cholinergic Synapse (4) (PNS) | Ca2+ channels activate via action potential and vesicles fuse to pre-synapse --> expulsion of Ach into synaptic cleft -process blocked by drug Botulinum toxin |
| Metabolism of Ach at the Cholinergic Synapse (5) (PNS) | released Ach can act on: muscarinic GPCR or Nicotinic ionotropic receptors or endplate of skeletal muscle |
| Metabolism of Ach at the Cholinergic Synapse (6) (PNS) | Ach is metabolized in the synapse by Acetylcholinesterase to acetate and choline |
| Metabolism of Ach at the Cholinergic Synapse (7) (PNS) | Ach can also bind to autoreceptors and heteroreceptors on the pre-synapse, to control further release |
| Catecholamines (SNS) | small molecule NTs -benzene with 2 ortho -OH & side chain amine |
| principal catecholamines in the body: | NE, EPI, Dopamine |
| Biosynthesis of NE & EPI: | Tyrosine>Dopa>Dopamine> (NE>EPI) (occurs only in adrenal medulla) |
| Tyrosine hydroxylase | converts Tyrosine>Dopa |
| Dopa decarboxylase | converts Dopa>Dopamine |
| Dopamine b-hydroxylase | converts Dopamine>NE |
| MAO & COMT enzymes | metabolize catecholamines to inactive metabolites (VMA & HVA) |
| Biosynthesis of NE at the Noradrenergic synapse (1) (SNS) | Tyr is transported into nerve terminal by Na+ dependent carrier |
| Biosynthesis of NE at the Noradrenergic synapse (2) (SNS) | Conversion in cytoplasm: Tyr>Dopa>Dopamine |
| Biosynthesis of NE at the Noradrenergic synapse (3) (SNS) | transport of Dopamine from cytoplasm into vesicle by VMAT -VMAT blocked by the drug Reserpine |
| Biosynthesis of NE at the Noradrenergic synapse (4) (SNS) | Conversion in the vesicle: Dopamine>NE |
| Release of NE at the Noradrenergic synapse (5) (SNS) | action potential opens Ca2+ channel, & vesicles fuse with surface membrane --> expulsion of NE, peptides, ATP into cleft -process blocked by Guanethidine & Bretylium |
| Release of NE at the Noradrenergic synapse (6) (SNS) | NE acts on GPCRs on postsynaptic neuron or neuroeffector organ (e.g. BVs) |
| Release of NE at the Noradrenergic synapse (7) (SNS) | NE can also diffuse out of cleft --> metabolized by liver enzyme MAO |
| Release of NE at the Noradrenergic synapse (8) (SNS) | NE can transport back into the nerve terminal by norepinephrine transporter (NET) -Cocaine and TCA drugs block NET |
| Release of NE at the Noradrenergic synapse (9) (SNS) | NE can also bind to autoreceptors and heteroreceptors on the presynaptic nerve ending, to control further release |
| Release of NE at the Noradrenergic synapse (10) (SNS) | NE can also be metabolized by enzyme COMT in the postsynaptic tissues |
| Botulinum toxin | blocks release of Ach into the Cholinergic synapse |
| Cocaine & Tricyclic Antidepressants (TCAs) | block norepinephrine transporter (NET) |
| Guanethidine & Bretylium | blocks release of NE, peptides, ATP into the Noradrenergic synapse |
| which synapse recycles the NTs? | Noradrenergic synapse |
| which synapse doesn't recycle the NT? (is a waster) | Cholinergic synapse |
| ANS effects on the eye | 1) pupil size 2) aqueous humor synthesis 3) far & near vision (accommodation) |
| Mydriasis | SNS a1 receptor activation contracts radial (dilator) fibers of iris (pupil dilation) |
| Miosis | PNS M3 receptor activation contract SPHINCTER (circular) fibers of iris (pupil shrinkage) |
| effect of a2 receptors on ciliary body epithelium (aqueous humor) | decrease secretion of aqueous humor |
| effect of b2 receptors on ciliary body epithelium (aqueous humor) | increase secretion of aqueous humor |
| effect of b2 receptors on ciliary muscles (accommodation) | ciliary m. relax, suspensory ligaments pull against lens, lens become less convex (more flat) -for FAR vision |
| effect of M3 receptors on ciliary muscles (accommodation) | ciliary m. contract, suspensory ligaments relax, lens become more convex (oval) |
| accommodation of the eye effects the ___ | curvature of the lens (see near or far) |
| Hemocholinium | inhibits --> Choline is transported in the pre-synapse by Na+ dependent choline transporter (CHT) |