Autonomic nervous system Flashcards

Question

3 major anomalies (exceptions to the rule) | for release of Neurotransmitter

Answer 1

Adrenal medulla (acts like a ganglia but releases NE and Epi as HORMONES) Norepi 20% Epi 80% Sweat glands Innervated anatomically by SNS Post ganglionic nerve releases Ach onto a muscarinic Ach receptor Thus … “sympathetic cholinergic fibers” Blood vessel smooth muscle Almost all have no innervation by PSNS However, there are muscarinic Ach receptors present on the blood vessels (activate NO with eventual vasodilation if you had a situation with circulating Ach)

Answer 2

``` Cholinergic Receptors(responde to acetycholine)Parasympathetic side Nicotinic Ach receptors Nm and Nn Muscarinic Ach receptors M1-5 ``` Adrenergic receptors(responds to NE..sympathetic) Alpha (1,2) Beta (1, 2, 3)

Answer 3

 (1,2) |  (1, 2, 3)

Answer 4

Activation of G-protein coupled receptor (D,Beta and alpha)) NT binds receptor & activates a G-protein G-protein will activate or inhibit an intracellular enzyme (adenylate cyclase→cAMP, phospholipase C) or will open or close an ion channel Usually the G-protein “cascade” has an eventual positive or negative effect on the amount of intracellular Ca2+ = physiological effect Receptor type will dictate the activity of the G protein Example Beta-1 receptors increase cAMP via G proteins. cAMP stimulates the Na-K pump and protein phosphorylation reactions leading to metabolic and pharmacologic effects we see clinically (increased heart rate and contractility, etc.)

Answer 5

Different parts of the body have different types & densities of receptors (skeletal muscle VS venous smooth muscle VS myocardium VS bronchial smooth muscle etc.) The specific effect depends on the type of receptor stimulated, receptor density in a given tissue, and what the second messengers activate at a molecular level in the cell. Receptors will up or down regulate based upon plasma concentrations of catecholamines (endogenous or exogenous)

Answer 6

Adenylate cyclase activates cAMP = smooth muscle dilation (Bronchioles blood vessels) Increased cAMP = vasodilation (also increased strength of cardiac contraction*, and increased heart rate*) Decreased cAMP= vasoconstriction PLC(Phospholipase C) activated activates IP3 & DAG results in increased PKC and increased free Ca2+ = vasoconstriction * Again… do not forget that The specific effect depends on the type of receptor stimulated, receptor density in a given tissue, and what the second messengers activate at a molecular level in the cell.

Answer 7

The Big table

Answer 8

Muscarinic and Nicotinic receptors

Answer 9

Muscarinic receptors (G-Protein Coupled) M1, M3, M5 inositol phosphate pathway (primarily) M2, M4 inhibit adenylyl cyclase reduce cAMP (primarily) M1: CNS, stomach M2: Widely expressed cardiac (inotropy/chronotropy), ganglia smooth muscle bladder, GI, uterus M3: smooth muscle, glandular tissues, work with M2 M4: CNS (ganglia) M5: cerebral bld vessels, pupil, esophagus, parotid gland

Answer 10

Nm: skeletal muscle at NMJ Nn: autonomic ganglia, adrenal medulla, CNS All Nn receptors are not parasympathetic.

Answer 11

Synthesis Choline (active transport brings it into the cytoplasm) and acetyl coenzyme A (formed by mitochondria) form acetylcholine under the influence of the enzyme choline acetyltransferase Storage Stored in synaptic vesicles released in response to an action potential Metabolism Brief effect <1 ms rapid hydrolysis by acetylcholinesterase to choline and acetate Choline is transported back into nerve endings used for synthesis of new acetylcholine

Answer 12

Norepinephrine* alpha 1,alpha 2,beta 1.......no effect or need alot to activate beta 2 Epinephrine alpha1,alpha 2,beta 1 and beta 2 .release from Medulla Dopamine D1=D2 need more to affect beta and a lot more for alpha

Answer 13

Formation In cytoplasm dopamine formed Dopamine enters synaptic vesicle In synaptic vesicle converted to norepinephrine Storage and Release Norepi stored in vesicle until action potential With action potential the norepi is released from postganglionic SNS nerve endings into ECF via exocytosis Effect of Norepi is affected by reuptake… Termination of Action Reuptake back into postganglionic sympathetic nerve endings (#1- 80% of released norepi can be reused) Dilution by diffusion from receptors Metabolism by the enzymes monoamine oxidase (MAO- cytoplasm) and catechol-o-methyltransferase (COMT - liver)

Answer 14

Formation - synthesized in the medulla of the adrenal gland (chromaffin cells) in the same enzymatic pathway that coverts the amino acid tyrosine into NE and dopamine (epinephrine is the final step) Storage and Release – Released after simulation of the adrenal medulla by pre-ganglionic sympathetic neurons by Ach Termination of Action – COMT and MAO

Answer 15

pls go through it

Answer 16

Innervated by preganglionic fibers that bypass the paravertebral ganglia Fibers directly from spinal cord to adrenal medulla Cells of adrenal medulla are analagous to post-ganglionic neurons SNS stimulation results in release of catecholamine hormones (released into systemic circulation instead of the synapse) 80% epinephrine 20% norepinephrine

Answer 17

Release of epi & norepi by adrenal medulla occurs after acetylcholine is released by preganglionic cholinergic fibers Acetylcholine increases the permeability of calcium by acting on plasma membrane receptors of adrenal medulla cells Calcium ions result in the exocytosis of the hormones into systemic circulation Results = similar to direct stimulation by the SNS however prolonged response 10-30 seconds (COMT)

Autonomic nervous system Flashcards

(42 cards)