Download Free Medical Cns Neurotransmitters and Basis of Drug Action in The Cns PowerPoint Presentation

Cns Neurotransmitters and Basis of Drug Action in The Cns PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "CNS Neurotransmitters & Basis of Drug Action in the CNS".

This medical PowerPoint presentation tells us how neurotransmitters play a critical role in CNS function, and drugs that target these neurotransmitters or their receptors can be used to treat a wide range of neurological and psychiatric disorders.

The central nervous system (CNS) is responsible for coordinating and controlling most of the bodys activities, including movement, sensation, thought, and behavior. Communication between neurons in the CNS is mediated by neurotransmitters, which are chemical messengers that transmit signals across synapses.

There are many different neurotransmitters in the CNS, including dopamine, serotonin, norepinephrine, acetylcholine, glutamate, and gamma-aminobutyric acid (GABA). Each of these neurotransmitters has a specific role in regulating different aspects of CNS function, and imbalances in their levels can contribute to various neurological and psychiatric disorders.

Drugs that act on the CNS often do so by altering the activity of these neurotransmitters. For example, drugs that increase the availability of dopamine in the brain can help alleviate symptoms of Parkinsons disease, while drugs that block the reuptake of serotonin can be effective treatments for depression. Similarly, drugs that enhance the activity of GABA can be used to treat anxiety and seizure disorders, while drugs that block the action of glutamate can help reduce the symptoms of schizophrenia.

Other drugs act on the CNS by targeting specific receptors or enzymes involved in neurotransmitter signaling. For example, drugs that block the activity of acetylcholinesterase can be used to treat Alzheimers disease, while drugs that bind to specific types of opioid receptors can be used to relieve pain.

Tags : CNS Neurotransmitters, CNS function, neurological and psychiatric disorders, central nervous system, pharmaceuticals, pharmaceuticals PowerPoint presentations

Published on : Jun 23, 2023 | Views : 993 | Downloads : 2

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

CNS Neurotransmitters & Basis of Drug Action in the CNS
Slide 2-

Neurotransmitters in the CNS 1. Amino acids e.g., Glutamate, Aspartate, GABA, and Glycine 2. Biogenic amines e.g., Norepinephrine, Dopamine, Serotonin, & Histamine 3. Choline ester e.g., Acetylcholine 4. Purines e.g., Adenosine & ATP 5. Lipid-soluble gases e.g., Nitric oxide; carbon monoxide 6. Neuroactive peptides: Opioids (Enkephalins, dynorphins, & endorphins) Tachykinins; Secretins; Insulins, and Gastrins Pituitary Releasing, & Inhibiting hormones
Slide 3-

Consequences of Neurochemical Imbalance in the Brain – a Simplified View
Slide 4-

Life Cycle of Neurotransmitters
Slide 5-

Biosynthesis of Acetylcholine Choline + Acetylcoenzyme A (acetyl CoA) choline acetyltransferase Acetylcholine Acetyl coA comes from the oxidative decarboxylation of pyruvate from glycolysis Majority of choline comes from diet while small amounts are produced in the liver The rate-limiting step of the synthesis of ACh is choline transport into neuron ACh is stored in vesicles via Ach/H+ antiporter (against ACh conc. gradient; down H+ conc. gradient) Vesamicol inhibits Ach/H+ antiporter
Slide 6-

L-Tyrosine Derived Neurotransmitters
Slide 7-

L-Tyrosine Derived Neurotransmitters Endogenous catecholamines: Dopamine, Norepinephrine (NE), and Epinephrine (EPI ) are derived from L-Tyrosine Rate-limiting step of the entire cascade is the conversion of L-Tyrosine to DOPA (catalyzed by tyrosine hydroxylase)
Slide 8-

Biosynthesis of Serotonin Precursor – Amino acid L-Tryptophan; important enzymes: Tryptophan hydroxylase, and Aromatic L-Amino Acid decarboxylase Rate-Limiting step - The conversion of L-Tryptophan to 5-Hydroxytryptophan by Tryptophan hydroxylase.
Slide 9-

Synthesis & Metabolism of glutamate and GABA Glutamate is synthesized from α-Ketoglutarate (from the Krebs cycle), a transamination reaction catalyzed by GABA transaminase (GABA-T) Glutamate is subsequently decarboxylated by glutamic acid decarboxylase (GAD) to GABA GABA is stored in Presynaptic vesicles by a transporter (VGAT) – the same as neurons that release glycine
Slide 10-

ppt slide no 10 content not found
Slide 11-

Postsynaptic targets of CNS transmitters action Ionotropic receptors: Activation of these receptors results in direct opening of ion channels resulting in rapid excitatory or inhibitory postsynaptic potentials (EPSPs or IPSPs) Examples: glutamate NMDA , AMPA & Kainate (excitatory); GABAA receptors (inhibitory) Metabotropic or G-protein coupled Receptors: Activation of these receptors activates the Intracellular 2nd messenger cascade Examples: α-/β-Adrenoceptors; Histamine H1/H2; Muscarinic M1/M3; Serotonergic (except 5-HT3) receptors, etc. Autoreceptors – on pre-synaptic nerve terminals, and K+ channels – on glial cells
Slide 12-

Centrally-acting drugs act via Four Broad Mechanisms Neuron-specific actions – such drugs interact with the transporters and ion channels maintaining neuronal electrical properties. E.g. Sedatives-hypnotics, antiparkinsonian drugs. Transmitter-specific actions- drugs that interfere with the life cycle of specific transmitter molecules. E.g. antidepressants and antipsychotic drugs acts this way Signal-specific actions - drugs mimic or interfere with specific signal transduction systems shared by different receptors e.g. anticholinesterases (treatment of Alzheimer’s disease) “General” actions on molecules expressed by all cell types, e.g., DNA, lipids, & structural proteins
Slide 13-

CNS effects via Neuron-Specific Actions Inhibitory neurotransmitters, e.g., Glycine, GABA (γ-Amino butyric acid) opens Cl- channels , resulting in post-synaptic target hyperpolarization GABA can also open K+ channels resulting in pre- or post-synaptic target Hyperpolarization Excitatory neurotransmitters, e.g., Glutamate, Aspartate, Acetylcholine opens Na+ or Ca2+ channels, resulting in depolarization of post-synaptic targets (increase inward currents) Glutamate can also cause depolarization via closing K+ channels (decrease outward currents)
Slide 14-

INHIBITORY POSTSYNAPTIC POTENTIALS (IPSPs) K+, Cl- at the postsynaptic , Ca2+ at the presynaptic -70 mV
Slide 15-

EXCITATORY POSTSYNAPTIC POTENTIALS (EPSPs) Na+, K+, Ca2+ -70 mV