INTRODUCTION TO CNS PHARMACOLOGY
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1 INTRODUCTION TO CNS PHARMACOLOGY Central nervous system is nothing but a network of neuronal cells interacting each other with many inhibitory and excitatory neurotransmitters which regulate all the body functions and protect against various external and internal insults through immediate refluxes and long term compensative and regenerative processes. Complete understanding of the functional physiology and neuroanatomy of central nervous system is far beyond our knowledge at least for now.the term Central Nervous system refers to Brain and Spinal cord. Actions through which CNS regulate entire body functions to maintain homeostasis are classified into Psychic (manifested by thoughts, emotions and attitude), somatic (body movements)and autonomic(respiratory, circulatory, and visceral functions) signals. Based on the predominant manifestations CNS disorders could be classified into Neuroses, Psychoses and Affective disorders. WHO Classification of CNS Drugs 1. Anxiolytic sedatives (hypnotics, sedatives, minor tranquillizers) Drugs that cause sleep and reduce anxiety Examples:Barbiturates, benzodiazepines and ethanol 2. Antipsychotic drugs (neuroleptics, major tranquillizers, anti-schizophrenia Drugs that are effective in relieving symptoms of schizophrenic illness Examples :Phenothiazines and butyrophenone 3. Antidepressant drugs (thymoleptics) Drugs that alleviate the symptoms of depressive illness Examples :TCA, MAOI, SSRI 4. Psychomotor stimulants (Psychostimulants) Drugs that can cause wakefulness and euphoria Examples :Amphetamines, Cocaine, and caffeine 5. Hallucinogenic drugs (psychodysleptics, psychotomimetics) Drugs that cause disturbance of perception and of behavior in ways that cannot be simply characterized as sedative or stimulant effects Examples :Lysergic acid diethylamide (LSD), mescaline and phencyclidine
2 Others Analgesics (opiate) Katamine (anesthetics) Nootropics drugs (Piracetam) Most drugs that act on the CNS do so by changing ion flow through transmembrane channels of nerve cells. 2 MAJOR TYPES OF ION CHANNEL IN CNS VOLTAGE-GATED ION CHANNELS(Respond to changes in membrane potential) Distribution: Concentrated on the axons of nerve cells eg: Include the sodium channels responsible for action potential propagationcell bodies and dendrites also have voltage-sensitive ion channels for potassium and calcium LIGAND-GATED ION CHANNELS (Chemically-gated) These channels respond to chemical neurotransmitters (NTAs) that bind to receptor subunits of the channel NTAs also bind to G protein-coupled receptors (metabotropic receptors). Found on all cell bodies and on both the presynaptic and postsynaptic sidesof the synapses. TYPES OF RECEPTOR-CHANNEL COUPLING Through a receptor that acts directly onthe channel protein Through a receptor that is coupled to the ion channel through a G protein Through a receptor coupled to a G protein that modulates the formation of diffusible second messengers - Cyclic AMP, Inositol triphosphate (IP3), Diacylglycerol (DAG) ROLE OF THE ION CURRENT CARRIED BY THE CHANNEL SYNAPSE- Ion current carried by channel synapse develop either EPSPs or IPSPs depending on the receptor and neurotransmitter involved. These potentials are the basic tools of neuronal communication. 1. EXCITATORY POSTSYNAPTIC POTENTIALS(EPSPs) Depolarizing potential change generated by opening of sodium or calcium channels closing of potassium channels (EPSPs) Na+, K+, Ca+2.
3 2. INHIBITORY POSTSYNAPTIC POTENTIALS(IPSPs) Hyperpolarizing potential change generated by opening of potassium or chloride channels (K+,Cl- at the postsynaptic, Ca+2 at the presynaptic) SITES AND MECHANISMS OF DRUG ACTION Some drugs exert their effect through direct interactions with molecular components of ion channels on axons Carbamazepine, Phenytoin, Local anesthetics and some drugs used for general anesthesia.most drugs exert their effect mainly at the synapses. May act presynaptically to alter synthesis/ Storage/ Release/ Reuptake/ Metabolism of transmitter chemicals.drugs may Activate or block Pre- and postsynaptic receptors for specific transmitters, Interfere with the action of second messengers, Inhibits synthesis (eg; serotonin Reserpine), Inhibits storage (eg; catecholamines Amphetamine), Inhibits release (eg; catecholamines Anticholinesterase), Inhibits degradation. Most of the drugs acting on CNS are modulators of neurotransmission. There are three processes occurring in connection with impulse transmission with nervous system i.e. 1. Neurotransmission process by which impulse is transmitted across a synapse 2. Neuromediation elicitation of the responses to the released neurotransmitters through neuromediators (second messengers eg: camp, inositol phosphate) 3. Neuromodulation thought to occur at pre and post synaptic levels to modulate all the steps of neurotransmission including synthesis and release on neurotransmitters (NTs) and post synaptic excitability or induces long term changes through affecting gene transcription. Neuromodulators (e.g. Adenosine prostaglandins and nitric oxide) arise from neuronal and nonneuronal cells as well and are not stored or released like NTs. They have long latent period and duration of action. CRITERIA FOR NEUROTRANSMITTER STATUS 1. Should be Present in higher concentration in the synaptic area than in other areas (localized in appropriate areas) 2. Should be Released by electrical or chemical stimulation via a calcium-dependent mechanism
4 3. Should exhibit Synaptic mimicry (External administration of the candidate should produce effects similar to the stimulation of the nerve at which the chemical is proposed to be a neurotransmitter or in other words Produce the same sort of postsynapticresponse that is seen with physiologicactivation of the synapse). CHEMICALS ACCEPTED AS NTs IN THE CNS 1. ACETYLCHOLINE (Ach) - 5% of neurons has receptors for Ach (G protein-coupled muscarinic M1 receptors which produce slow excitation bydecrease permeability to potassium are the major type in CNS). 2. DOPAMINE - Inhibitory actions at synapses in specific neuronal systems (G proteincoupled D2 receptor which Increase camp and activates of K+ channelsis the main dopamine subtype. 3. NOREPINEPHRINE - Excitatory effects through α1 and β1 receptors by decrease in K+ conductance and Inhibitory effects by activation of α2 and β2 receptors by Increase in K+ conductance are major norepinephrine mediated action in CNS. 4. SEROTONIN -There are multiple 5 hydroxytryptamine (5-HT) receptor subtypes which are metabotropic- Inhibitory at many CNS sites and excitatory at some depending on the receptor subtype activated. 5. GLUTAMIC ACID- Is excitatory for most neurons, receptors for glutamate are named after some specific agonists.n-methyl-d-aspartate (NMDA) receptor, AMPA (αaminohydroxy methylisoxazole propionic acid) receptors and Kainate receptors. 6. GABA AND GLYCINE-GABA is the primary NTA mediating IPSPs. GABAA receptor activation opens Cl- conductance, GABAB receptor activation opens K+ channels, closes Ca+2 channels. Glycine is more numerous in the spinal cord, is inhibitory by IncreasingCl- conductance. 7. OPIOID PEPTIDES -Three major receptors mu, kappa and delta endogenous opioid peptides E.g.; Beta-endorphins, dynorphins areinhibitory (presynaptic)by decrease Ca+2 conductance, Inhibitory (postsynaptic) by Increase K+ conductance. Alcohol Major known constituent of all the alcoholic drinks are Ethyl alcohol or ethanol, only caffeine is used more widely for recreational, non-therapeutic purpose and may be are one of the world most abused chemical. Types of Alcohol 1. Ethanol (ethyl alcohol, grain alcohol) 2. Methanol (methyl alcohol, wood alcohol) 3. Isopropanol (isopropyl alcohol, rubbing alcohol) 4. Ethylene glycol
5 Routes of Administration 1. Topical 2. Inhalation 3. Intravenous injection 4. Oral ingestion Pharmacokinetics of alcohol Factors affecting absorption 80% absorption from upper intestine thus, rate limiting factor is stomach emptying but total absorption is unaffected by food 1. Alcohol concentration of the ingested beverage - Optimal absorption occurs for beverages with alcohol concentrations between 10% alc. v/v and 30% alc. v/v. Beverages <10 % alc. v/v do not present as large a concentration gradient. Beverages >30% alc. v/v will irritate the gastric mucosa and increase mucous production. 2. Changes in blood supply to the GI tract -Changes in motility will affect the speed with which ethanol enters the small intestine 3. Presence of food in the stomach- Food in the stomach will prolong gastric emptying time, resulting in a lower, delayed peak blood alcohol concentration Metabolism and excretion a. 95% of alcohol is metabolized by alcohol dehydrogenase enzyme and CYP450 enzymes b. 85% of that metabolism is in the liver c. up to 15% is done in the stomach i. All women, alcoholic or not, have 60% less stomach alcohol dehydrogenase than men ii. Women appear to be even more vulnerable than men to intoxication and chronic effects d. Two-step metabolism: step 1 Alcohol is converted by alcohol dehydrogenase to acetaldehyde (co-factor: NAD+ to NADH), step 2 Acetaldehyde is converted by aldehyde dehydrogenase (ALDH)to acetic acid, then to CO2 and water in the Krebs cycle (ATP to AMP) e. Zero order metabolism (?- refer general pharmacology)
6 f. Disulfiram- The ant abuse drug used in alcohol dependence treatment blocks the step two of alcohol metabolism (by competitive inhibition of ALDH) this raises the blood level of acetaldehyde which effects cardiovascular system. After a week s therapy with disulfiram even a small amount of alcohol leads to toxic reactions like flushing, perspiration, palpitation, marked nausea, vomiting and fall in BP. Distribution (90% + access to all body compartments) 1. Alcohol is hydrophilic and will distribute into fluids and tissues according to water content.total body water (TBW) is dependent upon Age,Sex, Body weight 1. Effect of sex: If Man weighing 150 lbs and Woman weighing 150 lbs consume 2 beer BAC of the man will be 57 mg/100 ml and BAC of the woman will be 67 mg/100 ml 2. Effect of weight: If Manweighing 150 lbs and Man weighing 200 lbs consume 2 beer BAC of the lighter man will be 57 mg/100 ml BAC of the heavier man will be 43 mg/100 ml Pharmacodynamics of alcohol Mechanism of action of alcohol is not unitary in the effects but vary according to the plasma concentrations 1. High doses may disrupt membrane functioning ( fluidization ) 2. Low doses act on synapses, particularly glutamate. 3. Inhibits NMDA receptors for glutamate and decreases glutamate release a. Intoxication produces memory loss; glutamate transmission is reduced at BAC of 0.03% b. Abstinence syndrome hyperexcitability from up-regulation of NMDA receptors i. Withdrawal seizures due to up-regulated NMDA receptors c. Increased glutamate release during withdrawal is excitotoxic on up-regulated NMDA receptors: brain damage 4. GABA effects a. GABAA-2L subunit: ethanol is an agonist
7 i. protein kinase phosphorylation ii. intracellular mrna changes iii. GABA antagonists picrotoxin (Cl- channel blocker) and bicuculline (GABA competitor) are partial antagonists for EtOH iv. GABA agonists increase ethanol s effects b. GABA-consequent effects on Ach, NMDA, and DA 5. Inhibits release of Ach: Cognitive impairment 6. Agonizes DA from VTA to nucleus accumbens, the reward center. - Addiction is thus a combination of DA positive reinforcement and GABA negative reinforcement. 7. Opioid effects Effects on body could be summarized into 1. Vasodilatation - Creates a feeling of warmth when alcoholic beverages are consumed and contributes to paradoxical undressing in hypothermia deaths 2. Disinhibition -Responsible for the stimulant effects of alcohol llikeeuphoria, talkativeness, sociability. 3. Central nervous system depressant causes non-selective depression of brain and spinal cord and effects occur on a continuum - with increased BAC, increased effects occur :Sedated Sleepy Stuporous Unconscious and effects are additive with other CNS depressant. Stages of Alcohol Intoxication
8 mg/100 ml Loss of motor function Response to stimuli Stupor, unconsciousness Vomiting, incontinence Hypothermia mg/100 ml Unconsciousness Coma Depression of reflexes Impairment of respiration, circulation Death Alcohol intoxication is the major risk factor for positional asphyxiation. Central nervous system depression causes relaxation of the muscles that keep the airway open during sleep Tolerance Chronic use of alcohol will result in a decreased susceptibility to the effects of alcohol,visible signs of intoxication are decreased, Increased survivability even after consumption of large amounts of alcohol. Tolerance to alcohol may be either functional and/or metabolic in nature.
9 Treatment of acute and chronic alcoholism. 1. Management of acute alcohol toxicity. Intoxication due to acute intake of ethanol is managed by maintenance of vital signs and prevention of aspiration of vomitus. Treatment of Hypoglycemia and ketosis can be made by giving I.V glucose, Thiamine [IV or IM] and correction of electrolytes also be required. 2. Management of chronic alcohol dependence Alcohol dependence is treated with pharmacological approaches. a. The first approach to pharmacotherapy is to render ethanol consumption unpleasant [aversion therapy] by giving disulfirum. Dose 1g on first day, reduce by 250mg daily. Keep 250mg for maintenance daily. b. Naltrexone an opioid receptor antagonist in a dose of 50mg once a day is used to treat alcohol dependence. It has been demonstrated that opioid antagonist inhibit craving for alcohol while opioids incrase craving for alcohol. c. Recently, it has been shown that the anticonvulsant drug topiramate is also effective in reducing craving in chronic alcoholics. The drug potentiates the inhibitory effects of GABA [like benzodiazepine] but acts at a site different from benzodiazepine and barbiturates.
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