Ch. 8 Glossary of Terms – Flashcards
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Unlock answers| Adhesion Molecules |
| For ex, the integrins and selectins. These are molecules that mediate the binding of cells to other cells or extracellular matrix molecules such as fibronectin. |
| Alleles |
| Variations of a single genetic locus. |
| Anaphylatoxins |
| Fragments of complement proteins released during activation. Result in increased vascular permeability and attract leukocytes. |
| Antibody (Ab) |
| A protein produced as a result of interaction with an antigen. The protein has the ability to combine with the antigen that stimulated its production. |
| Antigen (Ag) |
| A substance that can react with antibody. Not all antigens can induce antibody production; those that do are also called immunogens. |
| B cell (also B lymphocyte) |
| Strictly, a bursa-derived cell in avain species and, by analogy, a cell derived from the equivilent of the bursa in non-avian species. B cells are the precursors of plasma cells that produce antibody. |
| Cell-mediated (cellular) immunity |
| Immunity in which the participation of lymphocytes and macrophages is predominant. Cell-mediated immunity is a term generally applied to the type IV hypersensitivity reaction. |
| Chemokines |
| Low-molecular-weight proteins that stimulate leukocyte movement. |
| Chemotaxis |
| A process whereby phagocytic cells are attracted to the vicinity of invading pathogens. |
| Complement |
| A set of plasma proteins that is the primary mediator of antigen-antibody reactions. |
| Cytolysis |
| The lysis of bacteria or of cells such as tumor or red blood cells by indertion of the membrane attack complex derived from complement activation. |
| Cytotoxic T cells |
| T cells that kill other cells, eg, cells infected with intracellular pathogens. |
| Endotoxins |
| Bacterial toxins released from damaged cells. |
| Epitope |
| Site on an antigen recognized by an antibody. Also known as an antigenic determinant. |
| Hapten |
| A molecule that is not immunogenic by itself but can react with specific antibody. |
| Histocompatible |
| Sharing transplantation antigens. |
| Humoral immunity |
| Pertaining to immunity in a body fluid and used to denote immunity mediated by antibody and complement. |
| Hypersensitivity Reactions: Antibody-mediated sensitivity Type I Immediate |
| IgE antibody is induced by allergen and binds via its Fc receptor to mast cells and eosinophils. After encountering the antigen again, the fixed IgE becomes cross-linked, inducing degranulation and release of mediators, especially histamine. |
| Hypersensitivity Reactions Antibody-mediated hypersensitvity Type II |
| Antigens on a cell surface combine with antibody, which leads to complement-mediated lysis or other cytotoxic membrane damage. |
| Hypersensitivity Reactions Antibody-mediated hypersensitvity Type III Immune complex |
| Antigen-antibody immune complexes are deposited into tissues, complement is activated and polymorphonuclear cells are attracted to the site, causing tissue damage. |
| Hypersensitivity Reactions Cell-Mediated Hypersensitivity Type IV Delayed |
| T lymphocytes, sensitized by antigen, release cytokines upon second contact with the same antigen. The cytokines induce inflammation and activate macrophages. |
| Immune response |
| Developement of resistance (immunity) to a foreign substnace. It can be antibody-mediated (humoral), cell-mediated (cellular), or both. |
| Immunity Innate Immunity |
| Nonspecific resistance not acquired through contact with an antigen. It includes skin and mucous membrane barriers to infectious agents and a variety of nonspecific immunologic factors, and it may very with age and hormonal or metabolic activity. |
| Immunity Adaptive Immunity |
| Protection acquired by deliberate introduction of an antigen into a responsive host. Active immunity is specific and is mediated by either antibody or lymphoid cells (or both). |
| Immunoglobulin |
| A glycoprotein, composed of H and L chains, thaat functions as antibody. All antibodies are immunoglobulins but not all immunoglobulins have antibody function. |
| Immunoglobulin Class |
| A subdivision of immunoglobulin molecules based on structural (amino acid sequence) differences. In humans there are 5 immunoglobulin classes: IgG, IgA, IgM, IgE, and IgD. |
| Immunoglobulin subclass |
| A subdivision of the classes of immunoglobulins based on structural differences in the H chains. For human IgG there are 4 subclasses: IgG1, IgG2, IgG3, and IgG4. |
| Inflammation |
| Local accumulation of fluid and cells after injury or infection. |
| Interferon |
| One of a heterogeneous group of low-molecular-weight proteins elaborated by infected host vcells that protect noninfected cells from viral infection. Interferons, which are cytokines, also have immunomodulating functions. |
| Leukocyte |
| General term for a white cell. |
| Lymphocyte |
| A mononuclear cell 7-10 um in diameter containing a nucleus with densly packed chromatin and a small rim of cytoplasm. Lymphocytes include the T cells and B cells, which have primary roles in immuniy. |
| Macrophage |
| A phagocytic mononuclear cell derived from bone marrow monocytes and found in tissues and at the site of inflammation. Macrophages serve accesory roles in immunity, particularly as antigen-presenting cells (APCs). |
| Major histocompatibility complex (MHC) |
| A cluster of genes located in close proximity, eg, on human chromosome 6, that encode the histocompatibility antigens (MHC molecules). |
| Membrane attack complex |
| The end product of activation of the complement cascade, which contains C5,C6,C7,C8, and C9. The membrane attack complex makes holes in the membranes of gram-negative bacteria, killing them and, in red blood or other cells, resulting in lysis. |
| Monoclonal Antibodies |
| Each B lymphocyte produces antibody of a single specificity. However, normal B cells do not grow indefinitely. If B cells are fused to a myeloma cell by somatic cell hybridization and fused cells that secrete the desired antibody specificity are selected, an immortalized antibody-producing cell line, known as a hybridoma, is obtained, and these hybrid cells produce monoclonal antibodies. |
| Monocyte |
| A circulating phagocytic blood cell that develops into tissue macrophages. |
| Natural Killer (NK) cells |
| Large granular lymphoid cells with no known antigen-specific receptors. They are able to recognize and kill certain abnormal cells, eg, tumor cells, and also activate the innate response. |
| Opsonin |
| A substance capable of enhancing phagocytosis. Antibodies and complement are the 2 main opsonins. |
| Opsonization |
| The coating of an antigen or particle (eg. infectious agent) by substances, such as antibodies, complement components, fibronectin, and so forth, that facilitate uptake of the foreign particle into a phagocytic cell. |
| Plasma cell |
| A terminally differentiated B cell that secretes antibody. |
| Polymorphonuclear cell (PMN) |
| Also known as a neutrophil or granulocyte, a PMN is characterized by a multiobed nucleous. PMNs migrate from the circulation to a site of inflammation by chemokines and are phagocytic for bacteria and other particles. |
| T cell (also T lymphocyte) |
| A thymus-derived cell that participates in a variety of cell-mediated immune reactions. |
| Thymocytes |
| Developing T cells found in the thymus. |
| Vaccination |
| Induction of immunity by injecting a dead or attenuated form of a pathogen. |
| MOA:Local Anesthetics |
-Modifies sodium channel function by blocking the Na channel -Enhancing membrane excitability
-No interaction with pain receptors |
| LA Analogs are developed from: |
| COCAINE |
| SAR Local Anesthetics |
Lipophilic portion (aromatic) lined to an ester or amide intermediate chain linked to a hydrophilic portion (except in benzocaine)
Usually weak bases pKa 7-9 Electron donating=increase potency Electron withdrawing=decrease potency Branching=hinders metabolism=may increase toxicity |
| Atypical LA |
| Benzocaine because no hydrophilic chain |
| Local Anesthetics MOA (cont.) |
-LAs are amphoteric
-They block the action potential generated by blocking the sodium channels
-LAs work by being charged (ionized) but have to cross the membrance unionized to have an effect. |
| Local Anesthetics block conduction in this order: |
1. Small myelinated axons 2. Non-myelinated axons 3. Large myelinated axons
Thus, nociceptive and sympathetic transmission is blocked first. |
| Side effects of Local Anesthetics |
CNS side effects: agitation,confusion, tremors, convulsions, respiratory depression (death)
Cardiovascular side effects: myocardial depression, vasodilation (decreased bp)
|
| LA drug administed all ways |
| Lidocaine |
| Methods of LA administration |
1. Epidural anethesia: injected into epidural space/ spinal anesthesia and childbirth/ lidocaine and sometimes bupivacaine 2. Spinal anesthesia: injected into subarachnoid space/ surgery to abdomen, pelvis, leg; used when gen. anesthesia can not be used/ mainly lidocaine 3. Nerve block anesthesia:injected close to nerve trunks to produce loss of sensation PERIPHERALLY/ dentistry/ most drugs come in this form 4. Surface anesthesia: used in nose, mouth, bronchial tree, cornea, and urinary tract/ lidocaine, tetracaine, amethocaine, benzocaine 5. Infiltration anesthesia: direct into tissues and nerve branches/ minor surgery/ most drugs 6. IV regional anesthesia: injected IV distal to a pressure cuff/ limb surgery/ lidocaine and prilocaine |
| Main metabolite for lidocaine |
Monoethylglyinexylidide (has CNS toxicities) This metablote is created from N-dealkylation |
| Ideal local anesthetic agent |
|
| TTX (Tetrotoxin) |
-Act from OUTSIDE the membrane. -Independent of wheteher channel is open or closed.
From puffer fish: causes severe weakness to complete paralysis or death.
Not used clinically bc too expensice and poor tissue penetration bc low lipid solubility. |
| STX (Saxitoxin) |
-Act from OUTSIDE the membrane. -Independent of wheteher channel is open or closed.
From marine microorganism: gives "red tide" phenomenon. Typically with shellfish.
Not used clinically bc too expensice and poor tissue penetration bc low lipid solubility. |
| Are there any clinically used inverse agonists for benzos? |
| NO |
| 3 Groups of Hypnotic Drugs |
|
| Benzodiazepines |
-Most preferred
-Used for: reduction of anxiety and aggression, sedation (induction of sleep), reduction of muscle tone and coordination, and anti-convulsant therapy (epilepsy)
-They are well-absorbed orally. |
| Non-Benzodiazepine GABAA Agonists |
-Fewer side effects -Very lipophilic=rapid absorption -No active metabolites -Can be administered without regard to meals |
| Sleep hygiene |
|
| Transient Insomnia |
-Lasts less than 3 days -Caused by brief stressor -May respond to sleep hygiene
-Drugs: Lowest dose for 2-3 nights |
| Short Term Insomnia |
-3 days to 3 weeks -Caused by personal stressor -Sleep hygiene education is 1st step
Drugs: adjunctively for 7-10 nights |
| Long term Insomnia |
-Lasts more than 3 weeks -No stressor indicated -Medical evaluation reqd.
Drugs: Hypnotics prescribed |
| Ideal sedative-hypnotic drug |
|
| Benzodiazepines MOA |
-Act selectively on GABAA receptors. -They enhance the response to GABA by facilitatitng opening of GABA activated chloride channels. -When they bind they bind specifically to a site on the receptor, distinct from the GABA site, and act allosterically to increase affinity of GABA for receptor. -GABA-enhancing effect of Benzos reach a max at low concentrations which is why drug really only exerts effects for a couple of weeks. |
| Flumazenil |
Benzodiazepine ANTAGONIST
-Mainly used to reverse the sedative action of benzos during anesthesia and also in acute benzo overdose.
-Acts quickly and effectively when giver by injection.
-Convulsions may rarely occur. |
| What metabolite of benzodiazepines is known for the "hangover effect"? |
N-desmethyldiazepam (Nordiazepam) -Has a half-life of 60 hours. |
What is the most common route of administration of benzos?
|
| -mouth |
| What is the main route of metabolism by benzos? |
| All are metabolized by CYPs and are excreted as glucuronide conjugates |
| PK: benzos |
-Well absorbed orally
-High lipid solubility |
| Which patients should be closely monitored while on benzos? |
| elderly |
| 3 types of benzos |
1. Long acting (Medazepam, Chlordiazepoxide, Chlorazepate,Diazepam : All go through nordiazepam)
2. Short acting (Lorazepam)
3. Mid acting (Triazolam, alprazolam, midazolam, clonazepam, and temazepam and oxzepam) |
| Benzos: Side effects |
Drowsiness, confusion, amnesia...more pronounced with CNS depressants.
Considered relatively safe overall.
Tolerance and dependence are the main drawbacks. Short acting benzos have MORE abrupt withdrawal effects. Long acting benzos have slower and less intense onset of withdrawal. |
| Non-benzodiazepine sedative-hypnotic drugs |
"Z" drugs Zolpidem (Ambien) and Zaleplon (Sonata) Have affinity for GABAa receptor complex. More efficacious with fewer side effects. Very lipophilic and have rapid absorption. No active metabolites. Approved for 7-10 days at a time. |
| MOA: Barbiturates |
| Acts by enhancing the GABA action but are less specific than Benzos and NON-selective |
| Barbiturates: Side effects |
Ranging from sedation and reduction of anxiety to unconciousness and even death from respiratory/cardiac failure.
Drug interactions bc induce hepatic drug-metabolizing enzymes (CYPs)
|
| Two pathways for metabolism of EtOH |
1) Alcohol dehydorgenase pathway (ADH) -Primary pathway NAD+ to NADH
2) Microsomal EtOH Oxidizing system (MEOS) -NADPH to NASP -Only induced with chronic alcohol consumption.
Both give same metabolite: acetalaldehyde
|
| Naltrexone |
-Drug used to treat alcoholism
-Long-acting opiod antaganist blocks effects of alcohol at opiod receptors. -Reduces craving for alcohol, reduced relapse rate -Patient must be opiod free before treatment |
| Acamprosate |
Drug used to treat alcoholism
-Actions on GABA, glutamte, serotonin, noradrenergic, and dopaminergic receptors. -No drug-drug interactions -ADRs: GI related |
| Disulfarim |
Drug used to treat alcoholism
-Inhibitor of ALDH pathway-accumulation of acetaldehyde. -Causes extreme discomfort in patients that drink. -Drug inhibits metabolism of many other drugs. -Very low adherence with this medication. |
| Depression |
Most common affective disorder
-Can be very mild to severe -Emotional symptoms include misery,apathy,pessimism,low self-esteem,loss of motivation -Biological symptoms include: retarddation of thought, loss of libido, decrease in energy, sleep issues, loss of appetite. |
| Mania |
Excessive exuberance,enthusiasm, and self-confidence with very impulsive actions.
Combined with irritability, impatience, aggression, and sometimes delusions. |
| Unipolar depression |
Two types: 1) Endogenous depression: 25%; show familial pattern; unrelated to external stressors.
2)Reactive depression: 75%; Non-familial; caused by triggers. May also have symptoms of anxiety and agitation. |
| Bipolar depression |
-Depression alternates with mania. -Usually appears in early adult life. -Less common than other forms of depression but has a STRONG hereditary tendency.
|
| Monoamine theory of depression |
Most widely accepted depression theory. Proposed by Schildkraut in 1965. States: Depression is caused by a functional deficit in monoamine transmitters at certain sites in the brain. ex)serotonin, dopamine, etc. Mania is caused by excess.
Controversy with this theory bc many anomilies amongst the evidence. |
Tricyclic Antidepressants |
Block NE and 5-HT reuptake
Increase mood |
| Monoamine oxidase inhibitors (MAO) |
Increase stores of NE and 5-HT
Increase mood |
| Reserpine |
Inhibits NE and 5HT storage
Decreases mood |
| Alpha-methyltyrosine |
Inhibits NE synthesis
Decreased mood (calming of manic patients) |
| Methyldopa |
Inhibits NE synthesis
Decreases mood |
| ECT |
Increases CNS responses to NE and 5HT
Increases mood |
| Tryptophan |
Increases 5HT synthesis
Elevated mood in some studies |
| SERT (serotonin transporter) |
| Reuptake of 5HT is dependent on the COTRANSPORT of Na and Cl and COUNTERTRANSPORT of K. |
| NET (NE transporter) |
| Reuptake of NE is dependent on the COTRANSPORT of Na and Cl with intracellular K stimulation but WITHOUT the efflux of K. |
| Tail suspension Test |
Mice determine there is no escape and eventually stop struggling. Anti-depressants INCREASE struggling (not giving up) and sedatives DECREASE |
| Forced swim test (FST) |
"Persolt test of swimming despair"
Animal confined to inescapable test chamber
Anti-depressants increase time of animal not giving up. |
| SSRI drugs |
Selective inhibitors of serotonin reuptake
fluoxetine paroxetine sertraline fluvxamine citalopram |
| MAOI drugs |
phenelzine tranyclpromine isocarboxazid |
| Atypical antidepressant drugs |
Act like TCAs but have a different structure: maprotiline
Compounds with different pharmacological actions. These drugs do not affect amine reuptake: venlaflaxine, trazodone, buproprion
Atypical vs. TCA Atypicals have fewer side effects and produce action with less delay. |
| SAR: TCA |
Tricyclic ring (3 rings fused together) Center ring is always 7 membered Tertiary amine: rapidly N-dealkylated to 2nd amine Secondary amines are active compounds themselves and are administered as drugs. |
| TCA drugs |
Same pharmacophore just differnt R1s and R2s
Amitriptyline nortriptyline imipramide desipramide clomipramide |
| SSRI MOA and side effects |
Inhibits 5HT reuptake. Less likely than TCAs to cause side effects. Less dangerous in overdose than TCAs. Less effective than TCAs in severe depression.
Can cause serotonin syndrom=tremor,hyperthermia, and cardio collapse which can result in death. This is from too much serotonin in the synapse. |
| MAOI side effects |
-Among 1st used as antidepressant NOW third choice as one. -Side effects: hypotension, weight gain, severe hepatotoxicity (rare) -"Cheese reaction": Tyramine is normally metabolized by MAO, when given an MAOI the tyramine builds up and enhances its sympathomimetic effects. Results in hypertension, a severe headache, and can create an intracranial hemorrhage. |
| Anxiety |
anxiolytics used by 10% population
-expressed complaint: feeling of anxiety as a symptom -somatic effetcs: restlessness, agitation, tachycardia, sweating, weeping, GI disorders, and sleep disturbance.
|
| ECT |
-treatment for severe depression -at least as effective as antidepressant drugs -response rates range from 60-80% -most effective treatment for suicidal depression -main disadvantage: causes confusion and memory loss that lasts for days to weeks |
| Lithium |
-Controls the manic phase of bipolar and is effective in treating unipolar as well. -Given in an acute attack it is only effective in reducing mania. -MOA: not understood but we know it interferes with the formation of IP3 and cAMP. -Side effects are common. -Alternative mood stabilizing drugs: carbamazepine and valproate. |
| Phobic anxiety vs Panic disorder |
Phobic: triggered by specific circumstances (spiders)
Panic: attacks of overwhelming fear in association with marked somatic symptoms. |
| Elevated Plus Maze or Elevated Zero Maze |
-Animal models for testing anxiety drugs
-Rat placed in unfamiliar environment-normally stays immobile but alert (anxiety) -Immobility is reduced with administration of anxiolytics...also animal is more liekly to be in open spaces and is not afraid of falling off the maze. |
| Conflict Tests |
-animal model for testing anxiolytic drugs
-conflict element is introduced. -rat will cease to press the bar. -when drugs are admin. rat continues to press the bar in spite of punishment |
| What is the most important group of drugs for anxiety disorders? |
***Benzodiazepines
2nd most is 5-HT1A: no sedation)
Barbituates: now largely obsolete
Beta-adrenoceptor antagonists: used mainly to reduce physical symptoms of anxietyzx |
| Analgesia |
| Blocks pain and patient is still conscious. |
| Anesthesia |
| Causes insensibility to pain and all other stimuli and with or without consciousness. General anesthetics: unconcious Local anesthetics: concious |
| What is the most common route of anesthetics? |
| Inhalation |
| What chemical class do inhalation anesthetics belong to? |
| None |
| Lipid Theory (Meyer-Overton Correlation) |
| -There is a close correlation between anesthetic potency and lipid solubility. -MAC=minimal alveolar concentration An increase in MAC=a decrease in potency. (decrease in oil-gas partition) |
| Protein Theory |
| -Inhibit function of excitatory ionotropic receptors. (Glutamamte, ACh, 5HT) -Enhance function of inhibitory receptors. (GABA, glycine) |
| What are the most sensitive brain regions to anesthesia? |
| 1. Thalamus 2. Cortex 3. Hippocampus |
| What are the 4 stages of anesthesia? |
| 1. Analgesia (analgesia, amnesia, euphoria) 2. Delirium (excitment, combative behavior) 3. Surgical anesthesia (unconsiousness, decreased eye movt.) 4. Respiratory Paralysis (medullary depression,respiratory and cardiac arrest) |
| Which 2 anesthesia drugs do not have an effect on respiration? |
| NO and Ketamine |
| What is the main determinant of induction and recovery times with anesthesia? |
| -Blood/gas partition coefficient LOWER B/G FASTER induction/recovery LOWER solubility of blood, faster equilibrium process. ex)Ether has B/G 12 NO has B/G 0.5 =NO is much faster in induction and recovery. |
| MAC |
| Low # = Highly potent ex) Halothane has a MAC of 0.8 and NO has a MAC of 100. NO is not very potent while halothane is potent. |
| Ideal anesthetic agent |
| 1.Rapid and pleasant induction and recovery. 2. Adequate relaxation of skelatal muscles. 3. Potent enough to permit oxygen supply in mix. 4. Wide margin of safety. 5. Nontoxic 6. No adverse effect 7. Non-flammable 8. Nonreactive 9. Inexpensive |
| Halothane |
| -Widely used -Potent, non explosive -Hangover effect, High lipid solubility -With chronic use can cause liver damage bc of the halogens. |
| Nitrous Oxide (NO) |
| -Low potency -Rapid induction and recovery -Good analgesic |
| ENflurane and Isoflurane |
| Enflurane: Halogentated and very similar to halothane but less risk of toxicity. Faster ind/rec than halothane. Can cause seizures. Isoflurane: similar to enlurane but no seizures. Desflurane and Sevoflurane are also very similar to this but with faster onset/recovery. Isoflurane is better than enflurane which is better than halothane. -ane ending = general inhalation anesthetic |
| IV anesthetic agents |
| -Very fast ind/rec. -Can be supplemented with opiods and other drugs for combined effects. -Good for fast procedures. -Patient more at ease. -Primarily used to induce. |
| What are the IV anesthetic agents and which one is a barbituate? |
| Propofol, Etomidate, Thiopental Thiopental is a barbituate. |
| Ketamine |
| -Street drug...analog of PCP -Onset is slow (2-5 min) -Hallucinations and dysphoria can occur. -Used in minor procedures for kids. -Dissociative anesthesia: concious, but have amnesia and are insensitve to pain. |
| What are the 4 CNS drug targets? |
| 1. Ion channels 2. Enzymes 3. Receptors 4. Transport proteins |
| Receptors are: |
| -GPCR (metabotropic) -Kinase linked -Channel-linked (ionotropic) -Gene transcription recievers |
| Fast Transmitters |
| Ion channels glutamate, GABA, and ACh via ligand gated ion channels |
| Slow transmitters |
| GPCR monoamines, peptides, ACh via GPCR linked to ion channels with second messengers |
| Original vs Redefined concept of neurotransmission |
| Original: substance acts rapidly and at a short range on adjacent neurons. Redefined: chemincal mediators can be slow or fast and can be long-lasting. They can act at a considerable distance from their site of release. |
| Ionotropic receptors |
| Ion channel receptors -Subunits with 4 transmembrane domains -Exs) nicotinic, cholinergic, GABAa, glycine, glutamate, aspartate receptor, and 5HT3 receptors. |
| Metabotropic Receptors (GPCR) |
| Single subunit with 7 transmembrane domains. EXs) muscarinic, one subtype of GABA and glutamate, all amino acid and peptide receptors |
| What is the criteria for being a central neurotransmitter? |
| 1. NT must be PRESENT in presynaptic terminal of synapse. 2. NT must be released from presynaptic nerve concomitantly with presynaptic nerve ACTIVITY. 3. When applied to target cells effects of NT must be IDENTICAL. |
| Neurohormones |
| Site of release at posterior pituitary |
| Neuromodulators |
| Released by neurons and produce SLOWER responses...usually GPCR. |
| Neuromediators |
| Substances that participate in eliciting postsynaptic response to NT (cAMP and other 2nd messengers) |
| Neurotropic factors |
| Released mainly by NON-neuronal cells and act on tyrosine kinase receptors. They regulate gene expression and repair damage. |
| Major central NTs |
| -Amino acids: GABA, glycine, GLUTAMATE, and aspartate -ACh -Catecholamines: DA,NE,EPI -5HT |
| Minor central NTs |
| -Histamine -Peptides -Purines,diffusable mediators, cytokines |
| What are the inhibitory amino acid trnasmitters? |
| GABA and glycine |
| What are the excitatory amino acid transmitters? |
| Glutamate and Aspartate |
| GABAa |
| -ligand gated Cl-ion channel -3 subunits: alpha, beta, and gamma -MOST PROMINENT -GABA is the site of action for many neuroactive drugs (benzos, barbituates, ethanol, etc) -Agonists: Muscimol -Antagonists: Bicuculline, Flumazenil and Picrotoxinin |
| GABA b |
| GPCR 2 subtypes: 1a and 1b Agonitst: GABA and Baclofen Antagonists: Phaclofen and CGP35348 |
| GABAc |
| Transmitter gated Cl channel Not widely distributed |
| Glycine receptors |
| -Inhibitory -Many subtypes -Agonists: B-alanine ad Taurine -Antagonist: Strychnine |
| Glutamate and Aspartate |
| -Both have 4 subtypes and both have THREE ion channel receptors and ONE GPCR -Excitatory |
| Dopamine receptors(DA) |
| -GPCR only -Receptors are implicated in schizophrenia and parkinsons. |
| What is the most prominent catecholamine in the CNS? |
| Dopamine...it accounts for more than half in the CNS. |
| Norepinephrine (NE) |
| -Predominately inhibitory function -Important in: Arousel system, alertness, mood (deficiency=depression), BP regulation, and "reward system" |
| 5HT (serotonin) receptors |
| 14 subtypes with 4 broad classes: 1) 5HT1: GPCR 2) 5HT2: GPCR 3) 5HT3: Ligang gated ion channel 4) 5HT4-7: All GPCR |
| 5HT Functional aspects |
| 1) hallucination and behavioral changes 2) Sleep,wakefulness, moods, and emotions 3) Control of sensory transmission 4) Vomiting |
| Histamine receptors |
| 4 subtypes: All GPCR (H1 is most prominent) Located in hypothalamus Functions: Arousal, body temp, vascular dynamics *Blocking H1 receptors= sedation and has anti-emetic effect ...This is why antihistamines make you sleepy. |
| Effects of CNS drugs are? |
| Additive ex. Respiration depressed by morphine is further impaired by depressant drugs. |
| What are the 6 classes of CNS drugs? |
| 1. Anxiolytics/Sedatives 2. Antipsychotics 3. Antidepressants 4. Psychomotor stimulants 5. Psychotomimetics 6. Cognition enhancers |
