Term
|
Definition
| A common metabolite that is converted to a neurotransmitter from 1 or more enzymatic reactions |
|
|
Term
|
Definition
| Tyrosine -> (with TH) L-Dopa -> DA -> NE -> EPI |
|
|
Term
| tyrosine hydroxylase (TH) |
|
Definition
| The enzyme that produces L-DOPA from tyrosine. It is the slow step in the reaction of catecholamines, or the rate limiting step! |
|
|
Term
|
Definition
| Amino Acid precursor. the first precursor to the catecholamines (DA, NE, EPI) |
|
|
Term
|
Definition
| The second precursor for the catecholmaines (DA, NE, EPI. Avoids the rate limiting step, can be administered for the increase for all 3 of them. Administering LDOPA really helps with Parkinsons (increases Dopamine levels) |
|
|
Term
|
Definition
Very much like the catecholamine synthesis (other monoamines)
Tryptophan -> (with TrpH) -> 5-HTP -> 5-HT (serotonin) |
|
|
Term
|
Definition
| Amino acid precursor. The first precursor to serotonin synthesis. This combined with tryptophan hydroxylase is the slow rate limiting step |
|
|
Term
| Tryptophan Hydroxylase (TrpH) |
|
Definition
| The enzyme that creates 5-HTP from tryptophan. Is known as the rate limiting slow step |
|
|
Term
|
Definition
| the second precursor to 5-HT (serotonin) synthesis. Avoids rate limiting TrpH step. Can be used as a drug to create serotonin. Helps with anxiety and insomia! |
|
|
Term
|
Definition
| the drug that blocks the formation of tyrosine hydroxylase, which blocks catecholamine synthesis! |
|
|
Term
|
Definition
| This causes L-DOPA To create alpha methyl dopamine, not dopamine! Alphamethyl dopamine is a "fake dopamine", so there is no post synaptic action and therefore no dopamine effects on the body. this helps people with high blood pressure! |
|
|
Term
|
Definition
| p-chlorophenylalanine! This inhibits TrpH and therefore inhibits 5-HT (serotonin levels). Used mainly for research. |
|
|
Term
|
Definition
| AcetylCoA + Choline -> (With CAT) ACh |
|
|
Term
|
Definition
| One of the two parts for the precursor of Acetylcholine. Very commonly found in phospholipids |
|
|
Term
|
Definition
| One of the two precursors to ACh. It is a metabolite involved in energy for oxidation metabolism. |
|
|
Term
| Choline Acetyltransferase (CAT) |
|
Definition
| The enzyme that causes Choline and AceytlyCoA to form into ACh. *Most cells have Choline and AcetylCoA, but only ACh Neurons have CAT, the enzyme to make it turn into ACh |
|
|
Term
|
Definition
GABA is made from glutamate!
GLU -> (with GAD) GABA |
|
|
Term
| Glutamic Acid decarboxylase (GAD) |
|
Definition
| the enzyme that causes GLU to turn into GABA |
|
|
Term
| Peptide Neurotransmitter Formation |
|
Definition
Pepitde neurotransmitters are caused by cleaving larger peptides until they form them.
Enzymes cleave these peptides to create the true neurotransmitters (EX: Endogenous opiates like Endorphins, or the other types like Substance P (used for pain to spinal cord and motor movement))) |
|
|
Term
|
Definition
| A phospholipid that is very very high in Choline, which can be used to induce ACh synthesis! Can be used as a drug and found in many foods. Can help with Alzheimers patients by increasing the ACh levels. |
|
|
Term
|
Definition
| Taking an exogenous (outside) supply of a neurotransmitter precursor (like L-DOPA) as a drug, to increase neurotransmitter levels. |
|
|
Term
|
Definition
| Material of Phospholipid bilayer and transport membrane proteins to store neurotransmitters. Vesicles morph with neuron membrane and dump the neurotransmitters. Vesicles protect neurotransmitters from enzymes! |
|
|
Term
| 3 main functions of strorage |
|
Definition
1. Storage of transmitter for long periods of time
2. Protection of transmitters, from both external and internal cell enzymes
3. There is always a subset of vesicles that maintains neurotransmitters in pre release state (Always ready) |
|
|
Term
|
Definition
| Long term, Short term, and pre release state |
|
|
Term
|
Definition
Blocks vesicle storage in monoamine terminals by inhibiting the vesicular transporter that gets them there. Basically this drugs prevents monoamines from being stored and therefore leads to a depeletion of them (monoamines are DA, NE, EPI, And 5-HT)
*same drug as tetrabenazine |
|
|
Term
|
Definition
Blocks vesicle storage in monoamine terminals by inhibiting the vesicular transporter that gets them there. Basically this drugs prevents monoamines from being stored and therefore leads to a depeletion of them (monoamines are DA, NE, EPI, And 5-HT)
*same drug as resperine |
|
|
Term
| effects of resperine/tetrabenzine |
|
Definition
these drugs prevent vesile storage of the monoamines!
-This leads to a depletion of DA, which leads to antipsychotic effects.
-also depletes NE and EPI, so can be treated for high blood pressure
-too much DA/ 5-HT depletion leads to depression |
|
|
Term
|
Definition
| vesicle transporters, puts the neurotransmitter in the vesicle. Resperine and tetrabenazine block these VMATs |
|
|
Term
| What happens when Parkinsons Disease happens |
|
Definition
| DA neurons die. This is why resperine and tetrabenazine (block storage of DA) have been known to produce parkinsonian effects |
|
|
Term
|
Definition
| How much is stored into one vesicle! An action potential releases one quantum. It is one unit of neurotransmitter release |
|
|
Term
|
Definition
Occurs by the action potential opening the Ca2+ gates, which allows an influx of Ca2+ into the cell. This influx of Ca2+ causes the pre release state vesicle to merge with the neuron membrane, and drump out the quantum of neurotransmitters
*It has been seen that uptake of transport proteins can also cause transmitter release |
|
|
Term
| Amphetamine Family of drugs |
|
Definition
d-amphetamine (dexedrine)
l-amphetamine (Benzedrine)
Methamphetamine (methadrine/meth)
-All of these drugs can increase monoamine release!
-Can be used to treat ADHD
-ALL Block Reuptake of Monoamines! |
|
|
Term
| Drugs that Increase in monoamine release |
|
Definition
the amphetamines!
EX: Meth increases the amount of DA/NE/EPI/5-HT levels |
|
|
Term
|
Definition
| A drug that is a mix of d and l amphetamine. Causes an increase in monoamine synthesis |
|
|
Term
| Methylphenidate (ritalin) |
|
Definition
| A drug that stimulates catecholamin release! (so focuses on DA/NE/EPI). Used to treat ADHD, major stimulant |
|
|
Term
|
Definition
A cold medicine, but seen as "legal speed" (meth)
is a very big stimulant, increases release of the catecholamines!
*NE is the greatest change |
|
|
Term
| Why is Ephedrine a performance enhancing drug? |
|
Definition
| Ephedrine increases catecholamine release, but it targets NE. NE activates sympathetic nervous system, which increases bloodflow and blood preassure. It essentially activates Flight or Fight response, giving someone competitive advantage |
|
|
Term
|
Definition
| Actions of neurotransmitters at the receptors |
|
|
Term
| 2 actions of post synaptic effect |
|
Definition
1. binding
2. intrinsic biological activity
AKA, neurotransmitter binds, performs some kind of change. |
|
|
Term
| post synaptic effect binding |
|
Definition
| a neurotransmitter binds to the receptor protein. Each receptor has an affinity, or a strength of the tendency of a neurotransmitter to bind to a receptor. |
|
|
Term
|
Definition
the tendency of a ligand binding to a receptor
-"How much a ligand" is needed
-Affinity is specific to bidning |
|
|
Term
| Intrinsic biological activity for post synaptic effect |
|
Definition
| neurotransmitter instigates a biological change in the cell, known as an intrisic activity. |
|
|
Term
|
Definition
a measure of Affinity. it is how 50% of a ligand concentration occupies 50% of its receptors. It is the same as the ID50!
-It is inversely related to affinity, so the higher the Kd, the lower the affinity |
|
|
Term
|
Definition
inhibitory concentration 50. How much of a ligand is needed to bind to 50% of a receptors. it is a measure of Affinity, like Kd
The lower the IC50, the higher the affinity a ligand is! |
|
|
Term
| Differences in ED50 and IC50/ Kd (affinity and potency) |
|
Definition
ED50 measures potency (inversely), or how much of a drug is needed for 50% of its effect. IC50/ Kd measure affinity (inversely. They measure how much ligand is needed for 50% of an effect
-Affinity is binding specific
-Potency is for any effect |
|
|
Term
| Two types of signal transduction (intrinsic activity) |
|
Definition
1. ionotropic
2. metabotropic |
|
|
Term
| Ionotropic signal transduction |
|
Definition
When a ligand enters a recpetor, and a receptor is directly attached to an ion channel. The intrisic activity is then opening/ closing the channel so ionic currents can stop/ flow
EX: GLU binds with NMDA to open cation channel and produce EPSPs, which are graded and lead to action potential. |
|
|
Term
| metabotropic signal transduction |
|
Definition
When a ligand binds to a receptor, and it leads to a variety of biological changes (ie anything other than ion channels)
Most common change is the metatropic receptor is linked to a G protein, which then produces enzyme changes.
AKA metabotropic produces enzymatic change, which leads to 2nd messengers EX: C-Amp, Ca2+, etc. |
|
|
Term
|
Definition
Cyclic adenosine monophosphate. This is a 2nd messenger that is produced from enzyme action from metabotropic signal transduction. It changes the effects of phosphorylation, or the patterns and activities of different enzymes.
G protein Gs stimulates C-AMP, G protein Gi inhibits C-AMP. |
|
|
Term
|
Definition
| it is a 2nd messenger. When a metabootropic signal transduction from a post synaptic effect reaches the G protien Gq, it stimulates IP3. IP3 increases Ca++ concentrations in cells (which is used for release of vesicles) |
|
|
Term
| Dopamine Receptor Subtypes |
|
Definition
D1 family and D2 Family
-Blocking D2 is known to help with anti psychotic effects, while blocking D1 does nothing in this aspect
-Stimulating D1 causes an increase in C-AMP becuase they are metabotropically bound to Gs g proteins. But Stimulating D2 produces none or reduces C-AMP Activity |
|
|
Term
|
Definition
| They are the family of receptors shared by NE and EPI. They are split into alpha and beta andrenergic types |
|
|
Term
| AcetylCholine Receptor Subtypes |
|
Definition
Nicotinic and Muscarinic
-Nicotinic receptors are ionotropic, while Muscarinic receptors are metabotropic |
|
|
Term
|
Definition
Splits into 5-HT (serotonin) 1-7
*5-HT3 is a ionotropic receptor type, all the other ones are metabotropic |
|
|
Term
|
Definition
| Excitatory ones! glutamate biggest excitatory neurotransmitter. Binds with NMDA to open cation channels in neuron to form EPSPs and consequently action potentials |
|
|
Term
|
Definition
GABA-A and GABA-B!
-GABA-A is completely ionotropic,binds with GABA to open Cl- channels during hyperpolarization to restore resting membrane potential
-GABA-B receptors are both ionotropic and metabotropic, it depends |
|
|
Term
|
Definition
| Cells that detect and act on their own neurotransmitter. Autoreceptors typically provide negative feedback EX: a DA neuron detects DA, and decreases the DA it produces in order to avoid becoming too active. |
|
|
Term
|
Definition
| These are receptors that can act on more than one type of neurotransmitter. EX: a receptor is an ionotrobic one that opens Ca2+ gates when exposed to on neurotransmitter, and closes those same gates when exposed to another neurotransmitter. |
|
|
Term
|
Definition
| Drug binds to a receptor, and mimics the same intrisic activity/ signal transduction as that neurotransmitter |
|
|
Term
|
Definition
| When a drug binds to the receptor and stimulates maximum or near maximum levels of the intrisic activity it is copying from a neurotransmitter. It is essentially completely mimicking the neurotransmitter itself |
|
|
Term
|
Definition
| A drug that binds to a neurotransmitter receptor and weakly mimics its activity. It can also act as a blocking mechanism for a neurotranmitter, by taking the transmitters place and only doing a fraction of what it normally does |
|
|
Term
|
Definition
| A type of drug that binds to a receptor and blocks activity from the neurotransmitter. No intrisic activity/ signal transduction occurs |
|
|
Term
|
Definition
| A drug that binds to a receptor and does the REVERSE of what a neurotransmitter usually does. |
|
|
Term
| Noncompetitive Antagonist |
|
Definition
| When a drug doesnt compete with the neurotransmitter by not binding to the neurotransmitter binding site, but rather somewhere else on the receptor/ during the signal transduction that hinders the neurotransmitter effect |
|
|
Term
| Positive or Negative Allosteric Modulator |
|
Definition
When a drug binds to a different site on a receptor and regulates the receptors function
EX: Valium, a benzodiapine, facilitate inhibitory actions of GABA. They do this by attaching to GABA-A receptors and regulating their inhibitory actions. Positive ones, like valium on GABA, act as agonists and increase intrisic activity (in GABA-A case opening cation channels). Negative ones act as inverse agonists, regulating neurotransmitters effects by decreasing them |
|
|
Term
|
Definition
| Acts as a DA Full antagonist. it binds to D2 receptors and essentially replaces DA. This acts as an anti-parkinsonian drug, which makes sense because parkinsons is the death of dopamine neurons. Bromocriptine acts on D2 receptors and copies DA effects |
|
|
Term
|
Definition
| Acts as a canabinoid full agonist. it mimics effects of AN at CB-1 receptors. *Remember AN is a retrograde messenger that tells the previous cell messages about the neural activity, enhances Long Term Potentiation |
|
|
Term
|
Definition
| Acts as a Full Agonist on mew receptors of peptide neurotransmitter. Copies the endogenous opiates like endorphins, enekinphins, and dynophins on cells. Essentially gives off analgesic effects, or a "well being sensation" |
|
|
Term
|
Definition
| Nicotine is a ACh nicotinic receptor FULL agonist. It does what ACh does on nicotinic receptors to its maximum |
|
|
Term
|
Definition
| This is a drug that acts as a Partial Agonist on Nicotinic receptors for ACh. It is a good way to help people quit smoking, by giving them the Nicotine effect by not as much as the full antagonist from the drug. |
|
|
Term
|
Definition
| It is a Dopamine Competitive antagonist. It goes to D2 receptors and blocks DA from binding to it. Acts as an antipsychiotic drug (prevents too much DA) |
|
|
Term
|
Definition
| It is a Dopamine Competitive antagonist. It goes to D2 receptors and blocks DA from binding to it. Acts as an antipsychiotic drug (prevents too much DA) |
|
|
Term
|
Definition
| It is a Dopamine Competitive antagonist. It goes to D2 receptors and blocks DA from binding to it. Acts as an antipsychiotic drug (prevents too much DA) |
|
|
Term
|
Definition
| A type of drug that acts as competitive antagonists to NE and EPI beta receptors. By Blocking NE and EPI, Beta Blockers are recognized for helping with high blood pressure |
|
|
Term
|
Definition
| A competitive antagonist that blocks ACh muscarinic receptors. Blocking these receptors helps with parkinsons, but too high of a dose leads to hallucinations |
|
|
Term
|
Definition
| A competitive antagonist that blocks ACh muscarinic receptors. Blocking these receptors helps with parkinsons, but too high of a dose leads to hallucinations |
|
|
Term
|
Definition
| A drug that acts as an Inverse agonist on benzodiapines (on GABA-A receptors.) This causes reverse effects of whatever those are |
|
|
Term
|
Definition
| Acts as an Inverse agonist against AN or delta 9 THC (Weed). it binds to C-1 cannabinoid receptors and produces effects opposite of them |
|
|
Term
|
Definition
| Acts as a non-competitive antagonist on GABA-A receptors. It binds to the GABA-A receptor but not where GABA does and stops/ blocks some of its intrinsic activity, such as opening CL- channels for IPSPs. |
|
|
Term
|
Definition
| A drug that acts as a non competitive antagonist on NMDA receptors. It binds to the receptor but not where the GLU binds, and blocks some of its intrinsic activity, or some of the EPSPs from sodium channels |
|
|
Term
| Benzodiazepines (Valium, Xanax, Librium) |
|
Definition
| Examples are Xanax, librium, or valium. They all act as positive allosteric regulators of GABA-A receptors. In other words, they regulate GABA-A so that GABA produces more intrinsic activity, or Inhibitory activity |
|
|
Term
| Antagonists and Agonists seen in a Dose Response Curve |
|
Definition
| The Agonist alone produces its own effect. The agonist while also in the presence of a competitive antagonist has the same maximum value (eventually the agonist will win with enough of a dose), but a lower potency at all other doses after that (Higher ED50). This is because it is competing for the same spot, so it will require more of the dose to get to the same amount of receptors. The agonist plus a noncompetitive agonist has a lower maximum response level and a smaller potency (Greater ED50). This is because as much of the drug there is, the non competitive antagonist is going to be acting upon it no matter what and therefore inhibit its activity |
|
|
Term
| ACh and DA interaction of parkinsons |
|
Definition
| In the signal transduction part of metabotropic signal transduction, neurotransmitters can interfere with eachother at that phase as well. For Example, ACh and DA use the same pathway in the brain. When ACh is acting on the brain, DA cannot, so it blocks DA effects on the brain. By blocking the DA from the brain, it acts as though its parkinsonian! in addition, antagonists of ACh block the ACh, allowing the DA to flow and then prevents Parkinsonian effects |
|
|
Term
|
Definition
| Reducing the neurotransmitter level in the synaptic cleft. |
|
|
Term
|
Definition
| The balance of neurotransmitters are maintained in the synapse, not going to high or too low |
|
|
Term
| 2 Methods of Neurotransmitter inactivation |
|
Definition
Enzymatic Breakdown
Reputake Via transport protiens |
|
|
Term
|
Definition
| One of the two methods of neurotransmitter inactivation. It is when an enzyme breaks down the neurotransmitter into smaller pieces that cannot work on the post synaptic receptor. These pieces are called metabolites |
|
|
Term
|
Definition
| They are the pieces of the neurotransmitter after enzymatic breakdown during inactivation |
|
|
Term
|
Definition
| The enzyme that breaks down all of the monoamines during inactivation. Therefore MAO breaks down DA, NE, EPI, and 5-HT |
|
|
Term
|
Definition
| Catecholamine 0-methyl transferase. it is an enzyme that breaks down catacholamines during inactivation. Therefore, it breaks down DA, NE, and EPI |
|
|
Term
|
Definition
| AcetylCholine Esterase. It is the enzyme that breaks down ACh into Acetic acid and Choline. Choline is also a precursor of ACh, so these choline metabolites and taken back by transport protiens to the ACh neuron. This makes Choline an ACh precursor AND a metabolite |
|
|
Term
|
Definition
| A metabolite of DA. MAO and COMT break down DA into DOPAC |
|
|
Term
|
Definition
| A metabolite of DA. MAO and COMT break down DA in HVA |
|
|
Term
|
Definition
| A metabolite of NE. MAO and COMT break down NE into MHPG |
|
|
Term
|
Definition
| A metabolite of 5-HT (serotonin). MAO breaks down 5-HT into 5-HIAA |
|
|
Term
|
Definition
| They are produced by Acetylcholinesterase. They are acetic acid and Choline. Choline is also a precursor of ACh, so it is reuptaken back into the cell via a transport protien and reused |
|
|
Term
|
Definition
| A drug that is an MAO inhibitor. By inhibiting MAO, it stops MAO from breaking down DA, NE, EPI and 5-HT. breaks down all types of monoamines, is not selective. THIS is used as an antidepressant! |
|
|
Term
|
Definition
| MAO-A blocker and MAO-B Blocker |
|
|
Term
|
Definition
| A drug that is a MAO-A Blocker, and is an antidepressant |
|
|
Term
|
Definition
| This is a MAO-B inhibitor, prevents the breakdown of some monoamines, and serves as an antiparkinsonian drug |
|
|
Term
|
Definition
| These block the breakdown of ACh from AChEsterase. This prevents Alzheimers disease |
|
|
Term
| What happens with Alzheimers disease |
|
Definition
| Alzheimers is a degenerative brain disease, but one of the main functions that goes away is the ACh projections of the brain. When blocking a drug like Acetylcholinesterase, or AChEsterase, which breaks down ACh, you actually help Alzheimers patients with their congitive ability by keeping more of their ACh. Therefore, this makes Tacrine (ACHesterase blocker) an Anti Alzheimers drug |
|
|
Term
|
Definition
These are drugs that block Acetylcholinesterase from breaking down ACh
Some of these are lethal however! |
|
|
Term
|
Definition
| A very lethal anticholinesterase (antiAChEsterase). it blocks breakdown of ACh to the point where theres too much ACh and it becomes lethal, and irreversible |
|
|
Term
| Nerve Gases (Tabun/ Sarin) |
|
Definition
| A very lethal anticholinesterase (antiAChEsterase). it blocks breakdown of ACh to the point where theres too much ACh and it becomes lethal, and irreversible |
|
|
Term
| High Affinity Uptake (Reuptake) |
|
Definition
| A method of inactivation where protein transporters move neurotransmitter molecules from the synapse back into the presynatpic terminal where it is either broken down or recycled |
|
|
Term
|
Definition
| Blocks Monoamine reuptake! Acts as a major stimulant because of it |
|
|
Term
|
Definition
| Blocks 5-HT reuptake, and therefore is an antidepressant (makes you use more of it) |
|
|
Term
|
Definition
| Blocks DA/ NE reuptake, and therefore makes it an antidepressant. (makes you use more NE/DA) |
|
|
Term
|
Definition
| Blocks Reuptake of NE. Is an antidepressant. |
|
|
Term
|
Definition
| The brain and the spinal Cord |
|
|
Term
| Peripheral Nervous system |
|
Definition
| All nerve tissue besides the brain and spinal cord |
|
|
Term
|
Definition
| A connection of motor neurons on Deals with the somatic nervous system! Striated Muscle for Voluntary muscle. They are acted upon nicotinic receptors of ACh! |
|
|
Term
| Nicotinic Antagonists can be lethal... |
|
Definition
| Because Ach regulates voluntary movement and striated muscle movement in the body. This straited muscle includes our diaphragm! so if you take too much of a ACh competitive antagonist, you will stop breathing |
|
|
Term
| Anticholinesterases can help the body... |
|
Definition
| These can help the body by preventing the breakdown of ACh, so they can act more on the nicotinic receptors of striated muscle (somatic nervous system). This helps people who have trouble with neuromuscular dysfunction |
|
|
Term
|
Definition
| A naturally occuring nicotinic antagonist. It blocks nicotinic Ach receptors, included ones on the striated muscle of Diaphragm, which can cause you to stop breathing! It is naturally ocuring and found in the blow darts from south africa |
|
|
Term
|
Definition
Controls the smooth muscles in the body, AKA the automatic/ involuntary functions.
EX: heart rate, digestion, exctretion, breathing, etc. |
|
|
Term
| Two types of Autonomic Nervous System |
|
Definition
| Sympathetic and Parasympathetic |
|
|
Term
| Sympathetic Nervous System |
|
Definition
| The nervous system that involuntarily "pumps you up" It is involved in promoting using energy. "Fight or Flight Response". Also when activated it makes the adrenal gland produce adrenaline! |
|
|
Term
| Parasympathetic Nervous system |
|
Definition
| Used for energy conserving processes/ calming the body down. For digestion, reducing heart rate, breathing rate, etc. |
|
|
Term
|
Definition
| The fibers that connect the brain/spinalcord to the post gangliatic fibers, and then the desired muscle via the neuroeffector junction |
|
|
Term
|
Definition
| These are the fibers that receive Ach from the Pre synaptic fibers, and then produce their own Neurotransmitter to the neuroeffector junction to the muscle |
|
|
Term
|
Definition
| The synaptic space between the post ganglionic neurons and the muscle. In sympathetic nervous system, the neuroeffector junction produces NE and send it to the Alpha and Beta receptors. When its the parasympathetic, it sends out more ACh. |
|
|
Term
| Path of Autonomic Nervous System |
|
Definition
| Messages in Brain and spinal cord are called preganlionic fibers, those send ACh to the post ganglionic fibers, which then send a specific neurotransmitter to the Neuroeffector junction. The sympathetic nervous system (one that pumps you up) exerts NE onto muscles! The parasympathetic nervous system produces Ach and puts that onto the muscarinic receptors of the muscles |
|
|
Term
| Sympathominetics (drugs that activate the SNS) |
|
Definition
Drugs that stimulate NE transmission, and therefore stimulate the sympathetic nervous system!
-this increases heart rate/ blood pressure
-found in cold medicines that act on NE to help pump you up |
|
|
Term
| Parasympathominetics (drugs that activate the PNS) |
|
Definition
Drugs that stimulate ACh transmission, such as muscarinic agonists or anticholinesterases (drugs that copy ACh or drugs that block the break down of Ach)
*known to stimulate SLUD |
|
|
Term
|
Definition
Salivation
Lacrimation
Urination
Defecation
SLUD, it is when you take drugs that increase ACh levels, and in turn stimulate the PNS. This stimulates the automatic parts of the body that calm you down/ are used for energy. So sleeping/ eating/ getting rid of waste all rise |
|
|
Term
|
Definition
| A drug that blocks muscarinic receptors. It prevents ACh from working on the parasympathetic nervous system. This causes people to have dry mouth (anti salivate), constipate (anti defecate) and dilate pupil (anti get sleepy) by blocking the ACh effects |
|
|
Term
|
Definition
| A drug that blocks muscarinic receptors. It prevents ACh from working on the parasympathetic nervous system. This causes people to have dry mouth (anti salivate), constipate (anti defecate) and dilate pupil (anti get sleepy) by blocking the ACh effects |
|
|
Term
|
Definition
| Forebrain, midbrain, hindbrain |
|
|
Term
|
Definition
| The outer suface of the forebrain, performs many complex functions of body, and is divided into LOBES! frontal parietal occiptial temporal |
|
|
Term
|
Definition
parietal - motor
occiptial - sight
temporal - hearing
frontal - ascribe meaning of stimuli |
|
|
Term
| 2 parts of Prefrontal Cortex |
|
Definition
| Prelateral and cingulate. Deals with memory |
|
|
Term
| Prelateral frontal cortex |
|
Definition
| The primary site for Working memory, AKA short term memory of things |
|
|
Term
|
Definition
| The primary site for judging value of rewards and making predictions |
|
|
Term
|
Definition
| a conglomerate that Involves the hippocampus, amygdala, and septum. all very important together for learning and memory |
|
|
Term
|
Definition
| A part of the brain critical for memory formation. It degenerates with patients with alzheimers |
|
|
Term
|
Definition
| One of the most important brain areas involving in emotion. Some of the antianxiety drugs work there |
|
|
Term
|
Definition
| Part of the brain that allows the two hemispheres to communicate with one another |
|
|
Term
|
Definition
| This includes the cerebellum, medulla, and pons |
|
|
Term
|
Definition
| Controls vital reflex functions, such as heartbeat, respiration, and blood pressure. Many drugs act here to have lethal effects of respiratory supression |
|
|
Term
|
Definition
Connects higher parts of the brain with the cerebellum, also includes the Locus ceruleus!
-The locus ceruleus plays a key part in dispersing NE to the brain |
|
|
Term
|
Definition
| A part of the brain located in the pons, it is key in the innvervation of NE to the brain (sending NE to the brain) |
|
|
Term
|
Definition
| Part of the brain with the Most important part of the motor system, aids with all movement and balance. Importance for drug induced ataxia (movement issue) |
|
|
Term
|
Definition
| Contains substantia nigra, ventral tegmental area, and the raphe |
|
|
Term
|
Definition
| A part of the brains midbrain. It is where DA neurons originate from |
|
|
Term
| Ventral tegmental Area (VTA) |
|
Definition
| A part of the brains midbrain. It is where DA neurons originate from. |
|
|
Term
|
Definition
| A part of the midbrain. It is where 5-HT neurons originate from |
|
|
Term
|
Definition
-Basal Ganglia (caudate/putamen AKA striatum, and the nucleus accumbus
-hypothalmus
-thalmus
-hippocampus
-amygdala
-septum |
|
|
Term
|
Definition
| Relays information to the rest of the brain, especially the neocortex (outer space of brain) |
|
|
Term
|
Definition
| Involves in motivation, emotion, autonomic regulation. Appetite suppressants work here. |
|
|
Term
|
Definition
Made up of the striatum (or putamen), nucleus acumbus, and global pallidus. It is important for motor control!
-Striatum is depleted with most DA neurons in parkinsons disease, antiparkinsonian drugs work here. |
|
|
Term
| Neurotransmitter Brain Systems |
|
Definition
| These describe where neurotransmitters are made, where they are projected to, and where they end up, in the brain. |
|
|
Term
| GABA and Glutamate brain systems |
|
Definition
| They are the common excitatory inhibitory and excitatory neurotransmitters, theyre EVERYWHERE IN THE BRAIN |
|
|
Term
|
Definition
3 of them!
-Nigrostriatal
-mesolimbic
-mesocortical |
|
|
Term
| nigrostriatal dopamine system |
|
Definition
| Goes from the Substania Nigro (SNc) to the striatum (CPU, Striatum). It is depleted in parkinsons disease, and mediates parkinsonian side effects of antipsychotics |
|
|
Term
| Mesolimbic Dopamine system |
|
Definition
| Goes from the VTA (ventral tegmental area) to the nucleus accumbens (in basal ganglia). It is involved with motivation, energy expernditure, depression, and aspects of drug abuse |
|
|
Term
| Mesocortical dopamine system |
|
Definition
| Goes from the VTA to the cingulate cortex (in prefrontal cortex). Involved in schizophrenia, learning, stress, and learning |
|
|
Term
|
Definition
2 of them
-intrinsic striatal
-basal forebrain |
|
|
Term
| Intrinsic striatal System of ACh |
|
Definition
| Goes from the CPU, and either ends there, or goes to the striatum (putamen). site of ACH/DA fight for parkinsonism. (More Ach in pathway means less of the DA, and more parkinson effect) |
|
|
Term
|
Definition
Orginates near the septum/ basal ganglia nucleus, ends up in neocortex/ hippocampus)
-depletes with alzheimers and involved in memory and cognition |
|
|
Term
|
Definition
2 of them!
-Ventral bundle
-Dorsal bundle |
|
|
Term
| Ventral bundle NE brain system |
|
Definition
| Goes from the brainstem to the hypothalmus. Involved with food and stress |
|
|
Term
| Dorsal Bundle NE brain system |
|
Definition
| goes from locus coeruleus (in pons) to neocortex and hippocampus. Involves in learning, attention, stress, depressiong |
|
|
Term
|
Definition
|
|
Term
| The raphe brain system of 5-HT |
|
Definition
| Goes from midbrain/pons to hypothalmus OR striatum OR cortex OR hippocampus. Involved with many stops in the brain. Involved with depression, anxiety, drug abuse, motor control, learning |
|
|
Term
|
Definition
|
|
Term
| Active ingredient of tea/ coffee |
|
Definition
|
|
Term
| Active ingredient in tobacco |
|
Definition
|
|
Term
| active ingredient in beer |
|
Definition
|
|
Term
| Active ingredient in coca leaves |
|
Definition
|
|
Term
| active ingredient in opium poppies |
|
Definition
|
|
Term
| Active ingredient in Rauwulfia |
|
Definition
| Reserpine (blocks storage of Monoamine) |
|
|
Term
| Active ingredient in Cannabis |
|
Definition
|
|
Term
| 1906 Pure food and drugs act |
|
Definition
| established the FDA, which regulated testing for usage and safety of drugs for medicine purposes |
|
|
Term
|
Definition
| Organization founded in 1906 which regulates testing, usage, and safety of drugs |
|
|
Term
| 1914 Harrison Narcotic Act |
|
Definition
| Put in place the modern regulatory structure of drugs |
|
|
Term
|
Definition
|
|
Term
| 1970 Controlled substance act |
|
Definition
| established a schedule for drugs, organizing according the abuse potential |
|
|
Term
|
Definition
| Drug enforcement agency. Regulates prescription licenses, identifies drugs with abuse potential, maintains "schedule list" |
|
|
Term
|
Definition
| An animal behavior test model used to asses stimulants or drugs that suppress movement |
|
|
Term
|
Definition
| An animal behavior test model. It Assess lack of coordination (how balanced you are) |
|
|
Term
| Operant conditioning rate |
|
Definition
| An animal test model that tests stimulants and drugs assessed with movement |
|
|
Term
|
Definition
| An animal test model that Tests anxiety levels in rats, see how willing they are to come into open to cross maze |
|
|
Term
| Radial Arm/ Morris Water maze |
|
Definition
| An animal test model that Tests for drugs that improve/ impair memory |
|
|
Term
| Oral route of administration |
|
Definition
|
|
Term
| IV route of administration |
|
Definition
| intravenous, directly into vein |
|
|
Term
| SubQ route of administration |
|
Definition
| subcutaenous, injected under skin |
|
|
Term
| IM route of administration |
|
Definition
| intramuscular, directly into ones muscles (like biceps) |
|
|
Term
| IP route of administration |
|
Definition
| Intraperitoneal, directly in fluid of gut/ abdomen |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Inhaling (smoking) a drug |
|
|
Term
| ICV route of administration |
|
Definition
| intracerebroventricular, or intraventicular. It is when you inject drug directly into ventricles of fluid filled spaces of brain. Avoids BBB altogether |
|
|
Term
| IC route of administration |
|
Definition
| intracranial, directly into some part of brain |
|
|
Term
|
Definition
| The effect of a drug on the organism. It is the Y axis measure of a drug dose response curve! can be measured plenty of ways |
|
|
Term
|
Definition
| "How much of a drug" is needed for a certain effect? it is an X axis measure for a drug dose response curve |
|
|
Term
|
Definition
| a measure of drug POTENCY. it states how much of a drug is needed to obtain 50% of behavioral activity (efficacy). It is inversely related to potency. The higher the ED50, the lower the potency |
|
|
