Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
103 Cards in this Set
- Front
- Back
|
What is psychopharmacology? |
The look at the effects of psychoactive drugs on BRAIN and BEHAVIOUR. Effects the brain by influencing NEUROTRANSMITTER SYSTEMS in the brain. different drugs = effect different NT systems. |
|
|
What is the deactivation of neurotransmitters? |
Immediatly after PS action, NT are cleared from the synaptic CLEFT = to carry new messages. NT that are NOT deactivated will continue to stimulate receptors indefinately. |
|
|
What are the deactivation mechanisms? How many processes are there? |
1) Enzymatic Breakdown Breakdown of NT by ENZYMES released into synaptic cleft by POST synaptic cell. eg. Enzyme - [Acetycholinesterase (AchE) breaks down (Ach) shortly after receptor binding. |
|
|
What is the reuptake of PSN? Is this another way the S-cleft is cleared of NT? |
Pre-synaptic cell reabsorbs the NT released via transporter molecules in the PSM. These attract the NT molecules back into presynaptic terminal for recycling. |
|
|
What is the process of dissemination of enzymes? |
1) NT molecules synthesized from precursors, under influence of enzymes 2) NT are stored in vesicles 3) NT that leak from vesicles are destroyed by enzymes. 4) AP cause vesicles to fuse with PSM then release NT into synapse. 5) Released NT bind with autoreceptos and inhibit subsequent NT release. 6) Released NT bind to PostSReceptors. 7) released NT are deactivated by reuptake and enzymatic degradation. |
|
|
How Leowi (1921) discover neurotransmitters? |
Leowi experiemented with frog hearts placed in electrolytes solution. Even with absence of neural input. Leowi placed frog heart in two fluid filled chambers, one connected to vagus nerve (parasymp Nerve) other heart was not. |
|
|
What did Leowi's theory indicate? |
That chemical messengers - Neurotransmitters from the stimulated vagus nerve would slow down both hearts. Indicating the messengers in the fluid would slow it down. |
|
|
What is an agonist? what do they do? |
Agonists - increase neurotransmission. Two ways - Direct agonsit. Drug binds to/activates PostSR same as neurotransmitter does. = like bran operated & flooded with NT. eg. Nicotine binds to nicotine receptors/activates cells same way Ach does. LSD - activates serotonin receptors - as serotonin. Opiates - (heroin activated opoid recptors same way endorphins do. |
|
|
What does an indirect agonist do? |
The drug blocks deacitivating mechanism that removes NT from Synapse. - neve gases, block AchE, Cocaine blocks reuptake of dopamine. Prozac - bocks repuptake of serotonin. Others indirect agonists PROMOTE RELEASE eg. Meth - triggers release of dopamine/norepinephrine. / MDMA triggers release of serotonin. |
|
|
What do antagonists do? |
Reduce of block Neurotransmission. blocking receptors for particular NT. eg. Anti-psychotic drugs - bind to dopamine receptors without activating them. blocking dopamine binding to / activating dopamine receptors in the brain. |
|
|
What other example of antagonists are there? |
Opiate antagonists eg. Nalaxone/ Naltrexone block opoid receptors. can reverse H overdose by knocking off H receptors. Caffeine block receptors for an inhibitory modulator called adenosine. Inhibiting release of NT or promoting uptake. |
|
|
What does Acetylcholine (ACH) do? |
regulates - movement, cortical excitability, arousal and sleep, cognition/reward Inbitory at muscarinic receptros - found in cardiac/smooth muscles. Excitory at nicotinic receptors - found in skeletal muscles. for movement Synth. Cholinergic neurons found in choline, which from eggs, seeds, beans. After release into S-cleft, Ach is borken down into (AchE) |
|
|
What does nicotine do to Ach synapses? |
- An agonist at Nicotinic recepts -Nicotine binds to and activates nicotinic receptors in similar manner to Ach. Excitatory effect of nicotine in the cerebral cortex makes smokers more alert and focusd. too much causes muscle lock/ death by cardiac or respitory arrest.
|
|
|
What does Curare do? what are the effects of |
antagonist at nicotinic receptors. blocks nicotinic receptors, preventing Ach - from muscle contraction - paralysis. |
|
|
Botulinium Toxin do? |
Blocks Ach release Similar drug used to reduce wrinkling by parlysing facial muscles. |
|
|
What does Muscarine do? |
Agonist at muscarinic receptors Inhibits effect on certan cells in Autonoomic and brain. Highly toxic due to actions in ANS |
|
|
Arecoline, what does it do? |
Similar drug with less toxic effects. to muscuranic - stimulant |
|
|
what does Atropine and Scoplomine do? |
Antagonsits at muscarinic receptors (ati-muscarinics) Used for medical purposes (relieve nausa & cramps) |
|
|
So what are Acetylocholinesterase (AchE) inhibitors? |
Drugs used as insecticides and nerve gases. Block the enzyme (achE) breaks down Ach, Causing Ach to build in S-cleft. High dose - death and lockup of mucles/cardiac arrest. |
|
|
What are the three closely related chemical messengers? |
1) dopamine (DA) 2) Norephinephrine (NE) 3) Epenephrine (adrenaline) |
|
|
What do Catecholamines do? |
Tyrosine (amino acid) > dopa Dopa convertime to DA in dompaminergic neurons. DA converted to NE in noradrenergic neurons Ne converted to ephinephrine in adrenal glands. DA - NE cleared from S-cleft - reuptake into presynaptic terminal. |
|
|
What does Monoamine oxidasa (MAO) do? |
Regualates amount of Catecholamine into axon terminal breaks down excess catecholamine stored in the vesicles. |
|
|
Whatdoes Epinephrine do? |
Hormone secreted by the adrenal glands for response to precived threat. Apmpliefies the fight - flight reaction |
|
|
What does Norepenephrine (non - adrenaline) do? |
Relaesed by the sympathetic NS at various internal organs/glands to trigger - fight / fllight response. IMPOTANT NT for the brain. Locus Coreuleus (lC) meani nucleus of NE - releasing cells. Part of RAS. LC sends neurons to axons throughout higher levels of brain increases vigilance/alertness/axiety. |
|
|
How many subtypes of the Ne receptor are there? https://www.youtube.com/watch?v=xVeyHsC4P20 |
Some excitatory and inhbitory |
|
|
What does dopamine do? |
Inhibitory NT that has crucial roles in the brain. Motor activity Psychoses Reward and Reinforcement |
|
|
What are the important DA release nuclei? Where are they located? |
1) Substantia Nigra 2) Ventral Tegmental Area Top of the brainstem. |
|
|
What is substania nigaraalos known as? What is it's function? |
Known as the mosestriatal dopamine system. IT sends DA releasing axons into Basal Ganglia, where DA helps voluntary movement. |
|
|
What is Parkinson's disease is effected? |
Neurons of the substantia nigar start dying off at rapid rate. - standard treament L-DOPA Potential chemical poisoning can be the issue PD |
|
|
What is the Ventral Tegmental Area? what else is it known as? What is it's function. |
Also known as the meslimbic dopamine system (reward/reinforcement centre) Sends DA releasing axons into nucleus accumbens of PFC. Electric stimulation of system so rewarding rats will press a lever to receive direct stimulaton Primary biological basis of drug addiction - drugs that acitivate this part of brain. cocaine, heroin, nicotine, alcohol. |
|
|
What do amphetamines do? What type of agonists are they? |
Promote release NE and DA into synaptic cells. (indirect agonists) - Release of Da promotes increased activity/mood elevation. |
|
|
What does Cocaine do? |
Block reuptake of DA/NE/Serotonin. Indirect agonist for all three NT Intense euphoria, local anasthetic / blocks sodium channel. |
|
|
What are sympathomemtic effects? |
- sympathomimetic effects - increase HR, elevated BP, pupil dilation, rapid breathing
|
|
|
How can a drug increase activity of inhibitory NT act as stimulant? |
Brain area that dopamine inhibits PFC normals serves inhibit behaviour in some way. |
|
|
What is disinhibition? |
The release of behavour, is inhibited. eg. cocaine reduces cortical activity, but the person is talkative and feels energised. |
|
|
What drugs affect the catecholamine synapses? |
Anti-psychotic drugs. eg. Thorazine, Olanzapine. Used to treat Schizophrenia. DA antagonists - block Da receptors in the brain. Supresses delusion and hallucinations. |
|
|
What does Serotonin do? What is the procces for the process of serotonin? |
Synth. into serotnergic neurons from the amino acid tryptophan. -12 different subtypes of serontonin receptor in the brain - excitatory. - removed from the synaptic celft by reuptake/ amount in axon terminal regualted by MAO. IMportant NT in RAS releasing raphe nuclei along with NE and Ach. |
|
|
What do Psychedelics do? |
Powerful/mind altering Naturally psychedelics - psilocin/ psilocybe. DMT/mescaline. -Produce hallucinations, loss reality/ extreme emotional reaction ranging from panic / spiritual ectsasy. - Serotonin - act as direct serotonin agonists. - stimulation of serotonin receptors results in strong activation cerebral cortex/ limbic system |
|
|
What do SSRI's do? |
Commonly prescribed anti - depressant. Blocks reuptake of SE - indirect serotonin agonists. Widley used to treat. Time to take effect widely uknown. |
|
|
What are two most common NT |
1) Glultamate 2) GABA (gamma aminobturyic acid) |
|
|
Where does glutamate do and where is it from? |
It is a major excitatory NT Comes from diet. Removed by Reuptake. |
|
|
What drugs affect the glutamate receptors? |
Dissociative Anesthetics? NDMA - receptor antagonists. Examples Phycyclidine (PCP - angel dust) & Ketamine (K) Blocks NMDA receptors (subtype of glutamate receptor) General painkiller (anesthesia) eg. laughing gas in high doses, hallucinogenic - lower dose. |
|
|
What is GABA? |
Major inbitory NT - most Common single transmitter of all types. Estimated by 20-40% of axons in brain release this. |
|
|
What are drugs that affect the GABA receptors? |
1) alcohol 2) Barbiturates - anti convulsants - painkilllers 3) Benzo's - diazepam, valium All these drugs make GABA more repsonsitve to GABA's inhibitory effect throughout the brain. |
|
|
What are depressants? |
Slow down or depress the CNS. |
|
|
What are indirect GABA agonists? |
Through high doses of barbs(pain killers also have direct agonists actions. |
|
|
What are endorphins? How were they discovered? What else are they called? |
-Enkephalins/ edogenous opiods - Group of inhibitory neuromodulators -made of short chain amino acids (peptides) First discovered 70's, researchers were studying the effects of opioid drugs in the brain. Opiates - morphine/codeine Semisynthetic derivatives - (herion) & Vicodin. Purely synthetic opioids - methadone/ meperidine |
|
|
What are inhibitory neuromodulators? |
These brain chemical bind to endorphins . (endogenous morphine) Called endorphins. 5 different types Opiates and Synthetic Opiates. Subtypes of opioid receptors. |
|
|
What are the affects on the endorphin system? From opiates and synthetic opiates ? |
Produce euphoria - opiates bind to promtoes DA - release from meslimbic dopamine system. Produce relaxation - Inhibits LC (alertness NE releasing) Produce Pain relief - Opiates bind to opioid receptors (pain inhibitory system) usually active during emergency. - E highly addictive. |
|
|
What are other drugs that affec endorphin system. |
Nalaxone - synthetic drug - blocks opiod receptors. Can revers H overdose. Used in opiate addiction. - treat H addicts. Used in treating heroin addiction. |
|
|
What does adenosine do? |
Common inhibitory neuromodulator found through the brain and body. - promotes sleep / caffeine (antagonist) block adenosine. Inhibitor leads to stimulation. - |
|
|
What is anandamide? 2-AG? How do they function in the brain? |
Recently discovered neuromods in higher brain - hippo and cortex. - discored by researher investigating brain effects of cannabis. THC were found to bind to specific receptors - canabinoid. Are released by PSC to GABA or glutumate receptors. |
|
|
What are retrograde neuromodulators? |
Diffuse backwards across the syanpes to inhibit futher release of GABA and glutamate. |
|
|
What are affects of canabis? |
Stimulant, depressant - mind altering effects. |
|
|
What is the different between addiction and dependance? |
Addiction - behavioural disorder, compulsive drug seeking behaviour, impaired self control Dependence - physiological from heavy use. mostly depressants - opiates, alchohol , barbituates |
|
|
What are the components of dependence? |
1) Tolerance - larger doses of drug are needed to produce same effect. 2) Withdrawal - when drug wears off/ hyperexcitability gone. eg shakes / anixety. eg. chronic alcoholism - fatal reaction. |
|
|
Neural adaptation, what is it what are the factors in the brain that indicate NA? |
NA reflection of Neural adaptation. |
|
|
What are effects of alcohol on the brain in terms of NA. |
1)Increase in excitatory glutumate receptors thtroughout the brain. 2) Decrease number of inhibitory GABA receptors throughout the brain. Drug is present - change = tolerane Drug is absent - change = withdrawal symptons |
|
|
what happens in the brain when chronic use of alcoholism or opiates are present / not present? |
Function of nervous system adapts to deppressive effects of substance allowing function but increases excitability. When drug is removed - neural activity skyrockets dramatically - withdrawal symtoms. Physical dependence - changing = detoxification. |
|
|
Can there be addiction without dependence? Can there be dependence without addiction? |
Yes, eg. cocaine, gambling, methamphetiaminces Yes, morphine use following surgery. |
|
|
Where in the body, does addiction occur? |
The brain's mesolimbixc dopamine system. Drug induced changes in the brain - appear to drug craving and impairments of self control characteristic of addiction. |
|
|
The development of the nervous system. |
The development of the nervous system is complex, poorly understood. All cells carry genetic instruction in EMBREYO |
|
|
Why is it some cells differ from others? eg become neurons instead of skin cells? |
In case of neurons, the questions are more complex than other types of cells. Many cases the target cells |
|
|
How many neurons are in the brain? How many synapses are in the brain? |
Neurons = 100 billion Synapses = trillion |
|
|
Questions to be answered. How are target cells reached, when growing axons are so far away? How do cells know which other cells to make synapes with? |
It's all incredibly complex, no complete answer. |
|
|
In what cases to synapses not form? |
eg. schizophrenia. |
|
|
What are the embreyonic layers? |
Ectoderm (outer) - develops skin Mesoderm (middle) - bone, organs Endoderms (inner) - digestive tract, sex cells |
|
|
Refer to diagrams on 8/9 slides |
May have fill in the blanks stage, however brain lobe diagram more important. |
|
|
What are the developing stages? How many are there? |
5 stages. Proliferation Migration Differentiation Mylinisation Synatpogenesis |
|
|
What happens in the first stage? |
Neural plate forms - 100,000 cells form, only. Proliferation increases growth rate to 300,000 N's p/m// also GLIA form at the same rate. |
|
|
What happens after the 4th week after conception. What forms? Refer to diagram on slide 12. |
Three main parts. 1) forebrain - becoming cerebral hemispheres 2) Mid brain 3) Hindbrain - cerebellum and brainstem Neural Proliferation complete at birth. 3 weeks - spinal cord. 7 weeks - cranial nerves. 11 weeks main pats are part formed. |
|
|
What other proliferation occurs during this period of fetal dev - birth? What is the first stage of cell dev? What is the process? |
Cell proliferaton - rapid division of stem cells - Neuroblasats and Glioblasts. - Neuroblasts = Neurons - Glioblasts = glial cells Cells proliferate = begin to migrate out of inner surface of neural tube. to final destination in NS |
|
|
What is the second stage? |
MIgration...most young neurons and glial cells are not actively migrating. -They are moved by PIONEER CELLS The movement is called AMOEBOID |
|
|
What influences the direction of the migration? |
CUES: 1) Radial Glia - type of astrocyte / sends radial extension (pathways/arms) from inner surface tube to target sites in dev. NS// extension form pathways for migration young neurons. 2) Chemical signals - concentration gradient of hormone like chemical - CHEMOKINES. release cells in target area. |
|
|
What is the third stage? What happens? |
Differentiation... Young neurons, arrive at target destination become like-neurons. They grown an axon /then dendrites. The chemical signals determine the kind of neuron they become. |
|
|
What is the fourth stage? Refer to diagrams on lecture 18 to study |
Myelinisation... Axons grow towards their targets - specialised glia form myelin around them. These are SCHWANN CELLS (in PNS)- oligodendrocytes (in CNS). Myelinisation - adulthood - frontal regions not fully myelinated until individuals reach 20's |
|
|
What are the critical periods? |
The brain is sensitive to toxins, disease and dietary deficiencies which can disrupt neural proliferation and migration. eg. - Feotal Alcohol syndrome - Cretinism - Rubella / influenza |
|
|
What is stage 5? |
Synaptogenesis.... Takes place after birth - especially in frist two years - through lifespan. Most post natal / then pre-natal. |
|
|
How must synapses form? What is growth cone? |
axons must find their way through a maze of dev issues to far away targets. - Leading edge of a growing neuron. |
|
|
What are the properiteis and process of growth cone? |
Filaments extend from the GC and attach to developing axons - as it grows. Chemicals signals from target cells guide with direction of axon growth. different chemical markers only attract certain axons. |
|
|
What is the role of chemical signalling? |
eg. frog optic nerve cut out, then regeneratd in exact specific connections. - opposite action to prior action to sever ensued. HOWEVER now connections are maladaptive, eye direction altered. Similar case in humans CHEMICAL GRADIENTS made b target cells. |
|
|
What guides the growth of dendrites. |
Unlikes axons = chemical signals. Dendrite growth is guided seperately. dendrites are developed before axons. not dependent on synaptic function. but synaptic function, dendrites will eventually wither away. |
|
|
What happens when axon reaches it target dendrite.? What has been created? |
Target cell releases chemical STOP, to stop axon growth and release NT. Axon releases another chemical - PSC to manufacture receptors for site of synapse. Functional synapse is created. |
|
|
What is Neural Darwinism? |
Synapses from earlier are destroyed later on. -1.5 years old is when we have the most synapses, then gradually eliminated from then. It is good as eliminating inappropriate/usuless connection help create function neural network. |
|
|
What is Apoptosis? |
The pruning process, where rejected axons die from target cells. - Programmed cell death is Apoptosis = normal part of brain develppment. |
|
|
What is Trophic Factor? |
A life sustaining factor that is released by target cells. That AXONS compete for. Absorptions stops Apoptosis. ONe neurotrophin is called nerve growth factor. - causes PREsynaptic cells to survive longer. |
|
|
What happens when an axons wins neurtrophin? |
Winning synaptic space, forming extra branches - for other synapses in same postsynaptic cell. |
|
|
What is an example of this? |
- The development of neuromuscular junctions. At birth one one motor neuron controls a given muscle cells. Axon has many branches. Lost axons then die. fetus (2months) has more neurons but half die...not enough space. - Natures ways of blancing CNS neurons to controlled cells. |
|
|
In most cases, how does a neuron survive? |
When it is most acitive, making the best conneciton for synaptic space. Lacking in connection also lack in neurtopin received from target cell. NT released at synapes, neurotrophin is also released maintaining the connection. PostS neurons are then retained better. |
|
|
What is an example of this? |
People who are blind have more neurons in the visual cortex, because pruning does not occur from usual devlepment. Experience guides the development of the brain during early childhood. |
|
|
What is the evidence proving that early experience alter development of the brain? |
1970's experiment with baby rat's Rats that had more stimulating environment demsontrated better learning performance compared non - active rats. = more complex dendritic tree (connection) Not reversible by adult experience. |
|
|
What is a way a brain can recover from brain damage? |
Neuroplasticity, recovery of function by self-altering function in the brain following brain damage. |
|
|
Why is brain recovery easier from children then adults? |
The amount of synaptic space and axons/neurons available. Partial recovery is possible however. |
|
|
What are some ways to brain can be damaged? |
Brain Tumour / Toxic substances / infection / stroke / direct trauma. |
|
|
What is the most common cause of localised damage. |
Stroke - oxygen to parts of the brain become blocked. From excitoxicity - Large amounts glutumate from damaged cells. Certain drugs such as THC, PCP, ketamin can reduce glutumate leels. |
|
|
What is Hemiplegia? |
A large stroke confined to one of the hemispheres. Damage to prefrontal cotex - problem solving, impulse control and socailly appropriate behaviour. How is this tested? Neurophysiological testing. |
|
|
What is the characteristic of brain damage? |
6 months after brain injury recover y may only be partial. Behavioural adjustments - to compenesate for disability - Plasticity is adaptive physiological changes in the brain. |
|
|
What is the difference in PNS versus CNS recovery? |
The PNS can re-grow and establish connections. eg. Limb re-attachment / permanenet spinal damage irreversible. i |
|
|
What is the role of glial cells for recovery? |
Part of the myelin sheath recovery. schwann cells (PNS) appear to produce trophic factors = helping axon re-growth. OLIGODENDROCYTES (CNS) do not do this and actually inhibit axon - regrowth. |
|
|
Do injured axons that fail to regenerate mean large changes won't occur? |
NO, as failing neurons will cause neurons in the nearby to sprout new branches (collaterals) for synapses in place of lost ones. If nearby axons serve a different function then (phantom limb pain) eg. heightened sensitivity in other fingers from lost one. |
|
|
What is Denervation Supersensitivity? |
Another process of recovery from brain damage. More receptors are made to compensate for loss of incoming axons. - Synaptic sites become more sensitive to missing NT. |
|
|
What is an example of Denervation Supersensitivity? |
Neuronal loss in parkinson disease can not be seen due to the basal ganglia - creating more receptors, for lack of Dopaminergic axons from substantia nigra. Sadly to SN will continue to degenerate - regardless of receptors. Therefore symtoms will |
|
|
What types of treatments / exercises are avaialable to help recovery? |
Intensive pracitve of behavioral skills. Physcisl stimulation and exercise of areas of the body that are weak or paralysied. THE SOONER THE BETTER OUTCOME = promotes collateral sprouting. PLASITICITY IS LEARNING |
