Chapter 3 Flashcards
(57 cards)
1
Q
what are exogenous ligand?
A
they are from outside the body (drugs have been used for ages to change the functioning of the brain and body)
2
Q
what are ligands?
A
molecules that fit into receptors and activate/block them
- neurotransmitters are ligands
3
Q
what are examples of exogenous ligands?
A
- agonists: substance that mimics or boosts action of transmitter/ other signaling molecule
- antagonist: substance that blocks/attenuates action of transmitter or other signaling molecule
4
Q
what are receptors?
A
proteins on plasma membranes of a neuron
- ligands will bind to it, which produces response (excitatory or inhibitory)
5
Q
what are receptor subtypes and which has the most?
A
different varieties of receptors for same neurotransmitter
- serotonin has the most with 15
6
Q
what are the different types of receptors?
A
- ionotropic receptors (quickly change shape and open/close ion channel- fast acting)
- metabotropic receptors (alter interworking of post neuron by second messenger to open ion channel or alter gene expression)- slow but longer effects)
7
Q
what are the five criteria for a neurotransmitter?
A
- synthesized in presynaptic neuron and stored in axon terminals
- released when action potentials reach axon terminals
- recognized by receptors on postsynaptic membrane
- causes change in postsynaptic membrane
- blocking its release interferes with presynaptic neuron ability to affect the post
8
Q
what are the 4 types of neurotransmitters?
A
- amino acid neurotransmitters (GABA & Glutamate)
- Peptide neurotransmitter (oxytocin & vasopressin)
- amine neurotransmitters (acetylcholine and monoamines like dopamine, serotonin & norepinephrine)
- gas neurotransmitter (nitric oxide & carbon monoxide)
9
Q
what are the two most common types of neurotransmitters?
A
- Glutamate is mostly excitatory (key for learning and memory) with AMPA and NMDA receptors
- GABA is most inhibitory (key for focus, reduction of anxiety, and motor control & vision) with GABAa and GABAb receptors
10
Q
what is co-localization?
A
the phenomenon where some neurons make and release more than one type of transmitter
11
Q
what does acetylcholine do?
A
plays a major role in transmission in the forebrain
- many cholinergic neurons found in basal forebrain- disruption interferes with learning & memory
- widespread loss leads to Alzheimer’s disease
12
Q
what does dopamine do?
A
plays key role in reinforcement learning & voluntary movement
13
Q
what are the two key pathways of dopamine?
A
- mesotriatal pathway- important for motor control and voluntary movement (originals in substantia nigra and projects to basal ganglia - Parkinson disease b/c of neuron loss here)
- mesolimbocortical pathway- important for reinforcement learning & reward (originals in ventral tegmental area and projects to nucleus accumbens and cortex)
14
Q
what does norepinephrine do?
A
important in control of many behaviors like alertness to mood to sexual behavior
- main transmitter of sympathetic nervous system
- noradrenergic neurons found in locus coeruleus and lateral tegmental area
15
Q
what does serotonin do?
A
does mood (depression), vision, anxiety, sexual behavior & aggression, and sleep
- originates in midbrain and brainstem in the raphe nuclei
16
Q
what do some neuropeptides do?
A
- opioid peptides are endogenous painkillers
- key for perception of pain (substance P)
- oxytocin and vasopressin contribute to memory and feeling of love
17
Q
how are neuropeptides synthesized?
A
synthesized from precursor proteins that are synthesized in cell body and shipped to axon terminals
- replenishment of neuropeptides slower
18
Q
what are endocannabinoids?
A
produce effects similar to THC - regulate & control many of critical body functions (learning & memory, emotional processing, sleep, temperature control, pain control, inflammatory & immune response, and eating)
- the receptor outnumber many other receptors in the brain
- act like traffic cops to control levels and activity of other neurotransmitters
19
Q
how do gas neurotransmitters differ?
A
- produced outside axon terminals (mainly in dendrites and diffuse out as it is produced)
- no receptors involved (diffuses into target cell and activates second messenger)
- function as retrograde transmitter by diffusing from post to pre
20
Q
how can drugs alter synaptic transmission?
A
- increase/decrease transmitter synthesis
- affect neurotransmitter storage/release
- stimulate/inhibit autoreceptors
- mimic/inhibit transmitter effect on receptor
- block transmitter breakdown/inhibit reuptake
21
Q
how do drugs increase/decrease transmitter synthesis?
A
- if a drug is a chemical precursor to the transmitter, then rate of transmitter formation increases
- can decrease by inhibiting key enzyme needed for transmitter synthesis
22
Q
how can drugs affect storage or release?
A
- can block storage (reserpine blocks storage of DA, NE and 5-HT in synaptic vesicles)
- stimulate release (amphetamine stimulate release of DA and NE)
23
Q
how can drugs mimic or block transmitter effect?
A
- nicotine can mimic ACh on receptors
- Curare and bungarotoxin block ACh receptors
24
Q
how do drugs stimulate or inhibit auto receptors?
A
- drugs stimulate autoreceptors and reduce amount produced
- drugs inhibiting increase the amount produced
25
What is a dose-response curve?
graph depicting the relationship between drug dose and resulting drug effects
26
what is the difference between effective dose and threshold for dose-response curve?
effective dose 50%: the dose of drug needed to show half of maximal effect
threshold: dose that produces smallest measurable response
27
what is potency?
amount of drug necessary to produce specific effect
28
how do you calculate the therapeutic index?
TD50: dose at which 50% of population experiences toxic effect
LD50: dose at which 50% of population experiences lethal effect
- Therapeutic index: TD50/ED50 or LD50/ED50
29
which is better for therapeutic index (wider or shorter)?
a wider therapeutic index indicates a safer drug
30
what is binding affinity with drugs?
degree of chemical attraction between ligand and receptor
- drug will bind strongly to one king of receptor
- at low doses, drugs will bind to their highest-affinity receptors
- at higher doses, drugs can bind to highest-affinity and lower-affinity
31
what is efficacy?
ability of bound ligand to activate receptor
- agonists have high efficacy while antagonists have low or no efficacy
32
what is drug affinity and efficacy?
combination of affinity (where it binds) and efficacy (what it does) determines overall effect of drug
33
what is tolerance with drugs?
condition in which, with repeated exposure to drug, an individual becomes less responsive to constant dose
34
what are the different types of tolerances?
1. metabolic tolerance: organ system becomes more effective at eliminating drug before it can have effect
2. functional tolerance: target tissue may alter sensitivity by changing number of receptors (down-regulation in response to agonist with fewer receptors and up-regulation with antagonist with more receptors)
3. cross-tolerance: tolerance to one drug generalized to other drugs in its class
35
what are psychoactive drugs?
chemical substance that changes function of nervous system and results in alterations of perception, mood, cognition, and behavior
- used for mental disorders, pain management, anesthesia, and recreation
36
what are the five classes of psychoactive/psychiatric drugs?
1. antipsychotics
2. antidepressants
3. anxiolytics/depressants
4. stimulants
5. mood stabilizers
37
what do antipsychotics do?
used to treat psychotic symptoms (those associated with schizophrenia or severe mania)
38
what is the difference between first and second generation antipsychotics?
first: also called neuroleptics; blocks dopamine receptors as it's selective antagonists of dopamine receptors
- reduction in psychotic symptoms associated with excessive dopamine
- has side effects of tardive dyskinesia with abnormal involuntary movements
second: acts on receptors in addition or other than D2 and may relieve symptoms resistant to typical antipsychotics
39
what do antidepressants do?
used to treat disturbances of mood called affective disorders
- two types: monoamine oxidase inhibitors (MAOI) and reuptake inhibitors (tricyclics, SSRIs, and SNRIs)
- all increase levels of monoamines but especially serotonin
40
what do monoamine oxidase inhibitors do?
prevent breakdown of monoamines
- allow transmitter molecules to accumulate in synapses to improve mood
41
what do tricyclic antidepressants do?
improve mood by blocking reuptake of norepinephrine and serotonin
- also block histamine and acetylcholine receptors and fast sodium channels in myocardial cells
42
what do selective serotonin reuptake inhibitors do (SSRIs)?
selectively block serotonin transporters
- promote accumulation of serotonin specifically at serotonergic synapses
43
what do serotonin-norepinephrine reuptake inhibitors do (SNRIs)?
block serotonin and norepinephrine transporters
- have applications beyond depression to include anxiety disorders
44
what is serotonin syndrome?
potentially life-threatening drug induced condition caused by too much serotonin in synapses
- present with neuromuscular, autonomic, and mental status symptoms
- caused by drug interactions (i.e. SSRI and MAOI taken together)
45
what are anxiolytics and different types?
used to reduce anxiety
- three types: depressants, barbiturates, and benzodiazepines
46
what are depressants?
drugs that reduce nervous system activity (alcohol and opiates)
- activates GABA receptors (agonist)
- strong potential for intoxication and addiction
47
what are barbiturates?
oldest sedative-hypnotics that relieve anxiety
- bind to specific receptors of GABA-A chloride ion channel, enhancing GABA activity
- Side effects: induces sleep but reduces amount of REM sleep; mental clouding; loss of judgement; slowed reflexes
- high doses: intoxication, coma, and death from respiratory distress; dangerous with alcohol
- tolerance develop and TI declines with withdrawal leading to seizures
48
what do benzodiazepines do?
used to treat GAD, panic disorder, OCD, and SAD
- enhance activity of GABA by increasing hyperpolarization but only if GABA is present by allowing more Cl- to enter
- does not work without GABA
49
what are opiates?
powerful painkilling effects by containing morphine (effective painkiller)
- bind to opioid receptors in brain (periaqueductal gray)
- endogenous opioids (enkephalins, endorphins, and dynorphins) produced by brain
50
what is the effect of opiates?
overall is inhibitory by hyper polarizing membrane potential, making neuron less excitable
- induce abnormal state of euphoria (powerful reinforcer) by actions within striatum (caudate nucleus)
51
what is cannabis generally?
used for relaxation and mood alternations
- effects range from relaxation, pain reduction, anti nausea, mood alteration, stimulation and paranoia
- delta-9-tetrahydrocannabinol (THC) is main ingredient
- risks: developing schizophrenia, respiratory problems, addiction, and cognitive decline
52
what does cannabis do?
exerts powerful inhibitory effect on neurotransmitter release (ACh, DA, NE, 5-HT, GABA, and glutamate)
- cannabinoid receptors on presynaptic neuron
- cannabis receptors are metabotropic (modulate gene expression by epigenetic changes and activity MAP kinase system- plays role in synaptic plasticity, learning, and memory)
- since metabotropic, could lead to epigenetic change like DNA methylation
53
what do stimulants do?
increase neural activity by increasing excitatory input or decreasing inhibitory activity
- caffeine blocks adenosine autoreceptors that result in increase transmitter release
54
what does nicotine do?
acts as stimulants and acts as agonist on nicotinic ACh receptors which enhance cognitive functions
- also affects DA (activating reward/addiction pathways) and NE (increase HR, BP, and alertness with sympathetic) pathways
55
what does cocaine do?
stimulate mood and behavior
- blocks reuptake of DA, NE, and 5-HT (inhibition of DA reuptake most important for cocaine behavioral effects and addictive potential)
56
what are amphetamines?
cause increased vigor and stamina, wakefulness, decreased appetite, and feelings of euphoria
- indirect catecholamine agonists by stimulating release of DA and NE by entering neuron to stimulate release from vesicles or alters transporter to act in reverse direction to release into synapse)
- NE released also affect sympathetic
57
what does alcohol do?
effects are biphasic with stimulant phase caused by activation of DA and NE followed by depressant phase caused by increased GABA and decreased glutamate
- inhibition results: social disinhibition, poor motor control, and sensory disturbances
