Chapter 3: Synapses Flashcards
describe Sherrington’s inferences concerning the speed of a reflex .
Sherrington=communication along an axon and between 2 separate axons is different
SPEED- reflexes (muscles reflex arc) is slower than conduction along axon (delay at synapse)
-one set of muscles is excited another different set become relaxed
temporal summation (Sherrington’s inference)
TEMPORAL SUMMATION- repeated weak stimuli over short period of time have cumulative effect, several weak stimuli presented at slightly different times produce strong reflex than single stimulus
spatial summation (Sherrington’s inference)
SPATIAL SUMMATION- inputs from separate locations combine effects on a neuron (pinch 2 points at the same time) *critical to brain functioning
mechanisms underlying the excitatory postsynaptic potentials
EPSP- excitatory postsynaptic potential
- depolarization
- Na+ into neuron
- if EPSP does not reach threshold it decays quickly
mechanisms underlying inhibitory postsynaptic potentials
IPSP- inhibitory post synaptic potential
- hyperpolarization (more -ve)
- decrease probability of action potential
- open K+ gates (K+ leaves or Cl- enters)
how synaptic potentials contribute to the firing rates of neurons and the integration of information.
- synapses vary in duration and effects
- most neurons have a spontaneous firing rate that EPSP or IPSP can change
- cells have different thresholds meaning same stimulus will not reach threshold of each cell
describe the contributions of T.R. Elliott and O. Loewi to the question of whether most synaptic transmission is electrically or chemically mediated.
T.R Elliot- applying adrenaline directly to the surface of heart, stomach, and pupils produces same effect as sympathetic nervous system therefore sympathetic nerves stimulate muscles by releasing adrenaline or something similar
describe the contributions of O. Loewi to the question of whether most synaptic transmission is electrically or chemically mediated.
O. Loewi- frog hearts experiment- transferred chemicals not electricity from 1 frog to another
conclusion: nerves send messages by releasing chemicals
- discovery led to development of drugs for psychiatric use
list the six major types of neurotransmitters
1) Amino Acids
2) Monoamines
3) Acetylcholine
4) Neuropeptides
5) Purines
6) Gases
role of diet in the synthesis of neurotransmitters
Almost all NTs are synthesized from amino acids in the diet
ex) Phenylalanine-> dopamine, norepinephrine, epinephrine (catecholamines)
ex) tryptophan -> serotonin
processes of transport of neurotransmitters.
Transport: NTs are transported in vesicles until released
processes of release of neurotransmitters.
Release: depolarization opens voltage dependent Ca2+ gates in presynaptic terminal, 1-2ms later NTs released in bursts from presynaptic neuron into synaptic cleft
processes of diffusion of neurotransmitters.
Diffusion: NTs diffuse across cleft to postsynaptic membrane and attach to receptors
-neurons release combinations of NTs
ionotropic effects of neurotransmitters
- begin quickly (less than 1ms post NT attaches)
- NT attaches and channel twists open
- convey visual info, auditory info, and anything that needs ASAP updates
- excitatory or inhibitory
- localized to point on membrane
metabotropic effects of neurotransmitters
- sequence of metabolic reactions
- slower (30ms or more after release of NT)
- last for a few seconds or longer
- NT attaches, bends protein, released G-protein, triggers 2nd messenger system
- influences activity in almost all of cell
- taste, smell, pain, arousal, attention, pleasure, emotion
describe the similarities and differences between neurotransmitters and hormones
NTs- message from sender to receiver
Hormones- chemical secreted by cell in one part of body and conveyed in blood to influence other cells
-long lasting changes in multiple parts of the body
-modify brain activity
-convey message to anyone that can receive it
difference in control mechanisms of the anterior and posterior pituitary and be able to list some of the hormones released from each.
Anterior Pituitary -glandular tissue -synthesizes 6 hormones -hypothalamus controls release by secreting releasing hormones -ACTH, TSH, Prolactin, GH, FSH, LH -works via -ve feedback loop Posterior Pituitary -neural tissue -considered extension of hypothalamus -oxytocin, vasopressin
why inactivation of neurotransmitters is important and the two major ways in which this is achieved
- if was not inactivated it would continue exciting or inhibiting receptor and amplifying response
- Acetylcholine- broken down by acetylcholinesterase in to acetate and choline, choline diffuses back to pre-synaptic neuron
- Serotonin or catecholamines- detach from receptor then reuptake via transporter membrane proteins, enzyme breaks it down and washes away broken down products (excrete in blood and urine)
- Neuropeptides- diffuse away
two mechanisms for producing negative feedback.
Autoreceptors- respond to release of NTs by inhibiting further synthesis and release
Stimulation by special chemicals- chemicals travel back to presynaptic terminal where they inhibit further release of NT
why our brains have receptors for plant chemicals
-all NTs and hormones that are the same as humans in other species so if a plant evolves a chemical to attract bees or repel caterpillars the chemical is likely to affect humans
difference between agonists, antagonists, and mixed agonist-antagonists
Agonist- drug that increases or minimizes effect of NT
Antagonist- blocks a NT
Mixed Agonist/Antagonist- agonist for some effects of NT and antagonist for others, can depend on dose of drug
difference between a drug’s affinity for a receptor and its efficacy at that receptor.
Affinity- if the drug binds to the receptor
Efficacy- drug activates the receptor
-drug can have high affinity but low efficacy if it binds to the receptor but doesn’t activate it
common mechanism of action of nearly all abused drugs
- share effects on dopamine and norepinephrine synapse
- activates nucleus accumbens (central to reinforcing experiences of all types)
- almost all abused drugs and addictive activities increase dopamine release in nucleus accumbens
relation of dopamine in the nucleus accumbens to motivation (“wanting”) and why dopamine does not seem to be related directly to pleasure (“liking”)
- wanting is not always the same as liking
- addiction (wanting) is triggered by dopamine release in nucleus accumbens
- you can want something and have an all-consuming drive to get it even though it doesn’t bring pleasure ex) drug addiction after a bit
explain the differences between the effects of amphetamine, cocaine, and methylphenidate
-all stimulant drugs that increase excitement, alertness, activity, elevate mood, and decrease fatigue
-Cocaine and amphetamine: stimulate dopamine synapses in nucleus accumbens by increasing presence of dopamine at presynaptic terminal by inhibiting dopamine transporters so there is no reuptake
AMPHETAMINE- has similar effects on serotonin and norepinephrine transporters
METHYLPHENIDATE (ritalin)- blocks reuptake of dopamine the same way as cocaine, pill
-difference relates to dose and release time
COCAINE- instant via sniff/inject
-people with ADHD are more likely to become addicted/use/abuse drugs/alcohol
different ways of increasing dopamine release in the nucleus accumbens used by nicotine
NICOTINE- stimulates acetylcholine receptor called nicotinic receptor in nucleus accumbens that are abundant on neurons that release dopamine in NA
-similar mechanism to cocaine (inhibit dopamine reuptake)
different ways of increasing dopamine release in the nucleus accumbens used by opiates
OPIATES- relieve pain by acting on receptors in the brain and producing endorphins
- endorphins synapses inhibit neurons that release GABA, a NT that inhibits firing of dopamine neurons, thereby increasing dopamine release
- endorphins also have rewarding effect on own (unrelated to NA and dopamine)
different ways of increasing dopamine release in the nucleus accumbens used by marijuana
MARIJUANA- binds to cannabinoid receptors
- cannot OD on marijuana because there are no cannabinoid receptors in medulla
- inhibit GABA release in ventral tegmental area (major source of axons that release dopamine into nucleus accumbens) and increase dopamine by inhibiting inhibitor
relationship of the prefrontal cortex to the nucleus accumbens in the facilitation of reinforcing experiences and how repeated drug use changes that.
- axons from nucleus accumbens travel to prefrontal cortex
- addiction takes over motivation and other kinds of reinforcing experiences become less powerful and less able to compete with the drug
- nucleus accumbens is restructured so the drug stimulates more dendrites and other events are less rewarding (ex- sex)
- repeated drug use impairs extinction
physiological effects of alcohol
ALCOHOL- facilitates response at GABAa receptors (inhibitory)
- this leads to decrease in brain activity
- decrease activity in areas of the brain that inhibit risky behaviour
- increased stimulation at dopamine receptors in nucleus accumbens
effects of Antabuse on alcohol metabolism
antagonizes effects of acetaldehyde dehydrogenase (makes people sick when they drink alcohol)
- accumulates acetaldehyde
- abusers take a pill and know if they drink they will get sick due to metabolism disruption
two types of alcoholism
TYPE 1 or A- develop gradually, after 25, may or may not have relatives with alcohol abuse
TYPE 2 or B- rapid onset, before 25, most are men and have relatives with alcohol abuse
differences between sons of alcoholics and sons of non-alcoholics
sons of alcoholics: less intoxication after drinking moderate amount of alcohol
- hold liquor well = increased risk of alcoholism
- lower stress more
- smaller amygdala in right hemisphere (predisposition not a result)
describe the genetic variations that may contribute to alcoholism
-genes that affect alcohol have similar effects on nicotine
-dopamine 4 receptor short and long types
-long form: less sensitive, people report stronger than average cravings for additional alcohol after having 1 drink, seek more alcohol to compensate for less than normal reinforcement
-COMT- enzyme that breaks down dopamine after release, more active or less active form
-more active: breaks down MORE dopamine therefore decreased reinforcement, people are more impulsive, choose immediate rewards instead of bigger rewards later, common in people with impulsive forms of alcoholism
OTHER GENES influence alcohol use by:
-> effect on risk taking behaviour
-> response to stress
-> reactions to anxiety provoking situations
why methadone can be used to treat addiction to heroin or morphine and why it does not end the addiction
- taken orally
- gradually enters blood then brain
- slowly metabolized= satisfy craving in less dangerous way allowing addict to live a relatively normal life and hold down a job
