MT 2 Flashcards
in the war of the soups and sparks who won?
soups
the “soups” (chemical transmission) side ultimately won against the “sparks” (electrical transmission) theory
what is the soups vs. sparks debate
a historical debate about whether nerve impulses are conducted chemically or electrically at the synapse
describe neurotransmitters
- released by neurons into synaptic cleft
- excitatory or inhibitory effect on adjacent post-synaptic cell
describe neuromodulators
- released ny neurons in larger amounts than NTs
- diffuses further than adjacent synaptic cleft
- affects genera; behavior (vigilance, arousal, pain, sensitivity)
- often neuropeptides (protein-like molecules)
describe hormones
- secreted by endocrine glands into extracellular fluid
- bloodstream transports to rest of body
- calls must have hormone receptor to be affected
- affects reproduction, growth, homeostasis (urine production, hunger, temp. regulation, etc.)
autoreceptor
on the presynaptic cell
prevents buildup of NT in synaptic cleft
they slow down NT release from the presynaptic cell when there is already an overabundance of NT in the synaptic cleft
drug / toxin effects on neurotransmission
positive regulation of neurotransmitter or negative regulation of neurotransmitter. can happen in presynaptic neuron or within synaptic cleft.
positive regulation of NT within presynaptic
- NT synthesis
- uptake into vessicle
- exocytosis
positive regulation of NT within synaptic cleft neuron
- diffusion in synaptic cleft
- postsynaptic receptor binding
negative regulation of NT within presynaptic neuron
- NT degradation
negative regulation of NT within synaptic cleft
- NT degradation
- reuptake
- autoreceptor binding
agonists
can facilitate positive regulatory effects of NT or inhibit negative regulatory effects of NT
i.e., a drug that facilitates the effects of the NT on the postsynaptic cell
antagonists
can inhibit positive regulatory effects of NT or facilitate negative regulatory effects of NT
i.e., a drug that decreases the effects of the NT on the postsynaptic cell
receptor-binding compounds (ligands)
ligand - any chemical that binds to the binding site
- they are direct agonists (they work directly on receptor protein)
- NTs
- drugs (medicinal and illicit) and poisons
- direct antagonists (receptor blockers)
- drugs (medicinal and illicit) and poisons
T/F - a drug that acts to speed up reuptake would be considered an antagonist
True
T/F - a drug that causes synaptic vesicles in the presynaptic neuron to leak inhibitory NT molecules into the intracellular fluid would be considered an antagonist
True
amino acids
some of the building blocks of proteins (i.e, glutamate, gaba, glycerine
amines
modified amino acides
- acetylcholine
- dopamine
- closely related to epinephrine (adrenaline, a hormone)
- serotonin
peptides
short chain of amino accids
endongenous opiodids
lipids
nucleosides
gases
gultamate
- receptors are widesspread in CNS
- most abundant excitatory NT
- excessive amounts = death
- increases activity in neural circuits
gaba
- receptors are widespread in CNS
- most abundant inhibitory NT
- decrease activity in neural circuits
glycine
- most common inhibitory NT in PNS
- postsynaptic receptors
- ionotropic receptor opens Cl- channel (causes IPSP)
- antagonist = strychnine (rat poison)
- causes convulsions
- synaptic release inhibited by tetanus toxin muscles become overstimulated and rigid. also inhibits GABA release.
acetylcholine
IN PNS:
- most common NT in PNS
- NT at the neuromusclular junction (synapse between motor neuron and muscle cell)
- stimulates muscle contractions in somatic nervous system and glands in autonomic nervous system
- usually excitatory (causes ESPS) but can be inhibitory
IN CNS:
- cholinergic neurons concentrated in brainstem
- axons have widespread projections to the cerebral cortex
- important for learning
which of the following would be an expected effect of a poison that acts as an acetylcholine agonist?
a. paralysis due to muscle weakening
b. paralysis due to involuntary muscular contractions
c. slowing of the heart rate
d. both A and C
e. both B and C
E (both B and C)
4 drugs that effects on ACh action
synaptic release affected by black widow spider venom
- stimulates release (exocytosis)
- spastic effect on muscles causes death –> diaphragm cannot be contracted to help breathe
botulinum toxin
- inhibits release of ACh
- poisonous and can kill people –> paralysis –> muscles become perpetually relaxed (diaphragm cannot be contracted to breathe in)
- swelling of a can of food
nicotinic receptor
- postsynaptic receptors nicotinic recepters
- direct agonist = nicotine
- direct antagonist = curare
muscarinic recpetors
- direct agonist = muscarine
- direct antagonist = atropine
acetylcholineresterase (AChE)
- deactivated in the synaptic cleft
- AChE inhibited by: several nucleotides physostigimine (or neostigmine) to counter effects of myasthenia gravis (autoimmune disease that destroys ACh receptors)
NTs that are amines
- acetylcholine
- dopamine
- norepinephrine
- epinephrine
- serotonin
dopamine
dopaminergic neurons located in brainstem and involved in motor control pathway from substania nigra to basal ganglia
- pathway damaged in parkinson’s disease
- symptoms relieved with L-DOPA (precursor molecule)
feelings of pleasure, reinforcement, and reward
- pathway from ventral tegmental area to nucleus accumbens, stimulated by pleasure associated with food, sex, money, addicted drugs
- reuptake blocked by cocaine, amphetamine (stimulants such as methamphetamine) and methyliphenidate (ritalin)
direct antagonists = chlorpromazine, clozapine
- antipsychotic drugs that alleviate symptoms of schizophrenia
pathway involved in the biological basis of reinforcement
ventral tegmental area –> nucleus accumbens –> prefrontal cortex
norepinephrine
noradrinergic neurons
- located in locus coeruleus in pons with axons projecting throughout brain regulate vigilance and attention
- 4 different types of norepinephrine receptors some cause IPSPs, others EPSPs
epinephrine
hormone from adrenal glands on the kidneys serves minor role as NT in brain
serotonin
serotonergic neurons located in rephe nuclei of brain stem, send axons widely throughout the brain.
- involved in regulation of mood, eating, sleep, dreaming, pain
- direct agonists = LSD, psilocybin, and peyote (hallucinogens)
- reuptake inhibited SSRIs
T/F after taking a high does of ecstacy, its common to go through a period of depression after the acute phase of the drug wears off
T
serotonin and ecstasy (short term effects)
MDMA (ecstacy) affects serotonergic system by
- inhibits serotonin reuptake
- increasing relase of serotonin (reverses the serotonin reuptake transporter)
- euphoria, positive emotions, colorful visual effects
serotonin and ecstasy (long term effects)
long term damage to serotonergic neurons
- axonal withering
- followed by abnormal regrowth (or none at all)
serotonin and psilocybin
metabolic breakdown of psyilocybin in liver results in psilocin
- psilocin is a serotonin direct agonist, indirectly triggers dopamine release
- wide range of effects
peptides
short chain or amino acids (made of two or more linked amino acids)
- endongenous opiods (“like opium produced with”)
- oxytocin, substance P, vasopressin
- involved in pain regulation
agonists = derived from poppies = opium, morphine, heroin, oxyContin
opioid addiction
- opioids act as antagonists for axoaxonic GABAnergic synapses in nucleus accumbens
- inhibiting release of GABA causes additional release of dopamine in this “reward center,” leading to euphoric feeling and addiction.
lipids
fat-like molecules
- endongenous cannabinoids increase dopamine release
- agonist: marajuana components THC and CBD
- released from postsynaptic cell
- regulates release of NT from presynaptic cell
nucleosides
- adenosine released when neuron and glia shory or fuel O2
- causes nearbu blood vesse;s to dialate
- inhibitory metabotropic receptors (i.e., causes IPSP)
- direct antagonist = caffeine –> binds to make you less tired
soluble hases
nitric oxide
- diffuses across cell membrane w/o vessicle or active transport
- can function as retrograde transmitters allowing postsynaptic neurons to affect presynaptic functiona
- important…
- agonist = viagra
T/F all drugs that have neurological effects directly alter some mechanism of typical synaptic function
False
tetrodotoxin
blocks sodium channels
- prevents transmission of action potentials in peripheral nervous system (can’t cross blood-brain barrier)
sensory transduction
process by which information (energy) in then environment is converted to information (energy) in the nervous system.
neuronal communication in the retina
light transduction hyperpolarizes the photoreceptor
glutamate in retina key
the glutamate receptor controls whether there is an excitatory or inhibitory signal sent to the next cell (ex. amacrine cell)
