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52 Cards in this Set
- Front
- Back
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characteristics of presynaptic ending
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axon expands into a terminal button or varicosity
has vesicles containing NT presence of electron dense regions |
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characteristics of postsynaptic nueron
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electron dense region underlies that of presynaptic membrane but not thrown into folds
contains receptors for the NT |
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what is the difference in sequence of transmission between an NMJ and your typical nueron?
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released NT may produce excitatory or inhibitory effects
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what is the EPSP
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Excitatory PostSynaptic Potential.
a transient depolarization produced, the membrane potential goes to a level less negative than the threshold increasing the probability that the postsynaptic cell will produce an AP |
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IPSP
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Inhibitory PostSynaptic Potential.
an inhibitory NT drives the membrane potential to be more negative (transient hyperpolarization) than the threshold, decreasing the probability of an AP |
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what is the trigger zone?
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the axon-hillock initial segment region where the AP originates
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what are the classifications of the synapses
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axodendritic - synapse on the dendrite of a nueron
axosomatic - synapse on the soma axoaxonic - synapse on the axon |
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what is the relationship of the triggerzone to AP input?
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since APs are triggered here, the AP activity is governed by the membrane potential at this site alone. This membrane potential is determined by the sum of all synaptic inputs merging onto this nueron at any given time
***imputs closer to the trigger have greater influence (decremental conduction) |
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how do spatial summations occur at the trigger zone
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arrival of two or more inputs either add (EPSP + EPSP) or subtract (EPSP + IPSP)
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how does temporal summation occur at the trigger zone
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build up of synaptic potentials during repetitive stimulation of SINGLE INPUT because of the overlap in time of postsynaptic responses
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What is facilitation? how does it affect presynaptic NT release?
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an increase in the size of the postsynaptic response during repetitive stimulation of the presynaptic nueron.
lasts less than 1 second results from increased # of quanta released with each succeeding stimulus due to the residual Ca left over from each preceding AP. |
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what is posttetanic potentiation?
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enchancement of the postsynaptic response after subjecting the presynaptic nueron to high frequency stimulation for several seconds. lasts up to several minutes, due to the increased # of quanta.
Saturation of Ca-buffering system, excess Ca increases availability of vesicles for release |
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what is long term potentiation?
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enhanced NT release after a strong tetanic stimulation, lasts for days or longer. involves both pre- and post- events.
1) mediated through NMDA receptors on post cell 2) activation of NMDA leads to production of retrograde messenger 3) the retrograde messenger diffuses from postsynaptic cell to presynaptic ending causing an increase in NT output by activating 2ndary messengers. serves as a cellular model for memory?? |
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what is depression?
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decrease in the amount of NT released after a train of stimuli
lasts a few secs to a few mins occurs at synapses with high quantal content due to depletion of vesicles available for release |
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describe the general characteristics of NTs
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stored in vesicles in presynapses
released upon nerve activity diffuse to the post- and combine with receptors produce change in conductance inactivation occurs by hydrolysis, uptake, or diffusion |
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How do gaseous transmitters (NO and CO) behave differently from classic NTs?
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not stored in vesicles but released as soon as synthesized
do not combine w/ receptors but go straight to 2ndary messenger systems inactivation by diffusion |
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Acetylcholine
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primary NT of the PNS
also participates in some CNS pathways degeneration of certain cholinergic paths occur in Alzheimer's disease |
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what are catecholamines? name 3
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NTs synthesized from the AA tyrosine
dopamine (DA) norepinephrine (NE) epinephrine (E) |
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Dopamine
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DA
found primarily in midbrain and diencephalon Parkinsonism involves degredation of DA pathways group of disorders classified as schizophrenia linked to DA |
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Norepinephine
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primary transmitter of postganglionic sympathetics
widespread NE projections from the locus coeruleus in the brainstem to the forebrain influence sleep, wakefulness, attention, and feeding |
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Epinephrine
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established role as hormone in stress response
NT in brain, unknown function |
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Serotonin
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5-hydroxytryptamine, 5-HT
synthesized from tryptophan widespread projections from raphe nuclei in brainstem to brain and cerebellum implicated in onset of sleep, mood, emotional behavior, and certain psychotic disorders |
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histamine
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synthesized from histidine
present in mast cells (non-nueronal) found in nuerons of hypothalmus mediate arousal |
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4 amino acid transmitters
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glycine (gly), gamma-aminobutyric acid (GABA), glutamate (glu), aspartate (asp)
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glycine
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inhibitory transmitter, found in spinal cord and brain stem
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GABA
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important inhibitory transmitters of CNS
GABA deficit implicated in Huntingtons Chora |
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Glutamate
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most prevalent excitatory transmitter in the brain
excess in CNS can act as excitotoxin causing cell death |
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aspartate
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nearly uniquitous excitatory transmitter
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what are nueropeptides
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polypeptides synthesized de novo in the soma
packaged in vesicles and transported via axoplasmic transport to axon terminals or sites of release. Fx as NTs, nueromodulators, and hormones |
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nueropeptides as NTs
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released from presynaptic nueron and produce a conductance change in postsynapse
action terminated by diffusion and perhaps peptidases |
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nueropeptides as nueromodulators
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alter some aspect of cell function e.g. excitability, amount of NT release, products synthesized
modulatory effects can be slow in onset and slow to dissipate (hours to days) all NMs activate G-protein coupled receptors that stimulate an intracellular signal cascade e.g. activation of adenylyl cyclase and elevation of C-Amp |
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classes of nueropeptides
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Opiods, gut-brain and hypophysiotrophic, NMs and NTs
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Endorphin
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Opiod NP derived from proopiodmelanocortin
bind preferentially to u-receptors |
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Enkephalin
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opiod NP derived from proenkephalin
bind to sigma-receptors |
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Dynorphin
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opiod NP derived from prodynorphin
bind to K receptors |
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Nitric Oxide
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Gaseous transmitter/modulator
first identified as endothelial-derived relaxing factor in blood vessels synthesized from L-arginine by NO synthase NOT STORED IN VESICLES does not bind to receptors |
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Carbon Monoxide
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synthesized from heme by heme oxygenase
diffused through cell membranes and released as synthesized one major action is activation of guanylyl cyclase |
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direct-gated ion channels
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aka ligand-gated or ionotropic receptors
transmitter receptor is part of the ion channel single macromolecule forms both the recognition site and ion channel binding of NT produces a conformation change in the macromolecule which results in opening of the channel |
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nicotinic ACh receptor
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Direct-gated channel.
binding of two ACh molecules initiates conf. change ion channel allows flux of Na into and K out of cell resulting in depolarization |
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how is the NMDA glutamate receptor more complex than the ACh
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ion channel is plugged by Mg at resting potential, needs sufficient depolarization (20-30mV) to drive Mg out of channel so it can be activated by glutamate
once unplugged the channel has high permeability to Ca as well as Na and K presence of glycine is required for efficient functioning of channel |
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how do the presence of non-NMDA glutamate receptors assist cells which contain NMDA receptors
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non-NMDA receptor activation depolarizes the cell, as depolarization increases NMDA channels are unplugged and current through them increases
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What is the result of Ca entry through NMDA channels?
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activation of Ca-dependent second messenger systems (Ca-calmodulin/kinase)
too much Ca results in cell death |
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what receptor is responsible for most of the inhibition in the CNS
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GABA-A
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what is the effect of GABA binding?
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opens CL- selective channels
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how is GABA modified by second-messenger pathways
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phosphorylation by either PKC or PKA reduces CL current
therefore 2ndary messengers can alter inhibitory activity in the CNS |
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what other substances can bind to additional sites on GABA receptors to modify activity
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Benzodiazapines (Valium) and Barbituates (phenobarbital) -increase the freq. of channel opening produced GABA and thus increase CL- current
steroids mimic the effects of barbituates ethanol increases the GABA-induced CL current |
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what receptor mediates the inhibition of CNS not mediated by GABA
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GLycine receptor
binding opens Cl selective channel |
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membrane-delimited pathway
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G-protein directly affects the ion channel
binding of NT to receptor activates GP and the beta/gamma subunits of the GP diffuse through the membrane to interact with nearby channels e.g. M2 ACh receptor on heart which increase K permeability ----these indirect receptors are relatively fast with latency period of 30-100 ms also relatively localized response b/c limited diffusion of the GP within the membrane |
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Indirect G-protein activation
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G-protein activates a 2nd messenger system
binding of NT activates GP GP activates an enzyme which gives rise to 2nd messenger (Ca, cAMP, cGMP, IP3, DAG, arachidonic acid) |
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activity of 2nd messenger
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created by enzyme activated by GP
directly modulates ion channel activates a kinase which phosphorylates a protein and causes channel to open or close |
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example of 2nd messenger system
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B1 receptor activation by NE in the heart leads to activation of adenylyl cyclase and an increase in C-AMP which activates protein kinase A that phosphorylates the L-type Ca channel leading to an increase in Ca influx
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properties of G-protein/2nd messenger system
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slow pathay with latency of 100's to 1000's ms
capable of widespread effects b/s of the production of soluble messengers which can diffuse through cytoplasm capable of a great deal of amplification can generate long-lasting changes in cells |
