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where the the places synapses can occur?
- between axon terminals of the presynaptic neuron
- across the synaptic cleft to the dendrite, cell body, or axon of the postsynaptic neuron
how does communication occur across a synapse? and how it is terminated?
- action potential
- volaged gated Ca+2 channels open
- calcium triggers exocytosis of neurotransmitters
- NT diffuses and binds to receptors
- response in cell
- teminated by degradation by enzymes, re-uptake by transporters and diffusion
what are the different receptors?
- channel linked (ionotropic): ligand gated channels, fast and direct acting
- G-protein linked (metabotropic) receptors: slow, indirect, direct coupling or second messengers
what is postsynaptic potential (PSP)?
change in membrane potential in response to receptor neurotransmitter binding
what is the movment of Cl- an example of? what does it do?
Cl moves in and either inhibits (IPSP-inhibitory postsynaptic potential) or stabilizes membrane potential
difference between divergent and convergent neural integrations
- divergence is a pathway that spreads information from one neuron to mutiple neurons
- convergence is when several nerons synapse with a single postsynaptic neuron
what is neural integration?
- the summing of input from various synapses at the axon hillock of the postsynaptic neuron to determine whether the neuron will generate action potentials
- -spatial (from mutliple axon terminals)
- -temporal (from one axon terminal)
what are the functional classification of neurotransmitters?
- substance must be in pre-synaptic nerve terminal and packaged into synaptic vesicles
- substance must be released from the nerve terminal upon arrival of action potential or depolarization
- specific receptors in post synaptic membrance for substance
- effects may be excitory or inhibitory, direct or indirect (determined by receptor type)
- found in PNS and CNS
- synthsized in cytosol of axon terminal
- choline acetyl transferase (CAT) is the enzyme for synthesis
- degradation occurs in synaptic cleft
typical choliinergic synapse
- action potential depolarize axon terminal
- calcium enter cytoplasm of axon terminal
- ACh release occurs through exocytosis, diffuses across synaptic cleft and binds to receptors on postsynaptic membrane
- sodium channels on postsynaptic surface are activated producing graded depolarization
- Ache release stops b/c calcium are removed
- depolarization ends as Ache is broken down to acetate and choline by AchE
- axon terminal reabsorbs choline from synaptic cleft and uses it resynthesize Ach
what are two types of cholinergic receptors that Ach activates?
- Nicoinic (ionotopic)
- muscarinic (metabotropic)
describe biogenic amines (monoamines) aka catecholamines
- all biogenic amine neurotransmitters are derived from amino acids
- catecholamines: derived from tyrosine (dopamine, norepinephrine-noradrenaline, epinephrine-adrenaline)
- all involved in reward pleasure and learning brain centers
- dopamine is the principle NT involved in addiction pathway
synthesis and release of catecholamines
- synthesis in the cytosol axon terminal, packaged in synaptic vesicles, released by neurons in CNS (dopamine and norepinephrine) and PNS (norepinephrine)
- epinephrine relased by some neurons in CNS but more commonly in adrenal medulla
- for epinephrine and norepinephrine NT
- alpha (1,2) Beta (1,2,3)
- G protein coupled and linked to second messengers)
serotonin, biogenic amines
- a CNS NT, broadly distributed in the brain
- derived from tryptophan
- involved in sleep, dreaming, hunger, arousal, emotional behaviors and biological clock
- depletion leads to depression
- inhibitory in pain pathways
histamine (biogenic amines)
- CNS NT, found in hypothalamus
- derived from histidine
- release from non-neuronal cells during allergic reactions
amino acid NT
- most abundant NTs in CNS
- Aspartate and Glutamate (most common) excitatory
- Glycine and GABA (most common) inhibitory
- short chains of amino acids synthesized in cell body like proteins
- most are co-localized in axon terminals with other neurotransmitters and modulate response caused by other NT
- depress physical functions like breathing and may produce physical dependence
- most known for actions as hormones
acetylcholine role in body
NT used by spinal cord neurons to control muscles and by neurons in brain to regulate memory. mostly excitatory
NT produces feelings of pleasure when relased by brain reward system, dopamine has multiple functions depending on where in the brain it acts. usually inhibitory
major inhibitory NT in brain
NT and hormone. In PNS, it is part of fight or flight response. in brain it acts as NT regulating normal brain processes. usually excitatory
how can drug interfere with neurotransmission?
- increase number of nerve impulses
- release NT from vesicles with or without impulses
- block reuptake or block receptors
- produces more or less NT
- prevent vesicles from releasing NT
how does methamphetamine alter dopmine transmission?
- enters dopamine vesicles in axon terminal causing release of NT
- blocks dopamine transporters from pumping dopamine back into NT neuron
- causes neurons to fire more often--euphoric feeling
- after drug wears off, dopmine levels drop, and user crashes
- -causes dopamine axons to wither and die
How does Nicotine work?
- binds to presynaptic receptors exciting neurons to fire more action potential causing an increase in dopamine release
- increase number of synaptic vesicles relased
- affects cognition, mood, and memroy by altering the serotonin neural pathway in several brain centers
- short term effects (changes in brain chemistry and behavior)
- alters neuron membranes, ion channels, enzymes and receptors
- binds directly to receptors for NT and hormones like GABA
- -when GABA attaches to receptor on postsynaptic membrane, it allows Cl- ions to pass into the neuron (hyperpolarizing)
- -alcohol binds to GABA receptors and amplifies the hyperpolization effect of GABA
- this accounts fro some of the sedative effects of alc
how to increase or descrease or no change in neurotransmitter release?
- increase impulses
- release NT from vesciesl with or without impulses
- release more NT in response to an impulse
- prevent vesicles from releasing NT
- block receptor wth another molecules (no change)
how to increase or decrease NT in synaptic cleft?
- block reuptake
- produce less NT