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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
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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
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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
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what is postsynaptic potential (PSP)?
change in membrane potential in response to receptor neurotransmitter binding
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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
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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
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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)
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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)
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Ach
- 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
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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
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what are two types of cholinergic receptors that Ach activates?
- Nicoinic (ionotopic)
- muscarinic (metabotropic)
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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
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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
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adrenergic receptors
- for epinephrine and norepinephrine NT
- alpha (1,2) Beta (1,2,3)
- G protein coupled and linked to second messengers)
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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
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histamine (biogenic amines)
- CNS NT, found in hypothalamus
- derived from histidine
- release from non-neuronal cells during allergic reactions
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amino acid NT
- most abundant NTs in CNS
- Aspartate and Glutamate (most common) excitatory
- Glycine and GABA (most common) inhibitory
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neuropeptides
- 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
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acetylcholine role in body
NT used by spinal cord neurons to control muscles and by neurons in brain to regulate memory. mostly excitatory
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dopamine
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
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GABA
major inhibitory NT in brain
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norepinephrine
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
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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
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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
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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
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ecstasy
- affects cognition, mood, and memroy by altering the serotonin neural pathway in several brain centers
- short term effects (changes in brain chemistry and behavior)
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alcohol
- 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
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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)
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how to increase or decrease NT in synaptic cleft?
- block reuptake
- produce less NT
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