Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
27 Cards in this Set
- Front
- Back
|
Electrical synapses |
Electrical current flows from one neuron to another through gap junctions Not common, Usually in brain Sending or not sending (no change in strength or any other variable) |
|
|
Chemical synapses |
Chemical NT carries info btw neurons Most synapses are chemical |
|
|
Presynaptic neuron |
Synthesizes and packages the NT in synaptic vesicles stored in the synaptic terminal Action potential cause release of NT The NT diffuses across the synaptic cleft(small gap for quick diffusion) and is received by the postsynaptic cell (where receptors are present) |
|
|
Ligand gated ion (ionotrpic) |
Involved in direct synaptic transmission by binding of NTs in postsynaptic cell NT binding causes ion channels to open generating a polysynaptic potention Depolarization = Na channels opening Hyperpolarization = K channels opening |
|
|
Excitatory postsynaptic potential (EPSP) vs inhibitory postsynaptic potential (IPSP) |
Excite: Depolarizations that bring membrane potential to threshold (Na) Inhibit: hyperpolarizations that move the membrane potential farther from threshold (K or Cl) |
|
|
Postsynaptic potentials |
Any single one is usually too small to trigger an action potential in a postsynaptic neuron Gets hundreds or thousands of synaptic terminal |
|
|
Summation |
Individual postsynaptic potentials combine to achieve threshold 2 type is summation |
|
|
Temporal summation |
2 EPSPs are produced in rapid succession |
|
|
Spatial summation |
EPSPs produced simultaneously by different synapses on same postsynaptic neuron add together |
|
|
A combo of both spatial and temporal |
Can start a action potential |
|
|
IPSP can counter effect of an EPSP |
The summed effect of EPSP and IPSP determines whether an axon hillock will reach threshold and generate an action potential |
|
|
2 Receptors on postsynaptic |
Ligand channel (ionotropic) and metabotropic |
|
|
Metabotropic |
NT binds to a receptor that activates a signal transduction pathway in the postsynaptic cell involving a second messenger Slower onset but last longer (due to 2nd messenger) Amplification such that many channels can be opened in response to a signal |
|
|
Many NTs have both |
Ionotropic and matabotropic |
|
|
NTs |
One NT binds to more than a dozen different receptors Receptor activation and postsynaptic response cease when NTs are cleared from the synaptic cleft Happens by: Simple diffusion, inactivation of enzymes, recapture into the presynaptic neuron |
|
|
Acetylcholine |
Common NT Involved in muscle stimulation, memory formation, and learning Myasthenia gravis: act receptors are broken down. Early symptoms are not opening eyelids and facial muscles |
|
|
2 classes of ACH receptor |
Ligand gated (nicotinic), at neuromuscular junction (NMJ), usually excitatory (opens Na channels), stimulating effects Metabotropic (muscarinic), results in open K channels so inhibitory, decrease cardiac output |
|
|
2 classes of ACH receptor |
Ligand gated (nicotinic), at neuromuscular junction (NMJ), usually excitatory (opens Na channels), stimulating effects Metabotropic (muscarinic), results in open K channels so inhibitory, decrease cardiac output |
|
|
Disrupting ACH |
Nerve gas (satin): inhibits actelcholinesterase (breaks down ACH in synaptic cleft). Symptoms impact cardiac output. Tx is an antagonist and block receptor (but only blocks physical effects) Botulism toxin: produced by certain bacteria (prevents release of ACH by presynaptic neuron so the not enough which can paralyze you). Used in Botox (botulism toxin) and treating migraines, cerebral palsy |
|
|
5 classes of NTs |
1. Amino acids 2. Biogenic amines 3. Neuropeptides 4. Gases 5. ACH |
|
|
Amino acids |
Active in CNS and PNS Known to function in CNS are: Glutamate, glycine, and GABA |
|
|
Glutamate |
Most common excitatory NT in CNS Forms long term memory Too much can cause neurodegenerative conditions or excitotoxicity |
|
|
GABA |
Most common inhibitory NT in brain Opens up Cl channels- hyperpolarization |
|
|
Glycine |
Inhibitory NT parts of CNS and brain |
|
|
Biogenic amines |
Made from amino acids: •Norepinephrine (tyrosine): excitatory in autonomic nervous system •Epinephrine: excitatory same as above •Dopamine (tyrosine): impact mood, sleep, attention, and learning •Serotonin (tryptophan): same as dopamine Active in the CNS and PNS Parkinson’s disease-decrease in dopamine Methamphetamines-increase dopamine release |
|
|
Neuropeptides |
Several, short chains of amino acids function as NTs Substance P and endorphins: affect our perception of pain Opiates bind to same receptors as endorphins and can be used as painkillers |
|
|
Gases |
Local regulators, not stored in vesicles. Made on demand and broken down quickly Nitric oxide and carbon monoxide CO in small amounts can synthesize and regulate release of hormones from hypothalamus. In PNS, inhibitory signal in intestines (laxative) NO causes vasodilation (erection) |
