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Download Chapter 11b Synapses and Neurotransmitters
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Chapter 11b Synapses and Neurotransmitters meurons communicate with other cells • • • signal sender neuron • signal = neurotransmitter signal transporter synapse signal receiver post-synaptic cell neuron muscle gland Synapse • • • = junction between neuron and effector cell pre-synaptic neuron – – axon terminal synaptic vesicles post-synaptic neuron (cell) – receptors for NT connections • • • • axodendritic axosomatic axoaxonic neuromuscular junction types of synapse • • electrical – – gap junctions ions pass between cytoplasm electrically coupled cardiac, smooth muscle ; brain chemical – – – – synaptic cleft neurotransmitter unidirectional CAM’s (cell adhesion molecules) signal sending • action potential reaches axon terminal • depol opens Ca++ channels • Ca++ stim exocytosis • – – – - voltage gated vesicles release NT Ca++ - calmodulin activates protein kinase protein kinase activates synapsins fuses synaptic vesicle to axon terminal membrane Ca++ pump Ca++ back outside signal transport • • • diffusion across synaptic cleft 30 - 50 nM synaptic delay signal reception • NT receptors • specific for each NT • ligand–gated Na channels open • • • – post-synaptic cell only one-way transmission nature wants ? termination of effect : enzymes destroy NT – made by post-synaptic cell re-uptake – by pre-synaptic cell post-synaptic potentials • effect of all NT : – – – open/close ion channels stim proteins that open/close ion channels change membrane polarization • goal: affect threshold at axon hillock • Excitatory postsynaptic potentials • • • – – EPSP depolarization open Na or close K channels Goal raise potential at axon hillock cause action potential Inhibitory postsynaptic potentials – – IPSP hyperpolarization open K or Cl channels Goal lower potential at axon hillock inhibit action potential summation • • • one EPSP can’t induce action potential all EPSP and IPSP are decremental summation = all EPSP + IPSP at axon hillock • temporal summation repeated stim of same receptor • spatial summation stim several receptors at once threshold revisited • • • • • potential at axon hillock is what matters all EPSP and IPSP are summed at axon hillock threshold - minimum increase in voltage to start AP sum > threshold action potential sum < threshold no AP synaptic modification • • • • plasticity – – - up-regulation down-regulation potentiation – – ability of synapse function to change synapse works better increase Ca++ influx NMDA receptors Ca++ increases NT receptor - # and sensitivity presynaptic inhibition – inhibits NT release axoaxonic connections recurrent axons neuromodulation – other chemicals affect synaptic activity ( hormones) Neurotransmitters • • • • secretions from neuron into a synapse made in axon terminal or cell body bind to ligand-mediated channels cheap ! chemical classes of NT • • • • • Acetylcholine (Ach) biogenic amines made from AA amino acids AA act as NT peptides short chains of AA others ATP , gases acetylcholine • • • • • • • • • acetyl-CoA + choline neuromuscular junction ; ANS receptors cholinergic receptors nicotinic receptors – – stimulatory open Na channels skeletal muscle ; ANS ganglia muscarinic receptors EPSP or IPSP open/close K channels (G protein mediated) • cardiac muscle • digestive smooth muscleclose open IPSP EPSP termination of effect acetylcholinesterase AchE re-uptake of choline biogenic amines • catecholamines – – – made from tyrosine dopamine brain ; basal ganglia motor, behavior, reward norepinephrine S-ANS ; CNS (epinephrine adrenal hormone) • • • G-protein mediated via cAMP termination: MAO monoamine oxidase indolamines – serotonin made from tryptophan mood, emotion, appetite – histamine made from histidine amino acids as NT • glutamate – – excitatory also stim NMDA receptors LTP, memory • aspartate • GABA • – – – – CNS excitatory CNS gamma-aminobutyric acid inhibitory most used NT in brain Huntington’s disease glycine – inhibitory spinal cord antagonist muscles glutamate and learning • • • • • • • increases LTP – long term potentiation glutamate stim NMDA receptors Ca++ flows in Ca++ stim calmodulin increase # receptors produce NO NO stim presynaptic NT release (retrograde messenger) peptide NT • substance P pain perception • endorphins reduce pain opiates • neuropeptide Y appetite other NT • ATP • NO • – – – – CO – CNS = nitric oxide (not Nitrous Oxide) synthesized on demand diffuses out of neuron increases LTP (cyclic GMP) smooth muscle relaxation = carbon monoxide may regulate LTP in brain drugs, poisons, and other problems • • • • • • • • • • AchE inhibitors neostigmine, TX myasthenia gravis MAO inhibitors block bioamine destruction nerve gas block AchE activity venom, curare block Ach receptors botulism block Ach release tetanus block IPSP SSRI serotonin-specific reuptake inhibitors Parkinson’s low dopamine Schizophrenia high dopamine memory glutamate (botox)
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