Chapter 11b Synapses and Neurotransmitters
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 voltage gated
* Ca++ stim exocytosis - 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 post-synaptic cell only one-way transmission
* specific for each NT
* ligand–gated Na channels open
* 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 - ability of synapse function to change
* up-regulation
* down-regulation
* potentiation synapse works better
* NMDA receptors increase Ca++ influx
* 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 open IPSP
* digestive smooth muscle close 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 CNS
* excitatory
* also stim NMDA receptors LTP, memory
* aspartate
* excitatory CNS
* GABA gamma-aminobutyric acid
* inhibitory
* most used NT in brain
* Huntington’s disease
* glycine spinal cord
* inhibitory 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 CNS
* NO = nitric oxide (not Nitrous Oxide)
* synthesized on demand
* diffuses out of neuron
* increases LTP (cyclic GMP)
* smooth muscle relaxation
* CO = 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 (botox)
* tetanus block IPSP
* SSRI serotonin-specific reuptake inhibitors
* Parkinson’s low dopamine
* Schizophrenia high dopamine
* memory glutamate
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