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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