PTP 512 Neuroscience in Physical Therapy Introduction Neurotransmitters Min H. Huang, PT, PhD, NCS.
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Transcript of PTP 512 Neuroscience in Physical Therapy Introduction Neurotransmitters Min H. Huang, PT, PhD, NCS.
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PTP 512Neuroscience in Physical Therapy
IntroductionNeurotransmitters
Min H. Huang, PT, PhD, NCS
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Concepts you should already know before this lecture
• Cell membrane ion channels• Resting membrane potential• Local potential
–Temporal summation–Spatial summation
• Action potential• EPSP• IPSP
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Types of Synapses in the CNS
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HETEROSYNAPTIC PLASTICITY
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Presynaptic Inhibition and Facilitation
• Axoaxonic synapses mediate presynaptic inhibition and facilitation, e.g. present in the spinal cord to regulate the propagation of information to the brain.
• Interneurons regulate the ability of the presynaptic neurons to release neurotransmitters by changing the amount of Ca++ influx to the presynaptic neurons.
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Presynaptic Facilitation1 Interneuron2 Presynaptic neuron3 Postsynaptic neuron
1 release transmitters
Transmitters bind to receptors on 2
This causes 2 to release more transmitters into the synaptic cleft between 2 & 3 when an action potential arrives
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Presynaptic Inhibition
1 Interneuron2 Presynaptic neuron3 Postsynaptic neuron
1 release transmitters
Transmitters bind to receptors on 2
This causes neuron 2 to release less transmitters into the synaptic cleft when an action potential arrives
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SYNAPSE
Syn – togetherHaptein – to clapse
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http://www.ncbi.nlm.nih.gov/books/NBK11164/
Electrical vs. Chemical Synapse
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Type Electrical ChemicalLength of synaptic cleft
3.5 nm 20-40 nm
Cytoplasmic continuity
Yes No
Structure Gap junction Presynaptic vesiclesPostsynaptic receptors
Agents of transmission
Ion current (electrical)
Neurotransmitters (chemical)
Synaptic delay Virtually absent > 1-5 msDirection of transmission
Bidirectional Unidirectional
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Dobrunz, 2002
Chemical Synapse
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Synaptic Communication
Lundy’s CD - Synapse
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Synaptic Communication• Total # of action potentials reaching the
presynaptic terminal directly influences the amount of neurotransmitter released
• ↑excitatory stimuli to the presynaptic neuron cause increased # action potentials reaching the presynaptic terminal
• ↑duration of excitatory stimuli to the presynaptic neuron cause a longer series of action potentials reaching the presynaptic terminal
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NEUROTRANSMITTERS AND NEUROMODULATORS
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What is a Neurotransmitter?• It is synthesized in the neuron• It is present in the presynaptic terminal• It is released in amounts sufficient to exert an
action on the postsynaptic neuron or effector organ
• It is removed from the synaptic cleft by a specific mechanism–Synaptic vesicle cycling
http://neuroscience.uth.tmc.edu/s1/chapter05.html
Schwartz, 2005
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What is a Neurotransmitter?
• When administered “exogenously” (e.g. drugs) in reasonable concentration, it mimics the action of the endogenously released neurotransmitter exactly. It activates the same ion channels or second messenger system in the postsynaptic cell.
Some define neurotransmitters to include neuromodulators that act away from the synaptic cleft (Blumefeld, 2010).
Schwartz, 2005
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What is a Neuromodulator?• Act at a distance away from the synapse• Modulate activity of many neurons• Released into extracellular fluid• The same chemical substance can act either
as a neurotransmitter or neuromodulator• Effects last minutes to days• Neurotransmitters and
neuromodulators can be released simultaneously
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Functions of Neurotransmitters• Mediate communication between neurons or
the end-organs through fast excitatory (EPSP) or inhibitory (IPSI) postsynaptic potentials (<1 ms)–Directly opening ligand-gated ion channels
on postsynaptic membrane• Slow-acting neuromodulation, occurring over
100ms to minutes– Indirect opening ion channels or activation
the cellular signaling cascades
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Neurotransmitter Receptors
• Receptors are often named according to the neurotransmitters to which they bind, e.g. GABAA, GABAB, 5-HT receptors
• The same neurotransmitter may bind to several types of receptors, e.g. Serotonin
• The effect of neurotransmitters on a postsynaptic neuron is determined by the type of receptors present on its membrane, e.g. Ach, Norepinephrine
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Signal Transmission Mechanisms: Direct Activation of Ion Channels
Neurotransmitters bind to receptors that are part of the ligand-gated ion channels and directly open the ion channels.
Lundy’s CD
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Signal Transmission Mechanisms: Indirect Activation of Ion Channels
Neurotransmitters bind to receptors that are separate from the ion channels, and indirectly open the ion channels by activating the G-protein. This process involves changes in the metabolism of the cell.
Lundy’s CD
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Signal Transmission Mechanisms: Activating Intracellular Signaling
Activation of the G-protein second-messenger system can trigger the intracellular signaling cascade. This process has long lasting effects on regulating genes expression and neuronal growth.
Byrne, 1997
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Termination of Synaptic Transmission• Removing neurotransmitters
–Diffusion: remove a fraction only–Enzymatic degradation: e.g.
acetylcholinesterase–Reuptake: most common, e.g. serotonin
• Desensitizing receptors by–Receptor internalization: folding the
postsynaptic membrane containing the receptors into the cell
–Receptor inactivation
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Common Neurotransmitters and Neuromodulators
• Amino Acid— GABA— Glutamate (Glu)— Glycine (Gly)
• Cholinergic— Acetycholine
(ACh)
• Amine— Dopamine (DA)— Serotonin (5-HT)— Norepinephrine
(NE)• Peptide
— Substance P— Endorphins
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Amino Acid: GABA
• Fast-acting MAJOR inhibitory neurotransmitter found in the entire CNS, e.g. inhibitory interneurons in spinal cord
• Prevents excessive neural activityBarbiturates mimics the action of GABA and
are used for sedation, as anticonvulsants.Baclofen, a muscle relaxant to control
muscle spasticity, increases presynaptic release of GABA
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Amino Acid: Glutamate (Glu)• Fast-acting MAJOR excitatory
neurotransmitter found in the entire CNS• Involved in learning and memory • Glutamate is present in a wide variety of
foods, e.g. MSGOveractivity of glutamate may cause seizuresExcitotoxicity: Excessive glutamate may
produce neuronal damage or death, e.g. TBI or CVA (X1000 higher than normal)
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Glutamate Receptors
• AMPA: ligand gated receptor• NMDA: ligand- and voltage-gated receptor
–Postsynaptic neuron must depolarize when the Glu binds to the NMDA receptor in order to open the gate
–Prolonged opening of ion channels resulting in long-term potentiation (LTP)
• Metabotropic glutamate receptor: indirect activation by G-protein pathway
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NMDA Receptor
Channel is permeable to Na+, Ca++, K+, opens and closes very slowly.LTP plays an important role in neuroplasticity.
Byrne, 1997
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Acetylcholine (ACh)• MAJOR neurotransmitters in PNS, ANS
–Fast-acting effect: act at neuromuscular junction, e.g. Nicotinic receptors
–Slow-acting effect: regulate HR, ANS function, e.g. Muscarinic receptors
• Primary as a neuromodulator in CNS –Controls locomotion, arousal–Facilitate attention, memory, learning
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ACh Receptors
Nicotinic Receptor Muscarinic Receptor
Byrne, 1997
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Nicotinic MuscarinicBind nicotine Bind muscarineLinked to ion channels Liked to 2nd messenger
system through G proteinFast and brief response
Slow and prolonged response
Located at neuromuscular junctions, autonomic ganglia, and some CNS
Found on myocardial muscle, certain smooth muscle, in some CNS regions
Mediate excitation Mediate inhibition and excitation
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Cholinergic Projection
Systems
Blumefeld, 2010
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AcetylcholineApplying electrical stimulation to
pontomesencephalic region of the brainstem elicits coordinated locomotor movements.
Drugs that block the cholinergic transmission in the brain causes delirium and memory deficits.
Degeneration of cholinergic neurons in the basal forebrain may be associated with memory decline in Alzheimer’s disease
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Myasthenia Gravis (MG)• ACh receptors on muscle membranes are
destroyed . Weakness becomes more severe with repetitive use of a muscle.
• Rx: Anticholinesterase inhibits the cholinesterase from breaking down ACh.
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Myasthenia Gravis (MG)
Reduced EMG amplitudes over repetitive muscle contractions.
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Case: a 12-year-old girl with cerebral paly
She walks on her toes and exhibits a scissor gait, with legs strongly adducted with each step. Standard physical therapy has not resulted in any significant improvements. Her physicians want to inject a small amount of Botulinum toxin (Botox) into the gastrocnemius and adductor magnus muscles of both legs to reduce involuntary muscle activity and improve gait.
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Questions• By what mechanism could the injection of
Botox reduce involuntary muscle activity?• At the neuromuscular junction, ACh acts via a
ligand-gated receptor. Is the action of ACh on the nicotinic, ligand-gated receptor the same as its action on the muscarinic, G-protein-mediated receptor?
The effect of Botox lasts about 12 weeks.Too much ACh leads to spasm or tremorToo little ACh leads to paralysis or delirium
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Amines: Dopamine (DA) • Produced in substantia nigra of basal
ganglia and ventral tegmentum• Primarily an inhibitory effect in CNS• All DA receptors are 2nd messenger systems
to suppress the activity of Ca++ channels.• Affects motor activity, motivation/reward
behavior, and cognition
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Dopamine Projecting System
BG Limbic Prefrontal Movement Reward Working Memory Addiction Attention
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Neurologic Conditions Associated with Dopamine (DA)
Parkinson’s Disease Case: ↓DA in basal ganglia
Depression/Cognitive: ↓DA in forebrainDrug addiction: cocaine and amphetamines
interfere with DA reuptake into the presynaptic neurons, allowing DA to activate receptors repetitively
Schizophrenia: too much DA
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Amines: Serotonin (5-HT)
• Produced in raphe nuclei and GI tract• Serotonin regulates sleep-wake cycle,
cognition, perception of pain, breathing, temperature, movements, and mood.
• Serotonin is associated with depression, anxiety, obsessive-compulsive disorder, aggressive behavior, certain eating disorders (release serotonin ↓appetite)
• Serotonergic neurons ↓firing during sleep
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Amines: Serotonin (5-HT)
Serotonin is “happiness hormone”. Serotonin ↓perception of pain. Low levels of serotonin are associated with depression.
Prozac (antidepressant) is a selective inhibitor of serotonin reuptake (so serotonin stays in the synaptic cleft longer to bind with receptors)
SIDS may be associated with defected serotonergic neurons.
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Serotonin Projecting
System
Noradrenergic Projecting Systems
Blumefeld, 2010
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Norepinephrine (NE)
• Regulate functions of ANS, thalamus, and hypothalamus
• Modulate attention, sleep-wake cycle–Noradrenergic neurons ↓firing in sleep–Attention-deficit disorders if often
treated with medications that enhance NE transmission
• ↑level of NE is associated with vigilance, ↑alertness, and “fight-or-flight” response
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Norepinephrine (NE)
• Noradrenergic neurons involve in sympathetic functions such as blood pressure control
Similar to Serotonin, NE also ↓perception of pain in the CNS, and plays a role in many psychiatric syndrome–↓NE can cause depression–↑NE can cause anxiety (panic attack)
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Serotonin Projection
System
Noradrenergic Projecting Systems
Blumefeld, 2010
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Histamine• Found mainly in the hypothalamus. • Found mostly outside the nervous system
in mast cells that mediate immune responses and allergic reactions.
• Role of histamine in the brain –Maintain the alert state–Excitatory effects on thalamus
Antihistamine medications can cause drowsiness by blocking CNS histamine receptors
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Peptides: Substance P• Released from the terminals of some sensory
nerve fibers• Neurotransmitter function in the nociceptive
pathway–stimulates free nerve endings at the site of
injury and transmit pain signals from the periphery to the CNS
• Neuromodulator function in the chronic pain syndrome– increase pain perception
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Peripheral sensitization following cell damage. Pain signals cause the free nerve endings to release substance P. 5-HT outside the nervous system stimulates the nociceptive free nerve endings.SP-substance PH-histamine5HT-serotonin
Hauser, 2010
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Peptides: Endogenous Opioids (endorphin, enkephalin,
dynorphin)• Body’s natural pain
killers• Inhibit CNS neurons
involved in the perception of pain
• Exercise increases endogenous opioids
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Nitric Oxide (NO)
• An free radical, highly reactive, diffusible gas molecule with neuromodulator effects
• NO is important in the regulation of cerebral blood flow, neurotransmission, long-term potentiation, excitotoxicity (i.e. neuronal death)
• NO cause blood vessels to dilate• NO in excess is toxic to cells
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Review
• What would be the functional implication of presynaptic facilitation and inhibition?
• Describe the structure of a chemical synapse and the events of signal transmission at the synapse.
• Compare and contrast neurotransmitters versus neuromodulators.
• Discuss the functions of neurotransmitters and the associated clinical implications.