neural transmission
DESCRIPTION
Neural transmission. The Reticular theory vs the Synaptic theory. The “resting Membrane Potential”. Ions are responsible for the Resting membrane potential. Hyperpolarization Moves potential away from zero (more negative) Depolarization Moves the potential toward zero (less negative). - PowerPoint PPT PresentationTRANSCRIPT
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Neural transmission
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• The Reticular theory vs the Synaptic theory
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The “resting Membrane Potential”
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Ions are responsible for the Resting membrane potential
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• Hyperpolarization– Moves potential away from zero – (more negative)
• Depolarization– Moves the potential toward zero – (less negative)
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“Threshold”
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What is special about “threshold?”
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The forces of Diffusion
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The Neurons membrane separates the different ions
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The membrane controls diffusion
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By opening or closingIon channels
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If ion channels are open; diffusion across concentration and electrostatic gradients will
occur
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Threshold Depolarization activates Na+ ion channels….and then Na+ influx will
occur
NA+ influx makes the potential more positive…K+ channels then open and K+ efflux occurs…the neuron moves back toward the RMP
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Once triggered, the AP is all or none, and “one-way.”
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Action potential arrives at terminals
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Causing the release of neurotransmitters into the synapse
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The action potential at the terminals causes Neurotransmitter release into the synapse.
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NTs bind to post-synaptic receptors
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EFFECTS OF NTs?
• IPSPs: inhibitory post synaptic potentials– Hyperpolarization– Decrease probability of action potential
• EPSPs: excitatory post synaptic potentials– Depolarization– Increase probability of action potential
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Ways that receptor activation can lead to IPSPs or EPSPs
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Neural Integration:if enough EPSPs occur threshold
depolarization will activate Na= ion channels
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EFFECTS OF NTs?
• EPSP or IPSP– Depends on the type of Neurotransmitter
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Know these:
Representative NTs
NTs Circuit involvement Effects
Acetylcholine NMJ, Autonomic ganglia +/-(Ach) Brain
Dopamine VTA, Subst. Nigra +/-(DA) accumbens
Norepinephrine RAS, many brain +/-(NE) regions
Serotonin Raphe, Ctx, +/-(5-HT) many regions
Gama-Amino- Ubiquitous -Butyric acid(GABA)
Glutamate Ubiquitous +(Glu)
Endorphin PAG, VTA, +/-Enkephalin(End/Enk)
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Ex: Why is ACH sometimes excitatory and other times inhibitory?Receptor subtypes
Effects depend on receptor subtype
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Neurotransmitters bind to receptor sites to produce postsynaptic effects
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NT-Receptor Specificity
Activation of a receptor will lead to either Excitation or Inhibition.
Lock & Key Model NT = key Receptor = lock
A given NT substance will only activate specific receptor proteins, and can not activate receptors for other NTs
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One Neurotransmitter may activate any of a “family” of receptor
subtypesACH in the ANS can activate the “Muscarinic” ACH receptor (mACH), a metabotropic receptor type.
ACH release in the somatic branch of the PNS activates the “Nicotinic” ACH receptor (nACHr). An ionotropic receptor type.
Activation of the mACHr leads to an inhibitory response.
Activation of the nACHr leads to an excitatory response.
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NT-receptor interactions must stop!Enzymatic degradation
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Nerve gases block ACHE-preventing breakdown of Acetylcholine.
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Different nerve gas compounds; all chemically related to Diisoflourphosphate (DFP) common in low concentrations
in insecticides and some pesticides.
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The effects of nerve gas poisoning reflect normal functions of ACH mostly in the PNS
Functional paralysis of muscle activity is a result of poisoning.
Death is most often due to anoxia, because you can not respire.
Antidotes involve drugs that block the effects of ACH
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The effects of other NTs are terminated by Reuptake. E.g. the serotonin transport
protein recycles 5 Ht from synapse.
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Drugs may affect neural transmission in many different ways
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Agonism and Antagonism
• Agonism- drug effects that are in the direction of or promote the natural effects of a given NTs at its synapse.
• Antatgonism- drug effects that are in the opposing direction of or inhibit the natural effects of a given NTs at its synapse.