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)

“Threshold”

What is special about “threshold?”

The forces of Diffusion

The Neurons membrane separates the different ions

The membrane controls diffusion

By opening or closingIon channels

If ion channels are open; diffusion across concentration and electrostatic gradients will

occur

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

Once triggered, the AP is all or none, and “one-way.”

Action potential arrives at terminals

Causing the release of neurotransmitters into the synapse

The action potential at the terminals causes Neurotransmitter release into the synapse.

NTs bind to post-synaptic receptors

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

Ways that receptor activation can lead to IPSPs or EPSPs

Neural Integration:if enough EPSPs occur threshold

depolarization will activate Na= ion channels

EFFECTS OF NTs?

• EPSP or IPSP– Depends on the type of Neurotransmitter

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)

Ex: Why is ACH sometimes excitatory and other times inhibitory?Receptor subtypes

Effects depend on receptor subtype

Neurotransmitters bind to receptor sites to produce postsynaptic effects

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

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.

NT-receptor interactions must stop!Enzymatic degradation

Nerve gases block ACHE-preventing breakdown of Acetylcholine.

Different nerve gas compounds; all chemically related to Diisoflourphosphate (DFP) common in low concentrations

in insecticides and some pesticides.

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

The effects of other NTs are terminated by Reuptake. E.g. the serotonin transport

protein recycles 5 Ht from synapse.

Drugs may affect neural transmission in many different ways

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.