1. Chapter 4 Neural Conduction and Synaptic Transmission
How Neurons Send and Receive Signals
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2. The Neuron’s Resting Membrane Potential
Inside of the neuron is negative with respect to the outside
Resting membrane potential is about -70mV
Membrane is polarized, it carries a charge
Why?

3. Ionic Basis of the Resting Potential
Ions, charged particles, are unevenly distributed
Factors influencing ion distribution
Homogenizing
Factors contributing to uneven distribution

4. Ionic Basis of the Resting Potential
Homogenizing
Random motion – particles tend to move down their concentration gradient
Electrostatic pressure – like repels like, opposites attract
Factors contributing to uneven distribution
Membrane is selectively permeable
Sodium-potassium pumps

5. Ions Contributing to Resting Potential
Sodium (Na+)
Chloride (Cl-)
Potassium (K+)
Negatively charged proteins (A-)
synthesized within the neuron
found primarily within the neuron

6. The Neuron at Rest Ions move in and out through ion-specific channels
K+ and Cl- pass readily
Little movement of Na+
A- don’t move at all, trapped inside

7. Equilibrium Potential
The potential at which there is no net movement of an ion – the potential it will move to achieve when allowed to move freely
Na+ = 120mV
K+ = -90mV
Cl- = -70mV (same as resting potential)

8. The Neuron at Rest
Na+ is driven in by both electrostatic forces and its concentration gradient
K+ is driven in by electrostatic forces and out by its concentration gradient
Cl- is at equilibrium
Sodium-potassium pump – active force that exchanges 3 Na+ inside for 2 K+ outside

9. Something to think about
What would happen if the membrane’s permeability to Na+ were increased?
What would happen if the membrane’s permeability to K+ were increased?

10. Generation and Conduction of Postsynaptic Potentials (PSPs)
Neurotransmitters bind at postsynaptic receptors
These chemical messengers bind and cause electrical changes
Depolarizations (making the membrane potential less negative)
Hyperpolarizations (making the membrane potential more negative)

11. Generation and Conduction of Postsynaptic Potentials (PSPs)
Postsynaptic depolarizations = Excitatory PSPs (EPSPs)
Postsynaptic hyperpolarizations = Inhibitory PSPs (IPSPs)
EPSPs make it more likely a neuron will fire, IPSPs make it less likely
PSPs are graded potentials – their size varies

12. EPSPs and IPSPs Travel passively from their site of origination
Decremental – they get smaller as they travel
1 EPSP typically will not suffice to cause a neuron to “fire” and release neurotransmitter – summation is needed

13. Integration of PSPs and Generation of Action Potentials (APs)
In order to generate an AP (or “fire”), the threshold of activation must be reached at the axon hillock
Integration of IPSPs and EPSPs must result in a potential of about -65mV in order to generate an AP

14. Integration
Adding or combining a number of individual signals into one overall signal
Temporal summation – integration of events happening at different times
Spatial - integration of events happening at different places

15. What type of summation occurs when:
One neuron fires rapidly?
Multiple neurons fire at the same time?
Several neurons fire repeatedly?
Both temporal and spatial summation occur simultaneously

18. The Action Potential
All-or-none, when threshold is reached the neuron “fires” and the action potential either occurs or it does not.
When threshold is reached, voltage-activated ion channels are opened.

19. The Ionic Basis of Action Potentials
When summation at the axon hillock results in the threshold of excitation (-65mV) being reached, voltage-activated Na+ channels open and sodium rushes in.
Remember, all forces were acting to move Na+ into the cell.
Membrane potential moves from -70 to +50mV.

21. The Ionic Basis of Action Potentials
Rising phase: Na+ moves membrane potential from -70 to +50mV.
End of rising phase: After about 1 millisec, Na+ channels close.
Change in membrane potential opens voltage-activated K+ channels.
Repolarization: Concentration gradient and change in charge leads to efflux of K+.
Hyperpolaization: Channels close slowly - K+ efflux leads to membrane potential <-70mV.

22. Refractory Periods
Absolute – impossible to initiate another action potential
Relative – harder to initiate another action potential
Prevent the backwards movement of APs and limit the rate of firing

23. The action potential in action

24. PSPs Vs Action Potentials (APs)
EPSPs/IPSPs
Decremental
Fast
Passive (energy is not used)
Action Potentials
Nondecremental
Conducted more slowly than PSPs
Passive and active

25. Conduction in Myelinated Axons
Passive movement of AP within myelinated portions occurs instantly
Nodes of Ranvier (unmyelinated)
Where ion channels are found
Where full AP is seen
AP appears to jump from node to node
Saltatory conduction

26. Structure of Synapses Most common
Axodendritic – axons on dendrites
Axosomatic – axons on cell bodies
Dendrodendritic – capable of transmission in either direction
Axoaxonal – may be involved in presynaptic inhibition

27. Synthesis, Packaging, and Transport of Neurotransmitter (NT)
NT molecules
Small
Synthesized in the terminal button and packaged in synaptic vesicles
Large
Assembled in the cell body, packaged in vesicles, and then transported to the axon terminal

28. Release of NT Molecules
Exocytosis – the process of NT release
The arrival of an AP at the terminal opens voltage-activated Ca++ channels.
The entry of Ca++ causes vesicles to fuse with the terminal membrane and release their contents

29. Activation of Receptors by NT
Released NT produces signals in postsynaptic neurons by binding to receptors.
Receptors are specific for a given NT.
Ligand – a molecule that binds to another.
A NT is a ligand of its receptor.

30. Receptors There are multiple receptor types for a given NT.
Ionotropic receptors – associated with ligand-activated ion channels.
Metabotropic receptors – associated with signal proteins and G proteins.

31. Ionotropic Receptors
NT binds and an associated ion channel opens or closes, causing a PSP.
If Na+ channels are opened, for example, an EPSP occurs.
If K+ channels are opened, for example, an IPSP occurs.

32. Metabotropic Receptors
Effects are slower, longer-lasting, more diffuse, and more varied.
NT (1st messenger) binds > G protein subunit breaks away > ion channel opened/closed OR a 2nd messenger is synthesized > 2nd messengers may have a wide variety of effects

34. Reuptake, Enzymatic Degradation, and Recycling
As long as NT is in the synapse, it is active – activity must somehow be turned off.
Reuptake – scoop up and recycle NT.
Enzymatic degradation – a NT is broken down by enzymes.

35. Small-molecule Neurotransmitters
Amino acids – the building blocks of proteins
Monoamines – all synthesized from a single amino acid
Soluble gases
Acetylcholine (ACh) – activity terminated by enzymatic degradation

36. Amino Acid Neurotransmitters
Usually found at fast-acting directed synapses in the CNS
Glutamate – Most prevalent excitatory neurotransmitter in the CNS
GABA –
synthesized from glutamate
Most prevalent inhibitory NT in the CNS
Aspartate and glycine

37. Monoamines Effects tend to be diffuse
Catecholamines – synthesized from tyrosine
Dopamine
Norepinephrine
Epinephrine
Indolamines – synthesized from tryptophan
Serotonin

38. Soluble-Gases and ACh Soluble gases – exist only briefly
Nitric oxide and carbon monoxide
Retrograde transmission – backwards communication
Acetylcholine (Ach)
Acetyl group + choline
Neuromuscular junction

39. Neuropeptides Large molecules Example – endorphins
“Endogenous opiates”
Produce analgesia (pain suppression)
Receptors were identified before the natural ligand was

40. Pharmacology of Synaptic Transmission
Many drugs act to alter neurotransmitter activity
Agonists – increase or facilitate activity
Antagonists – decrease or inhibit activity
A drug may act to alter neurotransmitter activity at any point in its “life cycle”

42. Agonists – 2 examples Cocaine - catecholamine agonist
Blocks reuptake – preventing the activity of the neurotransmitter from being “turned off”
Benzodiazepines - GABA agonists
Binds to the GABA molecule and increases the binding of GABA

44. Antagonists – 2 examples
Atropine – ACh antagonist
Binds and blocks muscarinic receptors
Many of these metabotropic receptors are in the brain
High doses disrupt memory
Curare - ACh antagonist
Bind and blocks nicotinic receptors, the ionotropic receptors at the neuromuscular junction
Causes paralysis