Psych 7 – Physiological Psychology – Neural Conduction – Dr. Mascolo
Chapter 4: Neural Conduction & Synaptic Transmission
All cells carry an electrical charge, but neurons take advantage of this
Neurons take advantage of this in order to conduct messages down their length and across to other neurons – their basic function.
A neuron’s electrical charge is called electrochemical – like your car battery the charge is based in chemistry – charged ions that are unequally balanced across the cell membrane – that is, inside the cell (“intracellular”) versus outside the cell (“extracellular”) – that’s why it is called the membrane potential.
To start, what exactly is an ion? Atoms with an unequal # of positively charged protons & negatively charged electrons. When # of protons > # of electrons, then the ion is positively charged. When # of protons < # of electrons, then the ion is negatively charged. Here are some examples we’ll be studying:
· Sodium (Na+) => 11 protons, 10 electrons – the “+” means 1 more proton than electron
· Potassium (K+) => 19 protons, 18 electrons – again, the “+” means 1 more proton than electron
· Calcium (Ca++ or Ca2+) => 20 protons, 18 electrons -- the “++” or “2+” means 2 more protons than electrons
· Chloride (Cl-) => 17 protons, 18 electrons – the “-“ means 1 more electron than proton
Summary your text’s presentation (from the previous edition, but I like it):
I will focus on 2 particular ions -- Na+ & K+ -- & 4 basic factors that affect their intracellular and extracellular distributions when the neuron is inactive – its “Resting Potential”:
#1 #2 #3 #4
Differential Concentration Electrostatic
Cell Membrane Sodium/Potassium Pump Gradient Pressure
Na+ Hard to cross extracellular intracellular intracellular
K+ Easy to cross intracellular extracellular intracellular
3 of these factors are “passive” – that is, they do not require energy:
· #1 is a characteristic of the cell membrane itself – called “semipermeable”, the imbedded channel proteins are differentially permeable to different molecules.
· #3 is actually a physical force called diffusion – substances flow down their concentration gradient – that is, from areas of higher concentration to areas of lower concentration.
· #4 is also a physical force involving electrical charge – substances flow away from areas with the same electrical charge to areas with the opposite electrical charge.
The last of these factors is “active” – that is, it does require energy:
· #2 is based on a particular channel imbedded in the cell membrane – just like #1 – but this one does require energy. This sodium-potassium pump in fact uses up 40% of the cell’s energy – an expensive little beast! It pumps 3 sodium ions out of the cell (efflux) for every 2 potassium ions into the cell (influx). This ratio of 3 positive ions out for every 2 positive ions in leads to a net negative charge of the cell.
If not for the activity of the sodium-potassium pump, the other 3 factors would even out the distribution of sodium & potassium, and the cell would end up with no electrical charge. The sodium-potassium pump is an energy hog – evolutionary theory suggests there must be a big adaptive advantage to maintaining this resting potential of -70mV.
A neuron receives messages from other neurons that alter its Resting Potential.
The neuron that sends the message is called “presynaptic” – the neuron that receives the message is called “postsynaptic”. We are focusing now on the postsynaptic neuron -- its resting potential is altered in 1 of 2 different ways. This is called a Graded Potential (GP):
· EPSP “Excitatory Postsynaptic Potential” alters the resting potential by depolarizing the postsynaptic cell – that is, the resting potential is reduced from -70mV to, say, -68 mV.
· IPSP “Inhibitory Postsynaptic Potential” alters the resting potential by hyperpolarizing the postsynaptic cell – that is, the resting potential is increased from -70mV to, say, -73 mV.
· The reason for the terms “Excitatory” & “Inhibitory” is that depolarization moves the postsynaptic cell closer to firing a message of its own – an explosive Action Potential (AP) -- but hyperpolarization moves the postsynaptic cell farther from firing an AP. The depolarization required to trigger an AP is called the “threshold of excitement” – it’s about +5mV – so the average neuron must depolarize from its resting potential of -70mV to -65mV in order to trigger an AP.
· All GPs – EPSPs & IPSPs – have these characteristics:
· their intensity can be anywhere between very strong very weak – they are graded
· they are conducted so rapidly they can be considered instantaneous
· they lose strength as they are conducted – so they are decremental.
The combined influences of various EPSPs and IPSPs gather at the Axon Initial Segment & determine whether or not the Postsynaptic Neuron fires an Action Potential
· Spatial Summation: Different presynaptic neurons create Graded Potentials on different places on the Postsynaptic Neuron -- these gather just below the Axon Hillock –first part of the Axon – the Axon Initial Segment
· Temporal Summation: One Presynaptic Neuron creates several Graded Potentials from one space on the Postsynaptic Neuron, & these gather at the Axon Initial Segment
Conduction of Action Potentials
Ionic Basis of Action Potentials
· Your text provides a detailed description of the step-by-step process of an AP. Once again, you can focus on the activities of 2 ions – sodium & potassium – the “voltage activated gates” that control their flow across the cell membrane.
· Basically, it is the influx of Sodium that causes the “Rising Phase” (depolarization), & it is the efflux of Potassium that causes the “Repolarization Phase” (hyperpolarization)
· Your text provides a Figure illustrating this process – including the actions of those voltage-activated gates – study it carefully
Refractory Periods
· Absolute Refractory Period – 1-2 milliseconds after the axon fires an AP, it cannot fire another one.
· Relative Refractory Period – a few milliseconds later, this portion of the axon can fire another AP, but only if it is depolarized more intensely than usual (i.e., more than +5mV)
Axonal Conduction of Action Potentials
Characteristic Graded Potential (GP) Action Potential (AP)
Voltage Activated
Channels? No – Passive Conduction Yes – Active Conduction
Decremental Yes (Time & Distance) No (Actively Regenerated)
Velocity Instantaneous Slow
Structures: Dendrite & Soma Axon
Conduction in Myelinated Axons
The difference here is that axons with myelin sheath can conduct the AP by “skipping” between instantaneous conduction (like GPs) & slower regeneration (why APs are nondecremental) – the former occur under the fatty myelin, the latter occur at the Nodes of Ranvier.
Synaptic Transmission
Structure of Synapses: they are named after the part of the presynaptic neuron (dendrite, soma, or axon) and the part of the postsynaptic neuron that are joining together to form the synapse, e.g.,
· presynaptic axon joins a postsynaptic dendrite – thus: axodendritic
· presynaptic axon joins a postsynaptic soma – thus: axosomatic
· presynaptic axon joins a postsynaptic axon – thus: axoaxonic (this last one allows for presynaptic inhibition/facilitation)
Directed vs. Nondirected synapses
Though we use the term “Neurotransmitter” very generally, we could be more specific by using these terms:
Neurotransmitters -- Neuromodulators -- Neurohormones
directed Nondirected Diffuse (bloodstream)
Release of NT molecules:
Exocytosis – the process by which NTs are ejected from the axon button
• NT molecules are transported from the soma to the axon button in vesicles – where they await release
• Release is dependent upon the arrival of an AP, but neither sodium nor potassium are involved in the actual process. That is, when Na+ & K+ channels are blocked at the axon button, NT molecules are still ejected.
• Instead, the arrival of an AP at the axon button causes Calcium (Ca++) channels to open. The influx of Ca++ is the direct cause of the exocytosis process – vesicles fuse with the cell membrane and empty their NT molecules into the synaptic cleft.
Activation of Postsynaptic Receptors by NT molecules: 2 Receptor “subtypes”
Ionotropic Receptors activate Ion Channels & so directly cause EPSPs or IPSPs.
These effects tend to be direct, quick, & brief. For example:
• Open Sodium Channels (Na+ influx) – EPSP
• Open Potassium Channels (K+ efflux) – IPSP
• Open Chloride Channels (Cl- influx) -- IPSP
Metabotropic Receptors are more complicated – a “2nd messenger” is involved.
These effects tend to be indirect, slow, & long-lasting
NTs land on Postsynaptic Receptor for just a few milliseconds
After that, they are pulled back into the Presynaptic Neuron through these processes
· Reuptake – most common
· Enzygmatic Degradation – less common (e.g., Ach is broken down by the enzyme AchE)
· Recycling – either way, NTs are pulled back into the Presynaptic Neuron & are used again
Glial Cells Revisited – there are many examples of neural structures credited with many more functions now than when I took this course! Glial cells may actually transmit information themselves.
Gap Junctions – Since we’re on this topic of “exceptions”, I may as well acknowledge research showing that some synaptic junctions directly transmit electrical charges without the use of NTs. That’s all I’m going to say about this!
Autoreceptors -- primarily inhibitory – the structural basis for Presynaptic Inhibition
Small vs large NTs -- see text
Types of Neurotransmitters (NTs) – listed in bold –
• Amino Acids -- simple building blocks of proteins -- earliest & most prevalent
• Glutamate -- most prevalent excitatory NT
• GABA -- most prevalent inhibitory NT
• Monoamines –
Catecholamines Indolamine
(Tyrosine -- Amino Acid Precursor) (Tryptophan--Amino Acid Precursor)
(L-Dopa -- Precursor) Serotonin (5-HT)
Dopamine
Norepinephrine
Epinephrine
• Acetylcholine (Ach)
• Unconventional NTs -- gases, endocannabinoids
• Neuropeptides (Endorphins)
Neurons are named after the NT they release:
Cholinergic Neurons Release Acetylcholine
Dopaminergic Neurons Release Dopamine
Serotonergic Neurons Release Serotonin
Adrenergic Neurons Release Epinephrine (Adrenaline)
Noradrenergic Neurons Release Norepinephrine (Noradrenaline)
How Drugs Influence Synaptic Transmission
· Your text first provides a Figure summarizing the steps involved in NT activity – from synthesis to deactivation.
· Next, your text describes the 2 basic categories of drug action:
• Agonistic -- Mimic or intensify a NT effect
• Antagonistic -- Impede or block a NT effect
(e.g., Botox is a Nicotinic antagonist
• and then provides a Figure summarizing these 2 effects