Detailed Notes on Electrophysiology
Slide 1: Introduction to Neuronal Electrophysiology
Electrophysiology studies electrical properties of biological cells and tissues,
particularly neurons.
Neurons generate electrical potential through charge separation across their
membranes.
Potential difference is measured in volts (V) or millivolts (mV).
Ion movement occurs across membranes through specialized structures:
o Ion Channels: Allow passive movement of ions.
o Gates: Regulate ion flow in response to stimuli.
o Pumps: Actively transport ions to maintain gradients.
Slide 2: Resting Membrane Potential (RMP)
RMP refers to the steady voltage across the cell membrane when the neuron is
unstimulated.
Typically ranges between -60 to -70 mV due to differential ion distribution.
Ion composition differences:
o Extracellular fluid (ECF): High Na+ and Cl- concentration.
o Intracellular fluid (ICF): High K+ and negatively charged
proteins/phosphate.
Forces governing ion movement:
1. Chemical force: Diffusion of ions down their concentration gradient.
2. Electrical force: Attraction and repulsion of charged particles.
Neurons are more permeable to K+ than Na+, contributing significantly to RMP
stabilization.
Slide 3: Depolarization
Occurs when membrane potential becomes less negative, increasing excitability.
Example: Change from -70 mV to -55 mV or even +30 mV.
Typically triggered by opening of voltage-gated Na+ channels, allowing Na+ influx.
If threshold is reached, an action potential is initiated.
Slide 4: Repolarization
Restores resting membrane potential after depolarization.
After Na+ channels close, voltage-gated K+ channels open.
K+ efflux leads to the return of a negative charge inside the neuron.
Slide 5: Hyperpolarization
When the membrane potential becomes more negative than RMP (-70 mV to -85
mV).
Caused by prolonged K+ efflux or Cl- influx.
Makes neurons less likely to fire an action potential, increasing inhibition.
Slide 6: Action Potential (AP)
A rapid and transient change in membrane potential used for neuronal signaling.
Phases:
1. Depolarization: Na+ influx through voltage-gated Na+ channels.
2. Repolarization: K+ efflux through voltage-gated K+ channels.
3. Hyperpolarization: Continued K+ outflow before stabilization at RMP.
APs enable fast, long-distance communication in neurons.
Slide 7: Threshold Potential and All-or-None Principle
Threshold potential (~-55 mV): Minimum voltage required to trigger an AP.
If threshold is reached, the AP occurs; otherwise, it does not.
APs follow an all-or-none principle, meaning strength does not affect intensity.
Slide 8: Refractory Periods
Absolute Refractory Period:
o No AP can be generated, as Na+ channels are inactivated.
Relative Refractory Period:
o A stronger-than-normal stimulus can trigger an AP due to partial recovery.
o K+ channels remain open, opposing depolarization.
Slide 9: Propagation of Action Potential
AP propagates along the axon, transmitting information.
Factors affecting conduction velocity:
1. Axon diameter: Larger axons conduct impulses faster.
2. Myelination:
Unmyelinated axons: Slow, continuous conduction.
Myelinated axons: Fast, saltatory conduction (jumping between nodes
of Ranvier).
Slide 10: Synaptic Transmission
The process of communication between neurons at synapses.
Steps:
1. AP arrives at the presynaptic terminal.
2. Voltage-gated Ca++ channels open, allowing Ca++ influx.
3. Synaptic vesicles fuse with the presynaptic membrane, releasing
neurotransmitters.
4. Neurotransmitters diffuse across the synaptic cleft.
5. Bind to receptors on the postsynaptic neuron, causing ion channel opening.
6. Postsynaptic potential changes, triggering an AP if threshold is reached.
Slide 11: Neurotransmitters and Their Effects
Excitatory Neurotransmitters: Depolarize postsynaptic neurons.
o Examples: Acetylcholine (ACh), Glutamate.
Inhibitory Neurotransmitters: Hyperpolarize postsynaptic neurons.
o Examples: GABA, Glycine.
Neurotransmitter Clearance Mechanisms:
1. Reuptake: Transport back into presynaptic neuron.
2. Enzymatic Degradation: Breakdown by enzymes (e.g., acetylcholinesterase
for ACh).
3. Diffusion: Passive movement away from the synapse.
Slide 12: Common Neurotransmitters and Drug Effects
Acetylcholine (ACh): Involved in muscle contraction and memory.
o Drugs: Nicotine stimulates ACh receptors; Alzheimer’s treatments enhance
ACh.
GABA: Major inhibitory neurotransmitter.
o Drugs: Alcohol enhances GABA’s effects, causing sedation.
Dopamine: Regulates movement and pleasure.
o Low levels: Parkinson’s disease.
o High levels: Schizophrenia.
o Drugs: Cocaine blocks dopamine reuptake, causing intense euphoria followed
by depletion.
Endorphins: Reduce pain, promote well-being.
o Drugs: Morphine and heroin mimic endorphins, leading to pain relief and
euphoria.
Norepinephrine (NE): "Feel-good" neurotransmitter.
o Drugs: Amphetamines enhance NE release, increasing alertness.
Serotonin: Regulates mood, sleep, and appetite.
o Drugs: Prozac blocks serotonin reuptake, used in depression treatment.
Conclusion
Neuronal electrophysiology is critical for brain and nervous system function.
RMP, AP, and synaptic transmission underpin communication between neurons.
Neurotransmitters regulate emotions, cognition, and movement, with drugs
modulating their effects.
Understanding electrophysiology helps in treating neurological and psychiatric
disorders.
