Receptor Potentials & Postsynaptic Potentials

Transcript

0:00 – 0:30  [Basic Definition]  The receptor potential is a voltage change that occurs in a sensory receptor when a sensory signal such as light or sound is transduced into an electrical signal, and this process is called signal transduction.  The postsynaptic potential is a voltage change that occurs in a postsynaptic cell when a presynaptic cell signals via a synapse, and this process is called synaptic transmission.  Importantly, both the receptor potential and the postsynaptic potential can be either depolarizing or hyperpolarizing.

0:30-2:30  

External stimuli are transduced into electrical signals by sensory neurons. These stimuli generate ‘receptor potentials’ which alter transmembrane voltage. There are a number of ways sensory signals are transduced, leading to increases or decreases in transmembrane voltage. In this example from an olfactory receptor neuron, odorant molecules bind to a metabotropic G-protein coupled receptor and initiate a second-messenger cascade that depolarizes the membrane potential.

Signals exchanged between neurons are called postsynaptic potentials. In this case, changes in transmembrane voltage rely on synaptic transmission. Another type of postsynaptic potential you may encounter specific to neuromuscular transmission is called the endplate potential. For synaptic transmission, spikes need to propagate to axon terminals to trigger neurotransmitter release. Staying with olfactory receptor neurons, receptor potentials generated in the cilia propagate toward the soma, reaching the spike initiation zone where a train of action potentials or spikes then propagate along the axon.

The pre-synaptic axon terminals of olfactory receptor neurons synapse with the post-synaptic dendrites of second-order interneurons within discrete glomeruli. These form the olfactory tract projecting to the brain. Within the brain post-synaptic potentials can lead to both increases and decreases in transmembrane voltage, otherwise known as excitation and inhibition.

Excitatory post-synaptic potentials (EPSPs) lead to increases in transmembrane voltage from rest that ultimately cross threshold. When spikes invade the axon terminal, there is an initial bolus of neurotransmitter release that decreases with time. This generates a transient excitatory post-synaptic current due to the synchronous activation of many individual postsynaptic receptors selectively permeable to cations. This means positively charged ions flow in and depolarize the membrane potential.

Inhibitory post-synaptic potentials (IPSPs) lead to decreases in transmembrane voltage that prevent the membrane potential from crossing threshold. They can be depolarizing from rest, but are ultimately hyperpolarizing near threshold. Inhibitory postsynaptic receptors are selectively permeable to anions. This means negatively charged ions flow in and hyperpolarize the membrane potential when they are activated by inhibitory neurotransmitters. Note, this is still considered an ‘outward’ current, since the inside is becoming more negative.

2:30-3:00  [Parallel Vocabulary] In introductory classes you learned about receptor potentials.  But Neuroscience is an interdisciplinary field, so there are many words for this term – For example, it may also be called a generator potential.  Postsynaptic potential is an umbrella term that includes the excitatory postsynaptic potential (EPSP) which is a postsynaptic voltage change that makes action potentials more likely, the inhibitory postsynaptic potential (IPSP) which is a postsynaptic voltage change that makes action potential less likely, and the miniature postsynaptic potential (mPSP) which is the postsynaptic voltage change that occurs when a presynaptic neuron releases a single vesicle of neurotransmitter.

3:00-4:00  [Here’s a real world example]  Receptor potentials and postsynaptic potentials are important in almost every aspect of neural communication including sensation, motor control, and cognition.  For example, did you know that many poisonous substances produce toxic effects in the body because they disrupt the receptor potential and / or the postsynaptic potential and therefore disrupt neural signaling even in the absence of sensory stimulation or presynaptic activity.  For example, the venom of a king cobra snake contains toxins that produce paralysis by blocking the nicotinic acetylcholine receptor.  Recall that the nicotinic acetylcholine receptor is found at the neuromuscular junction and is responsible for producing an excitatory postsynaptic potential in muscle cells that in turn leads to muscle contraction. When the nicotinic acetylcholine receptor is blocked,  this leads to an overall decrease in excitation of the muscle that  produces paralysis.  In extreme cases, the bite of a king cobra snake is lethal because muscle paralysis affects both heart-rate and respiration.

4:00-6:00 [Follow along with this example]

6:00-6:30 [Here are a few readings to help you review]
1) Neuroscience Exploring the Brain (Bear)

• Chapter 12: “The Somatic Sensory System” covers the receptor potential

2) Principles of Human Physiology (Stanfield)

• Chapter 5: “Synaptic Transmission”