The Synapse
Sherrington’s Theory
Q: Which of Sherrington’s findings resulted in him coining the term ‘synapse’?A: Sherrington conducted rigorous experiments on reflexes and discovered that the speed of reflexes was slower than the speed of an action potential. He deduced that this delay was due to the communication occurring between neurons, leading him to propose the term 'synapse' to describe this junction where neurotransmission occurs. Sherrington introduced the concept that reflexes involve a complex network of interactions between multiple neurons, highlighting the fundamental role synapses play in neuronal communication.
Gap Junctions
Q: What is the major difference between Gap Junctions and Chemical Synapses?A: Gap Junctions facilitate direct communication between neurons through the transfer of ions via specialized channels called connexons, allowing for nearly instantaneous signaling. In contrast, Chemical Synapses involve a more complex process of neurotransmitter release, diffusion across the synaptic cleft, and binding to receptors on the postsynaptic neuron.
Q: What are the benefits of using a Gap Junction over a Chemical Synapse?A: Gap Junctions provide several advantages including significantly faster transmission times, as the electrical signals can propagate instantly between adjacent neurons. They allow for the synchronization of neuronal activity, enabling groups of neurons to function in concert; this is particularly beneficial in tasks requiring rapid responses, such as defensive reflexes or rhythmic activities like breathing.
Q: What functions do Gap Junctions play in the overall functioning of the body?A: Gap Junctions are critically involved in functions that necessitate synchronous activity among groups of neurons. They play a vital role in processes such as cardiac muscle contraction, where rapid transmission of electrical signals is essential for coordinated heartbeats, and in certain neuronal populations in the brain that rely on synchronized firing for proper functioning.
Chemical Synapses
Q: Define the following terms:
Exocytosis: The process of releasing neurotransmitters into the synaptic cleft from vesicles fused with the pre-synaptic membrane.
Endocytosis: The cellular process of capturing external substances by engulfing them with the cell membrane, effectively bringing neurotransmitters back into the neuron following their release.
Q: What does an action potential reaching the axon terminals cause?A: The arrival of an action potential at the terminal boutons leads to the opening of voltage-gated calcium channels. This influx of calcium ions triggers a cascade of events leading to the fusion of neurotransmitter-filled vesicles with the pre-synaptic membrane and the subsequent release of neurotransmitters into the synaptic cleft.
Q: What are the two things that can happen to a neurotransmitter after use?A: Once a neurotransmitter has performed its function, it can either be recycled back into the presynaptic neuron through a process called reuptake or it can be broken down by enzymes in the synaptic cleft. This regulation is essential for maintaining synaptic health and functionality.
Q: What occurs during the process of reuptake/endocytosis?A: During reuptake, neurotransmitters are transported back into the presynaptic neuron by specific transporter proteins, such as Monoamine Oxidase (MAO). These neurotransmitters are then repackaged into vesicles for future release, ensuring that the synapse can promptly respond to subsequent action potentials.
Receptors
Q: Define the following terms:
Ligand: A molecule, typically a neurotransmitter, that binds to a specific receptor to initiate a biological response.
Agonist: A ligand that not only binds but also triggers a physiological response by activating a receptor.
Antagonist: A molecule that binds to a receptor but blocks or dampens the biological response initiated by an agonist.
Q: What are autoreceptors?A: Autoreceptors are specialized receptors located on the presynaptic terminal that respond to the neurotransmitter released by the neuron itself. These receptors provide feedback to the neuron regarding its own level of neurotransmitter release, often signaling the neuron to reduce further neurotransmitter release to maintain balance and prevent overstimulation.
Q: What are the things that a receptor can be connected to?A: Receptors can be connected to various intracellular mechanisms such as:
Ion channels (Ionotropic receptors): These receptors directly influence ion flow across the membrane upon ligand binding.
G-proteins (Metabotropic receptors): These receptors initiate a complex signaling cascade, altering metabolic processes and ion channel behavior indirectly.
G-protein coupled ion channels: These are integrated systems that link the activation of metabotropic receptors to the modulation of ion channels.
Ionotropic
Q: How do ionotropic receptors affect the voltage of the neuron?A: Ionotropic receptors change the membrane potential of the post-synaptic neuron by allowing specific ions (e.g., sodium, potassium, calcium) to flow in or out, leading to either depolarization or hyperpolarization depending on the ions involved and the direction of flow.
Q: What are the benefits and drawbacks of communicating using Ionotropic receptors over other kinds of receptors?A: The primary benefit of Ionotropic receptors is their rapid action, enabling quick synaptic transmission. However, they are often limited by a shorter duration of effect and a localized area of influence, constraining their ability to modulate broader neuronal activity over longer periods.
G-protein Coupled Receptors
Q: What are the two kinds of G-protein receptors?A: The two types of G-protein receptors are Metabotropic receptors and G-protein coupled ion receptors, which play pivotal roles in modulating neuronal signaling pathways.
Q: How do Metabotropic receptors affect the voltage of the neuron?A: Metabotropic receptors alter the voltage of the neuron indirectly by initiating a series of enzymatic reactions and signaling cascades through G-proteins, which can lead to changes in ion channel activity and metabolic processes within the neuron.
Q: What are the benefits and drawbacks of communication using Metabotropic receptors over other kinds of receptors?A: Metabotropic receptors provide prolonged and widespread effects on neuron signaling, often sustaining cellular activation for seconds or longer. However, their activation is slower relative to Ionotropic receptors, making them less efficient for immediate neurotransmission tasks.
Q: What molecule does the G-protein use as an energy source?A: The G-protein utilizes Guanosine Triphosphate (GTP) as its energy source for signaling processes.
Q: What happens when a neurotransmitter binds to a metabotropic receptor?A: When a neurotransmitter binds to a metabotropic receptor, it causes a conformational change in the receptor, transforming Guanosine Diphosphate (GDP) into Guanosine Triphosphate (GTP) and triggering the dissociation of G-protein subunits. These subunits then interact with either ion channels or Effector Proteins, initiating a secondary messenger system that can lead to either excitatory or inhibitory effects on the neuron. After the response is initiated, the subunits re-associate, and GTP is hydrolyzed back to GDP, completing the signaling cycle.
Example of a Secondary Messenger System:In Week 3’s lecture presented by Patrick, a secondary messenger system was described where effector proteins promote the release of calcium ions from intracellular stores, thereby increasing the excitatory voltage of the neuron. This demonstrates how complex interactions can modulate neuronal activity in response to extracellular signals.