Lecture #15: Impulse Transmission II
Topics: Postsynaptic Potentials, Graded Potentials vs. Action Potentials, Conduction Velocity, Neurotransmitters and Receptors
Neurotransmitter Activation of Ion Channels
Can activate different ion channels in the postsynaptic membrane.
Excitatory Postsynaptic Potential (EPSP)
Caused by:
Activation of Na+ channels (depolarization)
Nonspecific ion channel activation (more Na+ than K+, depolarization)
Ca2+ channel activation (depolarization)
Inhibitory Postsynaptic Potential (IPSP)
Caused by:
K+ channel activation (hyperpolarizing)
Cl- channel activation (hyperpolarizing)
Membrane Potential Levels
+30 mV (peak), -55 mV (threshold), -70 mV (resting)
EPSP and IPSP Effects
A single EPSP cannot induce an Action Potential (AP).
EPSPs can summate, influencing the postsynaptic neuron.
IPSPs can also summate; most neurons receive both inputs.
Action Potentials
Started only if EPSPs dominate, bringing membrane potential to threshold.
Temporal Summation
Multiple EPSPs occur in rapid succession at the same synapse.
Spatial Summation
Multiple EPSPs from different synapses add together.
Cancellation of Potentials
Changes in membrane potential can cancel each other out (e.g., overlapping EPSPs and IPSPs).
Graded Potentials
Activated by ligand-gated channels.
Varies with initiating event, decreases with distance.
Duration varies, both depolarizing and hyperpolarizing effects.
Can be summed (no threshold or refractory period).
Action Potentials
Activated by voltage-gated channels.
All-or-none response; amplitude remains constant along axon.
Only depolarizing effects, with a defined threshold and refractory period.
Factors Influencing Velocity
Axon Diameter: Larger diameter = faster conduction (less resistance).
Example: Squid giant axon.
Myelination: Myelin insulates and prevents charge leakage.
Action potentials in myelinated neurons propagate about 30 times faster than in unmyelinated neurons.
Saltatory Conduction: Charge jumps across myelinated regions via Nodes of Ranvier.
Overview of MS:
Autoimmune disease affecting primarily young adults.
Immune system attacks myelin in the CNS, leading to inflammation and scarring (scleroses).
Impulse conduction slows and can cease, leading to symptoms such as visual disturbances, weakness, and loss of muscular control.
Ionotropic Receptors:
Contain an ion channel; neurotransmitter binding opens the pore, resulting in either depolarization (Na+ or Ca2+ influx) or hyperpolarization (Cl- influx or K+ efflux).
Responses are immediate and brief.
Metabotropic Receptors:
Transmitter binds to G-protein-coupled receptors; indirect effects through second messengers (e.g., cyclic AMP).
Responses are complex, slow, and often prolonged.
Drug Interactions:
Agonists: Mimic neurotransmitters; Antagonists: Inhibit responses.
Nicotinic Receptors:
Ionotropic, excitatory; involved in somatic nervous system and some CNS pathways.
Muscarinic Receptors:
Metabotropic, excitatory or inhibitory; parasympathetic effects (e.g., heart, glands).
Compounds include epinephrine, norepinephrine, and dopamine.
All are metabotropic receptors, acting as G-protein coupled receptors, influencing sympathetic and parasympathetic responses.
Examples of Actions:
Heart rate modulation.
Respiratory and digestive system impacts.
Somatic Nervous System: Single neuron from CNS to effector organs, using ACh.
Autonomic Nervous System: Two-neuron chain (preganglionic and postganglionic), using ACh (parasympathetic) or NE (sympathetic).
Effect: Stimulatory or inhibitory, depending on neurotransmitter and receptor types.
Excitatory Neurotransmitter: Glutamate
Majority ionotropic (depolarization), some metabotropic (hyperpolarization).
Inhibitory Neurotransmitters: GABA (gamma-Aminobutyric acid) and Glycine.
GABA receptors can be ionotropic (Cl-) or metabotropic (hyperpolarizing).
Mixing alcohol or barbiturates with benzodiazepines should be avoided, as they can enhance GABA effects and potentially cause severe outcomes.