Psyc 362 Class Notes for Exam 1 Chapter 2 beginning of 3 at end 2 5 15 Properties of AP All or none event such that the initial depolarization will either reach threshold and neuron will fire or won t AP is spread down the axon membrane such that successive patches of the membrane are depolarized in non myelinated axons AP has a fixed amplitude a conduction velocity meters sec and a refractory period in which stimulation will not produce AP the firing rate is limited Saltatory Conduction conduction of AP by myelinated axons in myelinated axons the AP has to jump from node to node so depolarization takes place at each node Saltatory Conduction speeds up conduction velocity making myelinated axons faster Conduction velocity is also proportional to axon diameter such that the thinker the axon is the faster the velocity Fortunately myelination allows smaller diameter axons to conduct signals quickly As a result more axons can be placed in a given space if myelinated The length of the membrane must be specific so an action potential isn t lost due to resistance of the travel through nodes like a cable Due to this resistance there is gradual reduction of conduction of the AP under myelin sheath yet AP is regenerated at all nodes of Ranvier movement of ions in nodes is active movement under myelin sheath is passive done by diffusion The type of depolarization matters PSP Communication within the Neuron Rate Law with AP conduction the rate of firing determines the intensity of stimulus how many APs per unit time Variations in the intensity of a stimulus or What happens as a result of change in membrane potential is dependent on which channels are open ed Local grated potentials losing energy size as they move through the membrane They are carried along the membrane degrading with time and distance and can fail to produce an AP LP generally generates form dendrites and soma but AP mostly from axon occasionally dendrite Also amplitude change vs no change Intercellular communication Synapses synaptic cleft the physical gap between pre and postsynaptic membranes presynaptic is typically on the axon having axon terminals which contain 1 mitochondria to provide energy 2 vesicles that contain neurotransmitters and 3 cisternae parts of the golgi apparatus that recycle vesicles Vescicles lie docked near the presynaptic membrane until the AP arrives at the terminal the AP will open voltage dependent Ca channels which allows the entry of Ca into the axon the Ca ions change the structure of proteins that bind the vesicles to the presynaptic membrane resulting in the opening of fusion pores opens and merges the vesicles and presynaptic membrane to release the contents of the vesicle into the synapse The released neurotransmitters diffuse across the cleft and interact with the next neuron postsynaptic membrane can be a 1 dendritie axodendritic synapse 2 soma axosomatic synapse or 3 axon axoaxonic synapse Postsynaptic thickening lies under the axon terminal and controls membrane receptors for neurotransmitters Neurotransmitters bind to Postsynaptic receptors which when activated open alter postsynaptic ion channels that allow for the flow of ions through the membrane This can produce either hyperpolarization or depolarization PSP depending on which ion channel opens Ion channels can be altered by these receptors directly with ionotropic receptors 3 possible results 1 inflow of Na causes depolarization causing EPSP 2 outflow of K causes hyperpolarization IPSP 3 inflow of Cl causes hyperpolarization IPSP Ion channels can also be altered indirectly with metabotropic receptors There are two types and both require energy 1 Neurotransmitters attach to receptors which then release another chemical to activate G Protein which then activates an ion channel 2 Neurotransmitters may also bind to receptors activate the G protein which submits a breakaway that activates enzymes to produce messengers which would then open the channel Neural integration is the interaction of the effects of excitatory and inhibitory synapses on a particular neuron So if an excitatory and inhibitory synapse become active simultaneously the IPSP and EPSP would interact and the AP is not triggered in the axon involves the algebraic summation of PSPs This means a predominance of EPSPs at axon will result in an Action potential but if the PSPs don t drive the axon membrane past the threshold no AP will occur Termination of PSP can be done in the following ways Binding of Neurotransmitters to PS receptors resulting in a PSP with Reuptake of neurotransmitters back into the cytoplasm of the PS membrane This is energy efficient because the NT s can be recycled enzymatic deactivation Autoreceptors molecule located on neuron that responds to the neurotransmitters released by the neuron by regulating internal processes including synthesis and the release of neurotransmitters They do NOT change the membrane potential Axoaxonic synapse can produce presynaptic inhibition in which the presynaptic terminal buttons reduce the amount of neurotransmitters released by the postsynaptic terminal buttons can also produce presynaptic facilitation in which the presynaptic terminal buttons increase the amount of NT released by the next neuron Non synaptic chemical communication neuromodulators secreted substances that act like neurotransmitters but are not restricted to the synaptic cleft but are instead able to diffuse throughout the extracellular fluid Peptide amino acid chains that are joined by peptide bonds Most are hormones which means they are released from endocrine glands secrete chemicals into external fluid and capillaries blood stream and affect target cells contain receptors for particular hormones of other organs CH3 Neuroanatomy Neuroaxis imaginary line drawn through the spinal cord up to the rest of the brain Anatomical directions exist to help understand the brain body relative to the neuroaxis anterior rostral toward the head posterior caudal toward the kill ventral inferior toward the stomach belly dorsal superior toward the back top of head Location in brain Ipsilatural same side of the brain contralateral opposite side of the brain