BIOL 3170 Neurobiology 9-15.doc

BIOL 3170 Neurobiology 9-15 -review session possibility 2 forms of neural transmission Action potential Post synaptic potentials Inhibitory Excited Occur in cell body and dendritic arms Signal Type: Local signals (passive) Receptor potentials Synaptic potentials Both graded potentials, they are either hyperpolarizing or depolarizing Propagated signals (active) Action potential All-or-none Capacitance Two conductive plates that are separated by some kind of insulator, you can build up charge across the capacitance. Depends on the distance between the plates. The likelihood that the charges can be discharged The membrane can be thought of as a capacitance Myelin is a very good insulator, increasing the space between the positive and negative charges, reducing the capacitance It is also making the resistance of the membrane It DECREASES capacitance INCREASES membrane resistance Sufficient depolarization needs to be maintained to create another action potential: this regulates the size of the Node between the myelin sheath Want to use the minimal number of nodes, the smaller the amount of nodes, the quicker the potential. Want long distances for fast conductance velocity, but they need to be short enough not to mess up the action potential. To increase conduction velocity, decrease the internal (axial) resistance Axons that need fast conductance tend to be myelinated and very big Chemical Transmission Voltage gated Ca channels let calcium into the pre-synaptic terminal that fuses the transmitter (synaptic vesicles) and the release of the neurotransmitter. The post synaptic cell releases some sort of response EPSP (excited post synaptic potential) is depolarizing Inhibitory post synaptic potential (IPSP) Smaller than EPSP A result of increased intracellular negative charge by: Effluxing potassium or influxing chlorine Neuromodulatory Transmission Adenylyl cyclase signaling Actually generate cyclicAMP Use of a Gprotien PKA, the kinase, activation of PKA leads to phosphorilation of the channel Phosphoinositide signaling Activates a Gprotein, exchange of GDP for GTP, the primary affector is phosphoinositide, which hydrolizes a membrane lipid and IP3, which is soluble and diffuses through the cell, leads to release of calcium Receptor ? G protein ? 2nd messengers ? effector (Neuromodulatory Transmission) Alfred Gilman Discovered G proteins The signaling can have long term effects on the cell through the creation of proteins Our current understanding of the biophysical basis for the action potential was discovered by ______ in experiements on ____ -Hodgkin and Huxley; squid giant axon Sodium Ena = 55mV, Potassium Ek = -75mV The synaptic cleft: separates the presynaptic neuron from the postsynaptic neuron The Quantum Nature of Neurotransmitters How does an action potential in the presynaptic cell lead to the release of transmitter? In experiments they (they being the scientist that did the frog heart experiment Loewi and Dale) released TTX, tetrodotoxin, (a poison that blocks voltage gated Sodium channels), and as time elapsed and more channels became blocked, they measured the spontaneous effects; the action potentials in the pre synaptic cells are getting smaller and smaller, and the post synaptic potential get smaller until completely abolished. There is some kind of relationship between the presynaptic potential and the postsynaptic one. Membrane depolarization is required for transmitter release The post synaptic cell potential is increasing, so sodium infux is not necessary for transmitter release. Potassium efflix is NOT necessary for transmitter release either. Early evidence from del Castillo and Katz suggested that Calcium may play a role because: Increased extracellular calcium enhanced transmitter release Lowering extracellular calcium reduced transmitter release Removing extracellular calcium blocked transmitter release With increasing depolarizations, there was more and more calcium coming into the cell, the more calcium, the larger the signal in the post synaptic cell. Transmitter release is a function of Calcium influx into the presynaptic cell The time course of Calcium influx in the presynaptic cell determines the onset of synaptic transmission Neuromuscular Junction Acetylcholine is the neurotransmitter of the neuromuscular junction Changing Calcium does not change the amplitude of a unit Neurobiologist know definitively that a given synapse is inhibitory if stimulating the presynaptic neuron results in a reduction of the impulse frequency of the postsynaptic neuron. -inhibitory neurons reduce the frequency of action potentials Is the substance synthesized in the neuron? Is the present in the presynaptic terminal and is it released in amounts sufficient to exert a defined action on the postsynaptic neuron or effector organ? When administered exogenously in reasonable concentrations does it mimic the action of the endogenously released transmitter exactly? A specific mechanism exists for removing it from the site of action Once the transmitter is in the cleft, they have to be cleared to prepare the cleft for the next ?transmission?