CBIO 2200 1nd Edition Lecture 19 Outline of Last Lecture I. Overview of the Nervous SystemII. Subdivisions of the Nervous SystemIII. Nervous TissueIV. Classes of NeuronsV. Types of CNS NeurogliaVI. Types of PNS NeurogliaVII. MyelinVIII. Regeneration of PNS Nerve FibersIX. Electrophysiology of NeuronsOutline of Current Lecture I. The Refractory PeriodII. Chemical SynapsesIII. Memory and Synaptic Plasticity IV. Common Degenerative Disorders of the BrainCurrent LectureI. The Refractory Perioda. Two phases of the refractory period:i. Absolute refractory period – no matter the strength of the stimulus, you cannot generate another action potentialii. Relative refractory period – can generate another action potential but thestimulus would have to be extremely strongb. Action potential propagation called: These notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.i. Continuous conduction – in un-myelinated fiberii. Saltatory conduction – in myelinated fiber; at nodes of RanvierII. Chemical Synapsesa. Synapse between two neuronsi. First neuron in the signal path is the presynaptic neuronii. Second neuron is postsynaptic neuronb. Neurotransmitters and synaptic delayi. Neurotransmitters1. Fall into four major categories according to chemical compositionsa. Acetylcholine – acetic acid and cholineb. Amin acid neurotransmitters – e.g. glycine, glutamate, aspartate, and GABAc. Monoamines – synthesized from amino acids with carboxylgroup removed; i. catecholamines – norepinephrine, epinephrine, and dopaminesii. Seratonin and histamined. Neuropeptides – act in the brain; cholecystokin and substance Pii. Synaptic delay – ½ of a millisecond; for neurotransmitters to cross synaptic clefiii. Types of synapses with different modes of action1. Excitatory cholinergic synapse a. employs acetylcholine as neurotransmitter; b. excitatory in skeletal muscle but inhibitory in cardiac muscle2. Inhibitory GABA-ergic synapse a. Employs aminobutyric acid as its neurotransmitterb. When released, crosses synaptic clef and binds to GABA receptors which are also chloride channelsc. Chlorine cause hyperpolarization 3. Excitatory adrenergic synapsea. Employs norepinephrine as neurotransmitterb. Receptor is a trans-membrane protein associated with G protein; activates adenylate cyclase, which activates cyclic AMPc. Act through second-messenger systemsd. Enzyme amplification – one molecule has multiple effectsiv. Stopping synaptic transmission1. Two steps:a. Stop adding neurotransmitterb. Get rid of that which is already therei. Diffusionii. Reuptake into synaptic know; monoamine oxidaseiii. Degradation of neurotransmitter in clef and acetylcholinesterase breaks down acetylcholine and then choline is reabsorbed c. Postsynaptic potentialsi. Excitatory postsynaptic potential (EPP) – may or may not cause local depolarization1. Glutamate and aspartate are excitatory brain neurotransmitter that produce EPP’sii. Inhibitory postsynaptic potential (IPSP) – causes hyperpolarization1. Glycine and GABA produce IPSPs are inhibitoryd. Summationi. Process of adding up postsynaptic potentials and responding to their net effectii. Occurs in the trigger zone (axon hillock)iii. Temporal summation 1. Repeated release of excitatory neurotransmitter from a single presynaptic neuron2. Stimulus occurs at same location at different timesiv. Spatial summation1. EPSP’s generated from multiple presynaptic neurons at same timee. Facilitationi. One neuron increases the amount of neurotransmitter released by another neuron thereby enhancing the effectii. Ex: serotoninf. Presynaptic Inhibitioni. Process in which one presynaptic neuron suppresses the firing of anotherii. Ex: GABAIII. Memory and Synaptic Plasticitya. Memory trace (actual physical basis of our memory) or engrami. Synaptic plasticityii. Synaptic potentiation (one form of synaptic plasticity)iii. Kinds of memory:1. Immediate, short, and long term memoryb. Stages of memoryi. Encodingii. Storage – can’t happen with crammingiii. RetrievalIV. Common Degenerative Disorders of the Braina. Alzheimer’s diseasei. Generally among elderlyii. Diagnosis confirmed at autopsy1. Atrophy of gyri (folds) in cerebral cortex2. Accumulation of beta-amyloid plaque and neurofibrillary tanglesiii. Most common cause of dementia – loss of cognitive functionb. Parkinson diseasei. Progressive loss of motor function beginning in 50s or 60sii. Degeneration of dopamine-releasing neuronsc. Huntington’s diseasei. Accumulation of Huntington proteinii. Affects hippocampus, purkinje cells and