12.6 Neural Integration

12.6 Neural Integration 1 Expected Learning Outcomes: • Explain how a neuron “decides” whether or not to generate action potentials. • Explain how the nervous system translates complex information into a simple code. • Explain how neurons work together in groups to process information and produce effective output. • Describe how memory works at the cellular and molecular levels. 98 Neural Integration 2 Neural integration—the ability to process, store, and recall information and use it to make decisions • Chemical synapses allow for decision-making • Brain cells are incredibly well connected, allowing for complex integration • Pyramidal cells of cerebral cortex have about 40,000 contacts with other neurons • Trade off: chemical transmission involves a synaptic delay that makes information travel slower than it would if there was no synapse 99 12.6a Postsynaptic Potentials 1 Two types of postsynaptic potentials produced by neurotransmitters: • Excitatory postsynaptic potential (EPSP)—voltage change from the RMP toward threshold • An EPSP usually results from Na + flowing into the cell • Inhibitory postsynaptic potential (IPSP)—voltage becomes more negative than it is at rest • An IPSP can result from Cl- entry or K + exit from cell 100 Postsynaptic Potentials 2 Figure 12.25 101 Postsynaptic Potentials 3 Different neurotransmitters cause different types of postsynaptic potentials. • Glutamate and aspartate produce EPSPs in brain cells • Glycine and GABA produce IPSPs A neurotransmitter might excite some cells and inhibit others, depending on the type of receptors in the postsynaptic membrane • Acetylcholine (ACh) and norepinephrine work this way • ACh excites skeletal muscle but inhibits cardiac muscle due to the expression of different types of ACh receptors on the different types of muscle cells 102 12.6b Summation, Facilitation, and Inhibition 1 Summation—the process of adding up postsynaptic potentials and responding to their net effect • Occurs in the trigger zone • Some incoming nerve fibers may produce EPSPs while others produce IPSPs • A neuron’s response depends on whether the net input is excitatory or inhibitory • The balance between EPSPs and IPSPs enables the nervous system to make decisions 103 Summation, Facilitation, and Inhibition 2 Two ways EPSPs can be added to reach threshold: • Temporal summation—a single synapse generates EPSPs so quickly that each is generated before the previous one fades • Allows EPSPs to add up over time to a threshold voltage that triggers an action potential • Spatial summation—EPSPs from several different synapses add up to threshold at an axon hillock • Simultaneous input from multiple presynaptic neurons required for the postsynaptic neuron to fire • An example of facilitation—a process in which one neuron enhances the effect of another 104 Temporal and Spatial Summation Figure 12.26 105 Summation of EPSPs Figure 12.27 106 Summation, Facilitation, and Inhibition 3 Neurons can work in groups to modify each other’s actions • Presynaptic facilitation—occurs when one presynaptic neuron enhances another one • Increases necessary synaptic transmission • Example: facilitating neuron (cell “F” in figure) releases serotonin which makes voltage-gated calcium channels in axon terminal (“S” in figure) stay open longer 107 Presynaptic Facilitation Figure 12.28 108 Summation, Facilitation, and Inhibition 4 Neurons can work in groups (continued): • Presynaptic inhibition—occurs when one presynaptic neuron suppresses another one • Reduces or halts unwanted synaptic transmission • Example: Inhibiting neuron (cell “I” in figure) releases GABA which prevents voltage-gated calcium channels in axon terminal (“S” in figure) from opening and so little or no neurotransmitter is released 109 Presynaptic Inhibition Figure 12.29 110 12.6c Neural Coding Neural coding—converting stimulus information into meaningful pattern of action potentials • Labeled line code—mechanism for transmitting qualitative information (type of stimulus) • Depends on which neurons fire; for example, optic nerve input labeled as “light” • Quantitative information (intensity of a stimulus) encoded in two ways: • Weak stimuli only activate sensitive “low threshold” neurons; strong stimuli also activate less sensitive “high threshold” neurons through recruitment • Weak stimuli cause neurons to fire action potentials at a slower rate, strong stimuli cause higher firing frequency 111 An Example of Neural Coding Figure 12.30 112 12.6d Neural Pools and Circuits 1 Neural pools—functional groupings of neurons; each pool consists of thousands of interneurons concerned with a particular body function • Examples: • Control rhythm of breathing • Moving limbs rhythmically when walking 113 Neural Pools and Circuits 2 Discharge and facilitated zones • Information arrives at neural pool through input neurons • Within input neuron’s discharge zone, it can act alone to make postsynaptic cells fire • In its broader facilitated zone, input neuron makes fewer, less powerful synapses • Can only stimulate targets with the assistance of other input neurons Figure 12.31 114 Neural Pools and Circuits 3 Types of neural circuits: • Diverging circuit—one nerve fiber branches and synapses with several postsynaptic cells • Converging circuit—input from many different nerve fibers can be funneled to one neuron or neural pool Figure 12.32(top) 115 Neural Pools and Circuits 4 Types of neural circuits (continued): • Reverberating circuit—neurons stimulate each other in linear sequence but one or more of the later cells restimulates the first cell to start the process all over • Parallel after-discharge circuit—input neuron diverges to stimulate several chains of neurons • Neuron chains with different number of synapses converge on one or a few output neurons, but with varying delays • After-discharge—continued firing after the stimulus stops Figure 12.32(bottom) 116 Neural Pools and Circuits 5 Serial and parallel processing of information • Serial processing—neurons and neural pools relay information along pathway in relatively simple linear fashion • Can process only one flow of information at a time • Read a book or watch a television movie—you cannot do both simultaneously • May jump back and forth between one and the other, or only half understanding each 117 Neural Pools and Circuits 6 Serial and parallel processing of information (continued): • Parallel processing—information is transmitted along diverging circuits through different pathways that act on it simultaneously, for different purposes • For example, when you’re driving your car, your visual system (eye and brain) must simultaneously process information about color, shape, depth of field, and motion in the scene before your eyes • At the same time, you must process traffic sounds and signals from your body’s own motion sensors 118 12.6e Memory and Synaptic Plasticity 1 Memory trace (engram)—pathway of synapses through the brain; physical basis of memory • Along this pathway, new synapses are created or existing synapses modified to make transmission easier • Synaptic plasticity—ability of synapses to change • Synaptic potentiation—process of making transmission easier • Three kinds of memory: • Immediate memory, short-term memory, and long-term memory • Correlated with different modes of synaptic potentiation that last from a few seconds to a lifetime 119 Memory and Synaptic Plasticity 2 Immediate memory • Immediate memory—ability to hold something in your thoughts for a few seconds • Essential for reading ability • Feel for the flow of events (sense of the present) • Our memory of what just happened “echoes” in our minds for a few seconds • May depend on reverberating circuits 120 Memory and Synaptic Plasticity 3 Short-term memory • Short-term memory (STM)—lasts from seconds to a few hours • Includes working memory for taking action • Example: calling a phone number you just looked up • Synaptic facilitation—making it easier to transmit signals across a synapse; important in memory formation • Tetanic stimulation—rapid arrival of repetitive signals at a synapse • Causes Ca 2+ accumulation in terminal, more neurotransmitter released • Post tetanic potentiation—calcium level in axon terminal stays elevated, results in exceptionally large burst of neurotransmitter • May be involved in jogging a memory from a few hours ago • Little stimulation needed to recover memory 121 Memory and Synaptic Plasticity 4 Long-term memory • Long-term memory (LTM)—lasts up to a lifetime and can hold more information than short term memory • Two types of LTM: • Explicit (declarative) memory—memories you can put into words (numbers, names, dates, etc); must think to remember these • Implicit memory—reflexive or unconscious memory; includes emotional memories (bee stings hurt) and procedural (motor skill) memories • Some LTM involves formation or remodeling of synapses • New branching of axons or dendrites • Some LTM may involve molecular changes called longterm potentiation (LTP) 122 Memory and Synaptic Plasticity 5 How we forget • Long-term depression—low-frequency stimulation of a synapse results in low levels of intracellular Ca 2+ • Low calcium concentration activates protein phosphatases, which dephosphorylate synaptic proteins such as actin microfilaments that support dendritic spines • These proteins are then degraded by proteasomes, which tear down dendritic spines and remove little-used synapses from the neural circuits 123 Alzheimer Disease 1 Alzheimer disease (AD) causes 100,000 deaths/year; affects 11% of population over 65 and 47% by age 85 Symptoms: • Memory loss, moody, combative, and lose ability to talk, walk, and eat • Acetylcholine (ACh) and nerve growth factor (NGF) deficiencies Diagnosis confirmed at autopsy • Atrophy of gyri (folds) in cerebral cortex • Neurofibrillary tangles and senile plaques • Formation of β-amyloid protein from breakdown product of plasma membranes Treatment possibilities • Find ways to clear β-amyloid or halt its production, but research halted due to serious side effects 124 Alzheimer Disease 2 Figure 12.33 125 Parkinson Disease 1 Parkinson disease (PD)—progressive loss of motor function due to degeneration of dopamine-releasing neurons • Dopamine normally prevents excessive activity in motor centers (basal nuclei) Symptoms: • Involuntary muscle contractions • Pill-rolling motion, facial rigidity, slurred speech • Illegible handwriting, slow gait Treatment—drugs and physical therapy • Dopamine precursor (L-dopa) crosses brain barrier; bad side effects on heart and liver • MAO inhibitor slows neural degeneration • Surgical technique to relieve tremors 126 Parkinson Disease 2 Figure 12.34 127