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Nerves 2
Term | Definition |
---|---|
Regeneration | Occurs if the neurosoma is intact and at least some of the neurilemma remains; regeneration tube formed and guides growing axon stump back to target cells |
Regeneration tube | Tube formed by Schwann cells, basal lamina, and neurilemma near injury that guides axon back to original contact |
Degeneration Atrophy | Loss of muscle due to loss of nerve contact by damaged nerve |
Nerve Growth Factor | Protein secreted by gland, muscle, and glial cells; prevents apoptosis in growing neurons |
Resting Membrane Potential (Nerves) | -70 mV |
Na/K pumps | Brings out 3 Na for every 2 K it brings in, compensating for Na and K leakage. Active transport |
Local Potential | Disturbances in membrane potential when a neuron is stimulated; short-range change in plasma membrane that travels through trigger zone to trigger action potential |
Depolarization | Membrane voltage shifts to less negative value, due to Na rushing into the cell |
Threshold | -55 mV; critical voltage to which local potentials must rise to open voltage regulated gates |
Hyperpolarization | Drop of membrane voltage below original RMP due to more K leaving the cell than Na entering |
Spike | An action potential graphed, due to it happening so fast |
All-or-none law | Neuron fires at maximum voltage if threshold (-55 mV) is reached, and does not if threshold is not reached |
Nondecremental | Action potentials do not get weaker with distance |
Irreversible | Action potentials cannot be stopped once started |
Graded | Local potentials vary in magnitude with stimulus strength |
Decremental | Local potentials get weaker the farther they spread from the point of stimulation |
Reversible | Local potentials are able to return to normal resting potential when stimulation stops, due to K diffusion out of cell |
Excitatory and Inhibitory | Local potentials can either excite the cell or prevent it from firing an action potential |
Refractory Period | Period of resistance to stimulation |
Absolute refractory period | As long as the Na gates are open, no stimulus, regardless of strength, will trigger an action potential |
Relative refractory period | K gates are still open and will oppose incoming Na, but especially strong stimuli will trigger an action potential |
Continuous conduction | Unmyelinated fibers have voltage gated channels along entire length, and action potentials continuously travel down the axon, opening the channels. |
Saltatory conduction | Myelinated fibers have few voltage gated channels, but the signal travels quickly and stimulates the next node |
Presynaptic neuron | Neuron at a synapse that releases neurotransmitter |
Postsynaptic neuron | Neuron at synapse that responds to neurotransmitter |
Axodendritic | Synapse that connects an axon to a dendrite |
Axosomatic | Synapse that connects axon to the soma |
Axoaxonic | Synapse that connects axon to axon |
Electrical synapse | Gap junctions join cells instead of synaptic clefts and are fast, but cannot integrate information |
Acetylcholine | Class of neurotransmitter that is formed from acetic acid and choline |
Amino Acid neurotransmitters | Class of neurotransmitter that is made of amino acids, such as GABA, glycine, glutamate, and aspartate |
Monoamine | Class of neurotransmitter synthesized from amino acids by removal of -COOH group; contains several subcategories |
Catecholamines | Subclass of monoamine that contains a catechol group and an amine side chain |
Indolamines | Subclass of monoamine; consists of a bicyclic group with a benzene ring attached to a pyrroline group |
Neuropeptides | Chain of 2 to 40 amino acids that are stored in axon terminal as secretory granules |
Purines | Neurotransmitter that consists of a pyrimidine and a imidazole group, includes adenosine and ATP |
Gases | Neurotransmitter in a gaseous form, including nitric oxide and carbon monoxide |
Synaptic delay | Time from the arrival of a signal at the axon terminal of a presynaptic cell to the beginning of an action potential in the postsynaptic cell; 0.5 ms for all events to occur |
Excitatory cholinergic synapse | Employs acetylcholine, exciting some post-synaptic cells and inhibits others |
Postsynaptic potential | ACh receptors trigger opening of Na+ channels, producing this local voltage shift |
Inhibitory GABA-ergic Synapse | Functions like acetylcholine synapses, except GABA receptors are chloride channels, making the inside of the cell more negative and less likely to fire |
Excitatory Adrenergic Synapse | Employs norepinephrine; binds to transmembrane protein associated with G protein. Once NE binds to the transmembrane protein, the G protein dissociates and can do many actions |
Enzyme amplification | Property of excitatory adrenergic synapses, where one NE molecule can produce vast numbers of products in the cell |
Neuromodulators | Chemical signals secreted by neurons that have a long term effect on a group of neurons instead of a quick, brief effect. Can alter neurotransmitter release, synthesis, or breakdown, and can also alter number of receptors (e.x.: NO). |
Neural integration | Ability to process, store, and recall information and use it to make decisions, at the cost of information travelling slower |
Excitatory postsynaptic potentials | (EPSP); positive voltage change increasing chance of cell firing |
Inhibitory postsynaptic potentials | (IPSP); negative voltage change decreases chance of cell firing; mainly produced by neurotransmitters opening ligand gated channels, though can be produced by opening K channels, letting K inside |
Summation | Process of adding up postsynaptic potentials and responding to net effect; happens in trigger zone |
Temporal summation | A single synapse receives many EPSPs in a short time |
Spatial Summation | A single synapse receives many EPSPs from many presynaptic cells |
Presynaptic facilitation | A neuron enhances the effect of another |
Presynaptic inhibition | A neuron suppresses the effect of another |
Neural coding | The way the nervous system converts information into a meaningful pattern of action potentials |
Labeled line code | Each sensory nerve fiber leads from a receptor that recognizes a specific stimulus type |
Quantitative information | Information about the intensity of a stimulus; encoded either by different thresholds or firing frequency |
Neural pools | Neurons function in large groups, each of which consists of millions of interneurons concerned with a particular function |
Discharge zone | Single input neuron can make the postsynaptic cells fire |
Facilitated zone | Input neuron synapses with other neurons in the pool; there are fewer synapses on each of them, and can only stimulate those neurons to fire with the assistance of other input neurons |
Diverging circuit | One nerve fiber branches with several postsynaptic cells |
Converging circuits | Several nerve fibers funneled to one neuron or neural pool |
Reverberating circuit | Neurons stimulate each other in linear sequence but one cell restimulates first cell to start the process over |
Parallel after-discharge circuits | Input neuron diverges to stimulate several chains of neurons |
Memory trace | Pathway of synapses in the brain that encode memories |
Synaptic plasticity | Synapses can modify and change pathways |
Synaptic potentiation | Process of making transmission easier |
Immediate memory | Ability to hold something in thoughts for only a few seconds |
Short term memory | Lasts for a few seconds to several hours; needs to be recalled to send memory to long-term memory |
Tetanic stimulation | Rapid arrival of repetitive signals at synapse; Ca accumulates and cell more likely to fire |
Post-tetanic potentiation | Ca level in synaptic knob stays elevated, requiring only little stimulation to jog a memory |
Declarative memory | Long term memory involving retention of events that can be described in words |
Procedural memory | Long term memory involving retention of motor skills |
Long term potentiation | Changes in receptors and other features increase transmission across experienced synapses, effect is longer lasting |
Alzheimer's disease | Deficiencies of ACh and Nerve Growth Factor lead to memory loss and eventually loss of basic abilities like walking. Atrophies in cerebral cortex, and treatments include halting beta-amyloid production |
Parkinson's Disease | Progressive loss of motor function beginning in 50s or 60s; degeneration of dopamine-releasing neurons leads to involuntary muscle contractions |