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84 Cards in this Set
- Front
- Back
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From DNA to proteins
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1. Nucleus contains chromosomes
2. Chromosomes hold DNA 3. Genes produce mRNA 4. mRNA attaches to ribosomes produced by nucleolus 5. Ribosomes use mRNA info to produce proteins 6. Enzymes (proteins) catalyze reactions |
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Anterograde transport/Fast axoplasmic transport
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kinesin molecules transport molecules from soma to terminal end
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Retrograde transport
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dyenein molecules transport molecules from terminal end to soma
-can pick up toxins |
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7 Functions of glial cells
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1. Provide nutrients for neurons (neuroglia)
2. Provide structure to brain (neuroglia) 3. Myelinate neurons 4. Provide scaffolding during development (radial glial cells) 5. Function as phagocytes (engulf waste/damage, perform immune fuction; neuroglia) 6. Form scar tissue in brain (astrocytes) 7. Potassium buffering |
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Properties of the action potential
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1. All or nothing event (RMP either passes threshold or not)
2. Propogated down axon membrane 3. Fixed amplitude--do not change in height in relation to signal info 4.Has conduction velocity (m/sec) 5. Has refractory period in which stimulation will not produce an AP--limits firing rate |
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2 forces acting on ions across axon membrane
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1. diffusion--want to go from high to low concentration
2. electrostatic pressure--opposite forces attract |
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Ion Phases of Action Potential
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1. Sodium channels open, sodium begins to enter cell
2. Potassium channels open, potassium leaves cell 3. Sodium channels become inactivated, leads to refractory period, no more sodium enters cell 4. Potassium continues to leave cell--causes membrane to return to resting potential 5. Potassium channels close, sodium channels reset 6. Extra potassium outside membrane diffuses away |
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Saltatory conduction
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In myelinated axons, AP jumps from node to node, depolarizes membrane at each node
-speeds up conduction velocity |
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Neurotransmitter release
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1.Vesicles lie docked near pre-synaptic membrane
2.Arrival of AP at axon terminal opens voltage dependent calcium channels 3. Calcium ions change structure of proteins that bind the vesicles to the pre-synaptic membrane 4. Fusion pore is opened, results in merging of vesicular and pre-synaptic membranes |
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Postsynaptic receptors
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1.Molecules of neurotransmitter bind to receptors located on postsynaptic membrane
2. Receptor activation opens postsynaptic ion channels 3. Ions flow through membrane, either produce depolarization or hyperpolarization 4. resulting postsynaptic potential depends on which ion channel is opened (excitatory/inhibitory) --Postsynaptic receptors alter ion channels either directly (ionotropic, GABA, glutamate) or indirectly (metabotropic,using 2nd messenger=G-protein) |
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Termination of Postsynaptic Potentials
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1. Binding of neurotransmitter to postsynaptic receptor results in a postsynaptic potential
2. Terminations of PSP accomplished via A. Reuptake--> NT molecule transported back into cytoplasm of presynaptic membrane, NT molecule can be reused B. Enzymatic deactivation--> enzyme destroys NT molecule C. Reuptake by astrocytes |
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CNS
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brain, spinal cord
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PNS
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cranial/spinal nerves, peripheral ganglia
1. efferent nerves= motor nerves, project to target organs/muscles 2. afferent nerves= carry sensory info to brain |
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Divisions of PNS
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Autonomic (Involuntary), Somatic (Voluntary)
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Divisions of Autonomic Nervous System
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Sympathetic and Parasympathetic
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Sympathetic Nervous System
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1. Thorasic lumbar region
2. Fibers arranged short-long (ganglion in between spinal cord and organ) 3. Uses ACh at ganglion,Post-synaptic ganglion=norephinephrine secreting, Pre-ganglionic fibers=cholinergic 4. Concerned with energy expenditure because uses skeletal muscles digestion, automatic functions |
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Parasympathetic Nervous System
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1. Cranio and Sacral regions
2. Long presyn fibers, short postsyn fibers 3. Presynaptic fibers cholinergic (use ACh), Post-ganglionic fibers also secrete ACh 4. Concerned with energy conservation |
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Divisions of the Adult Human Brain
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Forebrain
Midbrain Hindbrain |
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Forebrain
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Diencephalon
Telencephalon |
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Midbrain
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Mesencephalon
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Hindbrain
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Myelencephalon
Metencephalon |
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Telencephalon
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Cerebral cortex
Basal ganglia Limbic system |
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Diencephalon
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Thalamus
Hypothalamus |
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Mesencephalon
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Tectum tegmentum
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Metencephalon
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Cerebellum
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Myelencephalon
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Pons
Medulla oblongata |
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Medulla
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controls vital reflexes
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Pons area
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many axons cross from one side of brain to other
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Reticular formation
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control motor areas of spinal cord, sends output to cerebral cortex, increasing arousal and attention
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Raphe system
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sends axons to much of forebrain, increases/decreases brain's readiness to respond to stimuli, has collection of cell bodies responsible for releasing serotonin in different parts of brain
-projection system |
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Cerebellum
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controls movement, shifts of attention, balance and coordination
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Superior and inferior colliculi
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important in routes of sensory info
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Thalamus
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contains nuclei that receive sensory info and transmit it to cortex, all senses meet in thalamus
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Hypothalamus
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contains nuclei involved in integration of species typical behavior e.g. fighting, feeding, sexual behavior
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Meninges
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series of membranes that protect brain and spinal cord
3 layers dura mater arachnoid pia mater |
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Ventricular system
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1. Travels through brain and along spinal column
2. Helps to get rid of waste 3. Epidemal cells line 3rd and 4th ventricles, help move along and produce CSF 4. Assists in cushioning brain |
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Cerebrospinal fluid
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1. Produced by choroid-plexus of ventricle
2. Brain floats in pool of CSF, reduces its weight from 1400 g to 80 g, increases its bouyancy 3. CSF also contained within 4 brain ventricles |
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Limbic system
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involved in learning, memory, and emotional states, involves olfactory system
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Structures of limbic system
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hippocampus
amygdala mammillary bodies fornix |
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Hippocampus
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involved in learning, memory
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Amygdala
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involved in emotion e.g. fear conditioning
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Fornix
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fiber bundle that interconnects the hippocampus with mammillary bodies
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Basal ganglia
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globus pallidus, caudate nucleus, putamen
-involved in control of movement |
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Pharmakinetics
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study of drug absorption/administration:
1. absorption 2. distribution 3. metabolism of compound 4. elimination |
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Depot binding
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drugs have a tendency to bind to various tissues in the body that are not necc. the site of action, prevents drug from binding to receptors at site of action in the same concentrations as it otherwise might
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Effects of depot binding
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1. Slows down rate of accumulation of the drug at the site of action
2. diminishes the concentration of the drug at the site of action 3. delays onset of the drug 4. prolongs action of drug |
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Common sites for depot binding
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1. Albumin in blood
2. Fatty tissues 3. Bone 4. Muscle 5. Liver 6. Kidneys |
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Dose-Response Curve
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relation between drug dose and magnitude of effect
-drugs can have more than one effect, vary in effectiveness |
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Therapeutic index
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effectiveness of drug relative to its safety
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Margin of safety
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area between dose-response curve for positive effect and dose-response curve for negative effect
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Tolerance
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1. Repeated drug administration results in diminished drug effect, or requires increased dosage to maintain constant effect
2. Withdrawal effects=opposite effect, often accompanies tolerance 3. Tolerance can reflect decreased drug receptor binding or reduced postsynaptic action of drug |
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Sensitization
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Repeated drug administration results in heightened drug effectiveness
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Direct agonist
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drug that binds to and activates a receptor
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Antagonist
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drug that binds to but does not activate, and can block, a receptor
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Indirect agonist
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drug that attaches to a binding site (not necc. the same as the neurotransmitter) and interferes with the normal action of the receptor
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Agonist actions on Synaptic Transmission
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1. Act as precursor, facilitate synthesis (e.g. LDOPA)
2. Stimulates release of NT (e.g. black widow spider venom) 3.Stimulate postsynaptic receptor (e.g. nicotine) 4. Blocks autoreceptors 5. Block reuptake 6. Inactivate enzyme |
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Autoreceptors
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receptors on cell releasing NT, bind to NT being released, involved in self-regulation of presynaptic cell
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heteroreceptors
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can exist on both pre and postsynaptic cells, tends to bind to NT that cell is not releasing
e.g. glutamate receptors on serotonin cell allow membrane potential to be depolarized |
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Antagonist actions on Synaptic Transmission
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1. Drug prevents storage of NT in vesicles (reserpine--monoamines)
2. Inhibits release of NT (botulinum toxin--ACh) 3. Blocks postsynaptic receptors (curare, atropine--ACh) 4. Inactivates synthetic enzyme (PCPA--serotonin) 5. Stimulates autoreceptors (apomorphine--dopamine) |
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Competitive binding
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Drug binds to same place as ligand, likelihood depends on affinities
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Noncompetitive binding
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Drug binds to site other than ligand, explains how drug can have additive/multiplicative effect
-keeps channel open more often and longer -bigger effect ultimately |
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Neuromodulators
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have longer, more distal, prolonged effects
-use metabotropic receptors, tend to have bigger effect on brain as a whole e.g. norepinephrine, dopamine, serotonin |
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Paracrine transmission
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You can release NT/neuromod in synapse but it escapes the synapse and can have effects on other cells in the surrounding area
e.g. serotonin acts on cells in surrounding area, not enough at synapse; Prozac works to change amount of serotonin available and thus change the system as a whole |
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NMDA receptors
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Important for learning induction, but not necessarily learning expression
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Carl Lashley
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1950s
-believed could find location in brain that had to do with memory (endogram) -taught rats to run mazes, looked at cortex to find location using cuts -tried to get rats to forget maze learning-->FAILED |
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Why Lashley failed
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1. Assumed memories started in cerebral cortex
2. Assumed memories stored in discrete location 3. Assumed all memories physiologically the same |
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Richard F. Thompson
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1980s
-Studied eyeblink response in rabbits, used classical conditioning (pair air puff with tone) -Figured out that lesioning nucleus in cerebellum (lateral interpositus nucleus) has an effect on conditioning -can interrupt learning -lesioning causes permanent loss of eyeblink response to tone |
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Effect of Red Nucleus on Eyeblink Response
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red nucleus= part of motor system, connected to cerebellum
-if you block activity of the red nucleus during training, rabbits do not show eyeblink response -after you let red nucleus recover, show very strong response dilemma=rabbit did not appear to learn behavior |
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Result of Thompson studies
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there is a location where a specific type of learning takes place
red nucleus=expression of learning interpositus nucleus=induction of learning |
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Donald Hebb
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1949
-at least 2 types of memory -short term and long term -brain damage effects both types -short term memory=self-activating circuit -memory=about how cells behave and the circuits they form -if circuits stabilize long enough, a permanent change occurs, either chemical or physical |
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Later evidence for Hebb's theories
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It is not length of time that strengthens memory, but emotional impact of the event
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Why emotional impact strengthens memory
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Emotional events cause a sympathetic reaction underlied by peripheral changes such as the release of adrenaline, increased conversion of glycogen to glucose
-stimulation of vagus nerve when something dramatic happens sends message to brain -increased loc. coer. activity, stimulation of amygdala (helps you remember negative events) -events that are emotionally arousing are underlied by a system to create memories esp. negative mechanism |
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Patient HM
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1950s
destroyed medial temporal lobes -anterograde amnesia (never able to form new memories) -temporary retrograde amnesia -removed amygdala, hippocampus -impaired declarative memory (hippocampus important in) |
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Hippocampal formation
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dentate gyrus
subiculum/subicular complex Cornu ammonis regions, CA3 and dentate gyrus (hippocampus proper) -hippocampus important for explicit memory |
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Hippocampal inputs
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1. entorhinal cortex-projects to CA1, CA3, dentate gyrus
2. perirhinal cortex-important for est. associations between pairs of stimuli |
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Hippocampal projections
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1. entorhinal cortex
2. perirhinal cortex 3. gyrus around hippocampus |
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Hippocampus important in
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1. explicit long term memory
2. spatial memory 3. retrieving info you have already learned |
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Patient RB
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Suffered cardiac arrest
Left CA1 regions damaged Caused severe anterograde amnesia, some retrograde amnesia -showed CA1 region important for forming new memories, somewhat important for retrieving old memories |
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Tseing
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created mice with knocked out NMDA receptors in hippocampus
-bad spatial memory -tried giving knocked-in NMDA receptors, but vulnerable to hypoxia, metabolic disturbances |
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condition most likely to produce retrograde amnesia
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damage to medial temporal lobes extending to hippocampus but not CA1 region
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Role of serotonin in hippocampal activity
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suppressive effect on LTP in hippocampal formation because decreases dendritic spines on parametal cells (release glutamate)
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Role of norepinephrine in hippocampal activity
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activation of norepinephrine beta receptors in dentate gyrus facilitates LTP
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Role of dopamine in hippocampal activity
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Facilitates LTP, blockage of dopamine can disrupt learning and memory tasks
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Role of ACh in hippocampal activity
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Faciliates LTP, generates a lot of theta waves
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