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49 Cards in this Set
- Front
- Back
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Neural Doctrine/ Nissl Stain vs Golgi Stain
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Golgi vs. Cajal
Cajal = not connected contact not continuity, golgi opposite Nissl Stain: distinguishes neurons and glia, establishing cytoarchitecture Golgi Stain: shows cell body, soma, dendrites, axons |
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Classifications of Neurons
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Unipolar-single neurite
Bi-polar- 2 neurites Multi-polar- 3 or more |
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Golgi Type 1?
Golig Type 2? |
Type 1-Long Axons-IE motor Neurons
Type 2- Short Axons Local Networks |
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Types of neurons
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1. number of neurites (unipolar, bipolar, multipolar)
2. pattern of dendrites (pyramidal, stellate) 3. connections (sensory, motor, interneuron) 4. axon length (Golgi type I, Golgi type II) 5. neurotransmitter (cholinergic, dopaminergic, serotonergic) |
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Glia?
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Astrocytes- most numerous in brain, fill spaces in between neurons, blood brain barrier
Ogliodendrites/Schwann cells- insulate neurons Nodes of Rainvier- no mylein |
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Axoplasmic Transports
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Anterograde transport= kinesin moving from soma to terminal
Retrograde transport= axon to soma, dynein moving |
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Nernst Equation?
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It tells us what the equilibrium potential for each ion is
Each ion has a unique equilibrium potential Note: The Nernst equation does not give us the membrane potential because it assumes only one type of ion crosses the membrane |
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NEURONS AND GLIA
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study
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Neural Doctrine/ Nissl Stain vs Golgi Stain
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Golgi vs. Cajal
Cajal = not connected contact not continuity, golgi opposite Nissl Stain: distinguishes neurons and glia, establishing cytoarchitecture Golgi Stain: shows cell body, soma, dendrites, axons |
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Classifications of Neurons
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Unipolar-single neurite
Bi-polar- 2 neurites Multi-polar- 3 or more |
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Golgi Type 1?
Golig Type 2? |
Type 1-Long Axons-IE motor Neurons
Type 2- Short Axons Local Networks |
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Ribosome factory= Nucleolus,
Rough ER/ Mitochondria = ATP energy KNOW WHAT THEY DO/WHERE |
study
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Types of neurons
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1. number of neurites (unipolar, bipolar, multipolar)
2. pattern of dendrites (pyramidal, stellate) 3. connections (sensory, motor, interneuron) 4. axon length (Golgi type I, Golgi type II) 5. neurotransmitter (cholinergic, dopaminergic, serotonergic) |
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Glia?
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Astrocytes- most numerous in brain, fill spaces in between neurons, blood brain barrier
Ogliodendrites/Schwann cells- insulate neurons Nodes of Rainvier- no mylein |
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Axoplasmic Transports
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Anterograde transport= kinesin moving from soma to terminal
Retrograde transport= axon to soma, dynein moving |
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NEURONAL MEMBRANE AT REST
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study
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Nernst Equation?
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It tells us what the equilibrium potential for each ion is
Each ion has a unique equilibrium potential Note: The Nernst equation does not give us the membrane potential because it assumes only one type of ion crosses the membrane |
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The resting membrane potential
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Na+ and K+
Both cross the membrane at different relative permeabilities K+ is much more permeable (this arises from the ion channels) RMP must account for K+ and Na+ moving through the membrane -65Mv |
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Equilibrium mV for
K+ Na2+ Cl- |
K+= -80
Na2+= 62 Cl- = -65 Ca2+= 123 Mv |
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Membrane is highly permiable to K2+,
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Remember: K+ is more permeable than Na+
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Goldman equation
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It tells us what the resting membrane potential is
It incorporates the different relative permeabilities of ions Remember: K+ is more permeable than Na+ |
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4 thing about RMP
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Small changes in ion concentrations --> large changes in Vm
Differences in electrical charge occur next to the plasma membrane surface Rate of movement of ions across the membrane proportional to Vm – Eion If ion concentrations inside and outside are known, Eion can be calculated |
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THE ACTION POTENTIAL Phases
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1: Resting Potential = -65, threshold -40
2: Rising Phase = Na rushes in 3: Overshoot 4: Falling Phase = K+ Rushes out 5: Undershoot |
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The rate of action potential depends on
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magnitude of deploarizing current
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Steps of synaptic transmission
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presynaptic action potential arrives
depolarization of the axon terminal voltage-gated calcium channels open calcium enters the axon terminal movement of “docked” synaptic vesicles exocytosis or release of neurotransmitter |
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What happens after the AP reaches the axon terminal?
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Vesicles are docked in the active zone and ready to go
Voltage-gated Ca2+ channels open Ca2+ entry triggers exocytosis Vesicles are recycled through endocytosis |
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Axon hillock
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Spike initiaztion zone, where axon meets soma
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When AP moves, sodium channels
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close behind it, K+ open
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Open stimulus, first channels that open are...
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Sodium mechanically gated
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SYNAPTIC TRANSMISSION
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Types of synapes: Dendritic, axonic, somatic
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Steps in the release of NT
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Presynaptic AP arrives
Deplorization of Axon Termina Voltage gated CA2++ channels open Ca2++ enters axon terminal Movement of Docked synaptic vesicles Exocytoss or release of NT |
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How does NT get to the presynaptic axon terminal Peptides vs Amines?
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Peptides: Synthesized in RER from large precursor proteins Golgi bodies,cleaved to smaller peptides Some part of Golgi bodies breakdown to form small vesicles (secretory granules) that carry the peptides along the microtubules (via motor proteins) to the axon terminal where they are stored and released following an AP.
Thus peptides synthesized in cell body shipped to axon terminal Amines and amino acids: Enzymes convert precursor molecules into neurotransmitter in cytosol of axon terminal. Transporter proteins will load them into synaptic vesicles in the terminal where they are stored and released following an AP. Thus amines and amino acids synthesized in axon terminal |
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How does the presynaptic neuron know when to stop releasing NT?
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Autoreceptors tell the neuron to stop releasing NT
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What happens to the NT after it is released into the synaptic cleft
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Autoreceptors
Broken down through enzymes (ACh only!) Transporters Diffusion Glia Receptors |
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Gap Junctions
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allow ionic current to pass bi-directionally
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Types of NTs
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Amino Acids
Glu, Gly, GABA Amines ACh, DA, NE, 5-HT Peptides Somatostatin, Enkephalins, Substance P, Oxytocin, |
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Grays type 1, 2 synapes:
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type 1: postsynaptic are thicker than pre
type 2: symmetrical thickness |
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when Ca2++ comes in presynaptic cell...
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releases NT
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EPSP?
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depolarization of postynaptic cell, excitatory
1. Impulse arrives in presynaptic, releases NT 2. molecules bind to NT gated ion channels. If N+ enters post synaptic cell, depolarization occurs 3. Resulting change, vM jumps |
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IPSP
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inhibitory, permiable to Cl-, caused by activation of glycine or gaba ion channels, post synaptic cell becomes hyperpolarized
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Glutamate (gives energy) agonists? ACH Antagonists?
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GLUTAMATE Agonists= AMPA, NMDA, Kainate,
ACH agonist Nicotine, Muscarine ACH antagonists= curare, atropine |
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Brain
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Cerebrum (anterior/rostral) to cerebrum (posterior, caudal)
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Body directional views
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Anterior/rostral = front
Posterior/caudal = back Dorsal = top ventral = down Medial= close to center lateral = extending |
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Planes of view
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Midsagital = cuts down the middle
Coronal = vertical sliver Horizontal= cuts horizontally |
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Layers of brain
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Dura->sub
Arachnoid -> sub Pia mater artery brain |
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Dorsal vs Ventral roots
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Dorsal, brings into spinal chord (sensory)
Ventral - brings away from spinal chord (muscles) |
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Stages of brain development
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Forebrain (future cerebrum)- Telencephalon, dienchephalon- retina
Midbrain- Mesenchephalon Neural Tube= enitre CNS Neural Crest = all neaurons with cell bodies in PNS Hindbrain- Metencephalon Myelencephalon |
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Ectoderm-NS
Diencephalon- thalamus mesencephalon - midbrain |
What leads to what
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Choroid Plexus
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Makes CSF -cerebral Spinal Fluid
Travels from lateral ventricles-> -> foramen of Monroe-> 3rd ventricle-> cerebral aqueduct-> 4th ventricle-> to EITHER subarachnoid space-> blood OR spinal column |
