Neurons Flashcards
Glia Cells
-non-neuronal cells
-supportive, homeostasis, regulation
Neuron function
Reception, integration, transmission, and transfer of information
Bipolar Neurons
-1 dendrite, cell body and 1 axon
-sensory
Pseudounipolar Neurons
Dendrites, axon and cell body on side
-motor
Multipolar Neurons
Multiple dendrites
-interneurons
-most common
Macroglia
-larger supporting cells
-Astrocytes
-Oligodendrocytes
-Schwann Cells
Microglia
-immune for CNS
-phagocytes
Astrocytes
-macroglia cells in CNS
-support, signal, nutrtients
Oligodendrocytes
-macroglia cells in CNS
-create myelin
Schwann Cell
-PNS macroglia
-support PNS and make myelin
-does all the job
Local Potential
-small, graded
-occurs in receptor or synapse
-spreads passively
Action potential
Large “all or none”
-depolarizing
Resting Membrane Potential
-70mV
Ion Cell Distribution at Rest
More Na+ outside, more K+ inside
-Extracellular positive charge outside
-Intracellular negative charge inside
-more permeable to K+M
Movement of K+ during AP
-diffuses down concentration gradient and towards negative charges
-chemical gradient force out, electrical gradient force in
2K+/3Na+
4 Membrane Ion channels
Leak (non-gated): small amount leak, K+
Modality-gated: Sensory neurons only; mechanical, temp or chemicals
Ligand-gated: opens when stimulated by neurotransmitters
Voltage-gated: opens when reaction; Ca+
Movement of Na+ during AP
-moves through leaky channels and then voltage gated negative charges
2K+/3Na+
Spatial Summation
I…..I……I……I
Temporal Summation
AP combine to form a large AP.
-Build up of multiple excitatory waves merging
Depolarization
-voltage gated channels release Na+ into cell
- polarity becomes positive
Repolarization
-Na+ channels close, K+ voltage channels open and release to the outside of the cell
Hyperpolarization
K+ gates remain open and cause hypo
-90mV
Absolute Refractory Period
completely unresponsive to stimuli
-Na+ has not reset yet
Relative Refractory Period
May respond to higher stimuli
-Most Na+ resets
Factors Influencing AP
-diameter of axon, larger=faster
-myelin, more=faster
-temperature, warm=faster
Nodes of Ranvier
-site of saltatory conduction
-location of AP generation and depolarization
-high density of voltage gated ion channels
Conduction Speeds of fibers
large myelinated: PNS sensory and motor
Thin unmeylinated:
-short axons in grey matter in CNS
-visceral ANS axons
-pain fibers
Muscle Cell AP
-90mV RMP
-AP 1-5msec
-18x slower than neuron
Presynaptic Terminal
-neuron conducting impulse toward synapse
-feet
-release neurotransmitters/neuromodulators
Postsynaptic terminal
-dendrite or cell body receiving neurotransmitter
Axosomatic Synapse
-synapse that binds to cell body of another nerve
-local membrane potential
Axoaxonic Synapse
-synapse that binds to axon of another nerve
-1st neuron activates second
-presynaptic effects
Axodendritic
-synapse that binds to dendrite of another nerve
-local membrane potential
Steps of Synaptic Transmission
- AP comes to presynaptic terminal
- Presynaptic membrane depolarizes and releases Ca+
- Ca+ causes vessicles to exocytose neurotransmitters
- Neurotransmitter binds to postsynaptic receptor
- Postsynaptic receptor opens ion channel or triggers intracellular messengers
Excitatory Postsynaptic potential (EPSP)
-local depolarization with Na+ or Ca+ into neuron
-facilitates AP generation
-common throughout CNS and PNS
Inhibitory Postsynaptic Potential (IPSP)
-local hyperpolarization with K+ out of neuron
Presynaptic Facilitation
-1st presynaptic neuron (Axoaxonic) releases neurotransmitters that attaches to 2nd neurotransmitter (axosomatic) and slightly depolarizes it to releases Ca+
Presynaptic Inhibition
-1st presynaptic neuron (axoaxonic) causes slight hyperpolarization to decreased Ca+ released from 2nd neuron (axosomatic)
Neurotransmitters
-fast
-released from synapse
-EPSP and IPSP
-ms to mins
Neuromodulators
-extracellular space
-alter gene expression, open iono channels, change metabolism, affects many neurons
-mins to days
Ligand-Gated Ion Channels
-fast response
-aka ionotropic receptor
-some excitatory and inhibitory
-inactivate due to lack of neurotransmitter and resorption
Guanine Nucleotide Binding Protein Activation of Ion Channels
-alters electrical excitability or neurons
-Neurotransmitter being to G protein and alter the shape
-Internal subunit breaks away and binds to membrane ion channel to change shape and open
-slower than ligand
-Mood disorders, Parkinson’s, Alzheimer’s
Agonist
-drugs the bind to receptors and copy actions of neurotransmitter
Antagonists
-drugs that block postsynaptic neurotransmitter
-drugs that inhibit release of neurotransmitter in presynaptic neurons
Acetylcholine (Ach)
-Neurotransmitter produced in basal forebrain above eyes and midbrain (at top of brainstem)
-Skeletal Muscles: Ach for neuromuscular junctions for muscle contraction. Blocking: causes weakness, fatigue, paralysis
-Autonomic NS: slows HR, constricts pupils
-Brain: Arousal, pleasure, cognitive function, movement and attention. Pleasure seeking behaviors and alzheimers
Glutamate
-amino acid principal fast neurotransmitter of CNS
-Neural changes w/ learning and development (neuroplasticity)
Excessive:
-excitotoxiciity and neuron death
-seizures
Associated with
-chronic pain, Parkinson’s, schizophrenia, neuron death, stroke
GABA
-Glycine and y-aminobutyric acid
-animo acid primary inhibitory neurotransmitter that prevent excessive neural activities in CNS (downers)
Glycine: inhibits postsynaptic in brainstem and SC
Low Levels:
-seizure, involuntary muscle contractions, anxiety
Huntington’s Disease
-causes loss of neurons that use GABA
-causes jerky, involuntary movements and cognitive decline
Dopamine
-amine neurotransmitter produced in substantia nigra of the brain
-affects motor function, cognition, and behavior, reward seeking behaviors (good for eating, bad for addiction)
-2nd messenger systems
Abnormalities seen in:
-Parkinson’s: not enough dopamine; bradykinesia, treat with precursor
-Schizophrenia: signalling pathways, treat with drugs that prevent binding
Excessive:
-drug abuse by preventing reuptake of presynaptic terminals
Norepinephrine
-amine neurotransmitter produced in brainstem, hypothalamus, and thalamus
-released by neurons of ANS and adrenal glands
-fight or flight
Excessive:
-fear, panic, PTSD
-beta blockers to treat
Low:
-sleeping
-depression
Serotonin
-amine neurotransmitter involved with mood, pain, arousal, and motor acitivities
High
-alert and during REM
Low
-depression
Opioid Peptides
-endogenous: endorphins, enkephalins, dynorphins
-produced in NS and bind to receptors for opium
-receptors in SC, hypothalamus, brainstem to inhibit pain
Substance P
-peptide that stimulates nerves at injury site
Neurotransmitter: acts on CNS to cary info to brain
Neuromodulator:
-pain syndromes
-hypothalamus and cerebral cortex during long duration excitation
-modulate immune activity during stress
Ways to Restrict of # Receptors
-internalize receptor
-inactivate receptor
Increase of # receptors
-infrequent activate
-low levels of neurotransmitters
Lamber-Eaton Syndrome
-antibodies damage Ca channels in presynaptic membrane
-no Ach release
-muscle weakness
Myasthenia Gravis
-antibodies damage receptors on muscle cells
-Ach released but cannot bind
-muscle fatigue
-life threatening
