Biological- Neurons And The Action Potential Flashcards
The nervous system
Central Nervous- brain and spinal chord
Peripheral nervous system
Neurons
-receive and transmit information
-100 billion neurons in the adult brain- combine to form consciousness sensory experience and controlled behaviours (william and Herrup 1988)
-vary in size and shape- all have the same basic structure
Types of neurons
Sensory- carry sensory signals from the skin, eyes,ears ect to the central nervous system (CNS)
Motor- carry signals from the cns to the muscles
Sensory neuron -Afferent- carry info towards the CNS
Motor neuron-Efferent- carry information away from the cns
Interneurons receive/carry info from/to other neurons
The anatomy of a neuron
Cell body (Soma)- contains the nucleus,and much of the machinery that maintains the neuron
Dendrites- information receiving part of the neuron. Receive information across a tiny gap called a synapse. Surface lined with synaptic receptors. Greater the surface are of the dentrite the more info can be received
Axon- the information sender. Transfers information from the cell body to the terminal buttons
Myelin sheath- protective, insulating substance, not continuous but consists of segments. The unmyelinated area between the segments is known as the Node of Ranvier
Presynaptic terminals- also known as terminal button/synaptic bulb or knob. When an action pote tial reaches the presynaptic terminal they secrete a transmitter substance which travels across the synapse to the next neuron
Always travels from the dendrites to the presynaptic terminal
Supporting cells
-neurons are not the only cells that exist in the nervous system
-most prominent is Glial cells
-provide the cells with nutrition, clear waste products and hold the neurons in place
-neurons need constant supply of oxygen and nutrients to survive
-different types- Oligodendrocytes ,Schwann cells, astryocytes, microglia
Oligodendrocytes and Schwann cells
-main function is to support neuron axions and produce the myelin sheath which surrounds axons
- oligodendrocytes- cns
Schwann cells- PNS
Astrocytes and microglia
Astrocytes- star shaped, provide physical support to neurons and clear debris
Some astrocyte extensions cover blood vessels - receive nutrients and release them to neurons
Microglia- smallest, protect cells in the brain from disease
Transmitting information
Neuron receives chemical message
Triggers and electrical response
Causes release of chemicals at presynaptic terminals
Inside the neuron
The fluid inside (intracellular) and outside (extracellular) the neuron contains electrically charged particles called ions
Sodium Na +
Potassium K+
Chloride Cl -
Organic A-
Membrane potential - difference in electrical charge inside as compared to outside the neuron
Resting potential
- when the neuron is completely a rest it shows membrane potential of -70mV
-This membrane potential of -70mV is called the neurons resting potential
Voltmeter measures volt, glass microelectode filled with liquid that conducts electricity, wire electrode placed in seawater connected to a giant squid axon
Ion distribution
Inside membrane
150 K+
15 Na+
10 Cl-
385 A-
Negative charge
Outside membrane
5 K +
150 Na +
110 Cl -
0 A -
Positive charge
Forces
- the outside layer of the neuron, the plasma membrane, made up to a double layer of lipid molecules
- allows small uncharged particles,water,oxygen,carbon dioxide to move through it
-Charged ions must pass through special openings called ion channels - organic ions cannot pass through (A-)
Diffusion and electrostatic pressure
Diffusion - particles are in constant motion. An array of particles in a solution will therefore tend to become evenly distributed
Electrostatic pressure- particles with the same charge repel one another while particles with different charges attract one another
Sodium- potassium pump
- when the neuron is at rest sodium and potassium can pass across the plasma membrane
- A so called ‘sodium potassium pump’ however expels sodium ions out and draws potassium ions in at a ratio of 3 sodium ions out to 2 potassium ions in
The action potential
- if we apply an electrical charge to a neuron this produces a brief period of depolarisation ie the inside becomes briefly positive then returns to negative
- if we apply a strong enough charge to reach a neurons so called ‘level of excitation’ teh neuron will produce an action potential
- action potential- membrane potential is rapidly reversed and becomes strongly positive (up to 40mV) compared to the outside
- then briefly overshoots and drops to -75mV (hyper polarisation)
The action potential
- ‘all or none law’- an action potential occurs or doesn’t. If it occurs its the same size regardless of the level of excitation
- rate law’- the strength of a stimulus is represented by the firing rate of an axon
- absolute refractory period - following an action potential the sodium gates are close for approx. 1ms - no further action potentials, regardless of simulation can be triggered during this time
- relative refractory period- after sodium gates open potassium gates remain open for a further 2-4 ms and flow out of the cell at a faster than usual rate, making an action potential less likely, a greater stimulus would be needed
Speed of nerve impulses
- in an unmyelinated axon- each point along the axon generates the action potential- passes down the axon like a wave
- in a myelinated axon- the sodium potassium exchange can only occur at the nodes of Ranvier the action potential therefore jumps from one node to another. This jumping is called saltatory conduction
Synaptic transmission
Process of communication between neurons,chemical
Stage 1 - synthesis
-Neurotransmitters
-Synthesised from modules derived from the diet
- small neurotransmitters- synthesised in pre synaptic terminals
- neuropeptides- synthesised in cell body
Stage 2 and 3- storage and transport
- stored in spherical packets called synaptic vesicles
- travel down the axon to the terminal buttons
-Collect next to the pre synaptic membrane
Closer look
Presynaptic neuron
Vesicle
Neurotransmiters
Synaptic cleft
Receptors
Postsynaptic activity
Stage 4- release
- Action potential reaches terminal button
- voltage dependent calcium channels open
-Calcium (Ca2+) ions enter terminal button
-Vesicles fuse with pre synaptic membrane - neurotransmitters released into synaptic cleft
-Whole process is called exocytosis
Exocytosis
Look at photo
Stage 5- Attachment
-Diffuse across the pre synaptic cleft to the post synaptic membrane
- neurotransmitter binds to the receptors in the postsynaptic membrane
- receptors can only work with a specific neurotransmitter
‘Key in lock’
- any chemical that attaches to a receptor is called a ligand
Stage 6- Activation
- once binding occurs postsynaptic receptors open ion channels in the neurons membrane which allow particular ions to pass into the neuron
Ionotropic effects
-Rapid but short lived
-Open ion channels directly
Metabotropic effects
-Slower and long lasting
-Activates second messenger
Excitatory post synaptic potentials (EPSPs)
- receptors open sodium channels (Na +) channels
-Depolarisation- neuron becomes more positive
-Makes an action potential more likely to occur
Inhibitory post synaptic potentials (IPSPs)
-Receptors open either potassium (K+) channels or the Chloride channels (Cl-)
-Hyperpolarisation - neuron becomes less positive
-Makes an action potential less likely to occur
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Neural integration
Spatial summation- summation over space
-Inputs from separate locations can have combined effects
Temporal summation- summation over time
-Repeated stimulating in a brief period of time can have a cumulative effect
Stage 7- removal
Deactivation
-Special enzymes breakdown the neurotransmitter
-Eg- acetylcholine (chlorine and acetate)
-The parts are drawn back to pre synaptic membrane
-Recombined to form more
Reuptake
-Detach from receptors and drawn back to the pre synaptic membrane
-Recycled
Neurotransmitters
-Inhibitory or excitatory effects
-Dopamine- implicated in movement,attention and learning. Degradation of dopaminergic neurons responsible for Parkinson’s disease. Linked to schizophrenia
Serotonin- implicated in the regulation of mood,eating,pain,sleep dreaming and arousal. Implicated in depression and eating disorders
Drug effects
-Psychopharmacology- the influence of drugs on neurotransmitter action
-Agonists- facilitate neurotransmitter effects
Antagonists- inhibit neurotransmitter effects
Ahonistic drug effects
-Drug increases the syntheses of neurotransmitter molecules (eg increasing the amount of precursor)
-Drug increases the number of neurotransmitter molecules by destroying degrading enzymes
-Drug increases the release of neurotransmitter molecules from terminal buttons
-Drug binds to auto receptors and blocks their inhibitory effect on neurotransmitter release
- drug binds to postsynaptic receptors and either activates them or increases the effect on them of neurotransmitter
- drug blocks the deactivation of neurotransmitter molecules by blocking degradation or reuptake
Antagonistic drug effects
- drug blocks the synthesis of neurotransmitter molecules (eg by destroying synthesizing enzymes)
- drug causes the neurotransmitter molecules to leak from the vesicles and be destroyed by degrading enzymes
-Drug blocks the release of the neurotransmitter molecules from terminal buttons
- drug activates auto receptors and inhibits neurotransmitter release
- drug is a receptor blocker it binds to the postsynaptic receptors and blocks the effect of the neurotransmitter
What makes drugs addictive?
- avoidance of unpleasant symptoms of withdrawal
- relative strength of the pleasant physiological effects of the drug
- the same thing that makes other behaviours ‘rewarding’
Adapting behaviours
-Anticipating financial reward
Attractive mates (Ie sex)
Feeding
Drinking when thirsty
Orgasm and sexual activity
Flight from danger
Hoarding (for rats?)
They all activated the ‘reward circuitry’ in the brain. Ie the nucleus accumbens
Something about rat brains
Location of the human and rat reinforcement system
Medial forebrain bundle
Approx 60 bundles of neurons
Dopamine levels in the nucleus accumbens are increased by?
-Amphetamine
-Cocaine
-Nicotine
-Morphine
-Alcohol
-Cannabis
-3,4-methylenedioxymethamphetamine (MDMA)
Negative reinforcement
-Taking some drugs provides negative reinforcement (Ie they make the aversive ‘withdrawal symptoms stimuli cease). This must be a factor in maintinence of the habit but not in addiction
-Eg- the strength of withdrawal effects is not related to addictiveness
-Eg- some medical drugs that don’t hit the nucleus accumbens have withdrawal effects but are not addictive
Speed of action
-Operant conditioning theory suggests that the sooner the reward is experienced after the stimuli the stronger will be the reinforcement
-This is seen quite clearly in the addictiveness of drugs. Note that addictiveness is not directly related to the strength of the effect
-Alcohol- slow onset- low addictiveness
-Morphine
-Heroin- smoked and injected
- cocaine
-Crack cocaine
-Cigarettes- not nicotine patches, injections ect
