Chapter 4: Neuron Function

antischizophrenic drugs

- amphetamines and cocaine produce a temporary disorder that resembles schizophrenia schizophrenia as excessive activity at dopamine synapses -> thus dopamine antagonists seem to be an effective treatment

Factors contributing to even distribution of Ions

- random motion (particles tend to move towards their lower concentration gradient - electrostatic pressure (like repels like, opposite attract)

Relative Refractory Period

A period following the absolute refractory period after firing when a neuron is returning to its normal polarized state and will fire again only if the incoming message is much stronger than usual

Action Potentials vs. EPSPs and IPSPs

Action potentials are nondecremental, meaning they do not lose strength over distance Action potentials are conducted more slowly because they are more active that the EPSPs and IPSPs are passive

Integration

Adding or combining IPSP and EPSP signals

The Hodgkin-Huxley Model

Based on the study of squid motor neurons Cerebral neurons are far more complex than motor neurons

Gap Junctions (Electrical Synapses)

Narrow spaces between adjacent neurons that are bridged by fine tubular channels called connexins that contain cytoplasm

Antidromic Conduction/ Orthodromic Conduction

Orthodromic conduction is axonal conduction in the natural direction from cell body to terminal buttons, while antidromic conduction is in the backwards direction from the axon back toward the cell body

Axon Hillock

The conical structure at the junction between the cell body and the axon It was believed that action potentials were generated there, but they are actually generated in the adjacent section of the axon

Steps in the Synthesis of Catecholamines from Tyrosine

Tyrosine L-Dopa Dopamine Norepinephrine Epinephrine

Factors contributing to uneven distribution of Ions

- selective permeability to certain ions - sodium potassium pump

Antagonist drug effect

1. Drug blocks the synthesis of neurotransmitter molecules (e.g. by destroying synthesizing enzymes) 2. Drug causes the neurotransmitter molecules to leak from the vesicles (are then destroyed by degrading enzymes) 3. Drug blocks the release of neurotransmitter molecules from the terminal buttons 4. Drug activates autoreceptors and inhibits neurotransmitter release 5. Drug is a receptor blocker, binds to postsynaptic receptors and blocks effect of neurotransmitter

Agonist drug effect

1. Drug increases the synthesis of neurotransmitter molecules 2. Drug increases the number of neurotransmitters by destroying degrading enzymes 3. Drug increases the release of neurotransmitter molecules from terminal buttons 4. Drug binds to postsynaptic receptors and either activates them or increases the effect on them 5. Drug blocks the deactivation of neurotransmitter molecules by blocking degradation or reuptake

Metabotropic receptor

1. neurotransitter binds to signal protein 2. a subunit of g protein breaks away and leads to a) subunit moves along the inside surface, binds to a nearby ion -> inducing IPSP/EPSP b) triggers the synthesis of a chemical called secondary messenger -> diffuse through cytoplasm and influence neurons (e.g. entering a nucleus and bind do DNA, thereby influencing genetic expression) More prevalent that ionotropic receptors and their effects are slower to develop, longer lasting, more diffuse, and more varied

Absolute Refractory Period

A period of time (1-2 milliseconds) following an action potential during which no additional action potential can be evoked regardless of the level of stimulation

Receptors

A protein that contains binding sites for only particular neurotransmitters Neurotransmitters produce signals in postsynaptic neurons by binding to receptors in the postsynaptic membrane Ligand- A molecule that binds specifically to a receptor site of another molecule

Resting Membrane Potential

An electrical potential established across the plasma membrane of all cells by the Na+/K+ ATPase and the K+ leak channels In most cells, the resting membrane potential is approximately -70 mV with respect to the outside of the cell

Axodendritic Synapses/Axosomatic Synapses

Axodendritic Synapses: Synapses of axon terminal buttons on dendrites Many terminate on dendritic spines (nodules of various shapes that are located on the surfaces of many dendrites Axosomatic Synapses: Synapses of axon terminal buttons on somas (cell bodies)

Neurotransmitters

Diffuse across the synaptic clefts and interact with specialized receptor molecules on the receptive membranes of the next neurons in the circuit. When neurotransmitter molecules bind to postsynaptic receptors they have one of two effects: They depolarize the receptive membrane (decrease resting potential), or hyper polarize it (increase the resting membrane potential)

Directed Synapses/ Nondirected Synapses

Directed Synapses: Synapses at which the site of neurotransmitter release and the site of neurotransmitter reception are in close proximity (common) Nondirected Synapses: Synapses at which the site of release is at some distance from the site of reception Molecules rereleased from a series of varicosities (bulges or swellings) along the axon and are dispersed to surrounding targets Referred to as "string-of-beads synapses" because of appearance

EPSPs and IPSPs

Excitatory postsynaptic potentials: postsynaptic depolarizations increase the likelihood that the neuron will fire Inhibitory postsynaptic potentials: postsynaptic hyperpolarizations increase the likelihood that the neuron will fire Both are 'graded responses' which means the amplitudes are proportional to the intensity of the signals that elicit them. Weak signals elicit small postsynaptic potentials and strong signals elicit large ones

Velocity of Axonal Conduct

Faster in large-diameter axons and myelinated Fastest: (mammalian motor neurons) 100m/s Slowest: 1 m/s Max for human motor neurons: 60 m/s

Threshold of Excitation

If the sum of the depolarization and hyperpolarization is sufficient to depolarize the membrane to the Threshold (Usually about -65mV( an action potential is generated near the axon hillock

Refractory Periods

Important because it is responsible for the fact that action potentials normally only travel along axons in one directions (they can't reverse directions) Also responsible for the fact that the rate of neural firing is related to the intensity of the stimulation

Voltage - Activated Ion Channels

Ion channels that open or close in response to changes in the level of the membrane potential After about 1 millisecond, the sodium channels close and marks the end of the rising phase of the action potential and the beginning of repolarization by the efflux of K+ ions

Neuropeptides

Large neurotransmitters, relatively short chains of amino acids Assembled in the cytoplasm of the cell body on ribosome's, packaged in vesicles by the cell body's Golgi complex and transported by microtubules to the terminal buttons

Coexistence

Many neurons contain two neurotransmitters: A neuropeptide in the larger vesicles and a small-molecule neurotransmitter in the smaller vesicles

Conduction in Neurons without Axons

Many neurons don't have axons or have very short ones, and do not normally display action potentials "Interneurons" are typically passive and decremental

Action Potential

Massive but momentary (1 millisecond) reversal of the membrane potential (-70 to +50) All-or-none responses: They either occur to their full extent or not at all

Autoreceptors

Metabotropic receptors with two unconventional characteristics: Bind to their neurons own neurotransmitter molecules, and located on the presynaptic membrane Function is to monitor the number of neurotransmitter molecules in the synapse and release more when levels are low, and reduce release when they are high

Myelinated Axons

Myelin is fatty tissue that insulates neurons from extracellular fluid Nodes of Ranvier- gaps between adjacent myelin segments that allow ions to pass through the axonal membrane Myelination increase the speed of axonal conduct Saltatory conduct is the transmission of action potentials in myelinated axons

Equilibrium Potential

Na+ = 120 mV K+ = 90 mV Cl- = -70 mV (same as resting potential)

Ions in Resting Potential

Na+ and Cl- are greater outside a resting neuron K+ more concentrated on the inside Negatively charged protein ions are synthesized inside the neuron and stay there

Location of a Synapse

On a neuron's receptive membrane has long been assumed to be an important factor in determining its potential to influence the neuron's firing

Properties-> Unequal Distribution of Ions

One of these properties is passive (does not consume energy): The different permeability to those ions. Specialized pores called ion channels let ions pass through. The active property is the sodium potassium pump that exchange three Na+ ions from the inside for two K+ ions outside. Other classes of transporters have been discovered as well.

Temporal Summation

Postsynaptic potentials produced in rapid succession at the same synapse sum to form a greater signal Postsynaptic potentials that stimulations of a neuron produce outlast the stimulation 1. Two EPSPs elicited in rapid succession sum to produce a larger EPSP 2. Two IPSPs elicited in rapid succession sum to produce a larger IPSP

Ionotropic Receptors/ Metabotropic Receptors

Receptors that are coupled to ion channels and affect the neuron by causing those channels to open - associated with ligand-activated ion channels

Spatial Summation

Simultaneous postsynaptic potentials 1. Two simultaneous EPSPs sum to produce a greater EPSP 2. Two simultaneous IPSPs sum to produce a greater IPSP 3. A simultaneous EPSP and IPSP cancel each other out

Amino Acid Neurotransmitters

Small-molecule neurotransmitter Four most widely studied: Glutamate (most prevalent excitatory), aspartate, glycine, and Gamma-aminobutyric acid (GABA)- simple modification of glutamate, most prevalent inhibitory neurotransmitter

Monoamine Neurotransmitters

Small-molecule neurotransmitter There are four: Dopamine, Epinephrine, norepinephrine, and serotonin Subdivided into two groups: Catecholamines (each synthesized from the amino acid tyrosine) Indolamines: Only serotonin, synthesized from tryptophan

Acetylcholine

Small-molecule neurotransmitter at neuromuscular junctions at many of the synapses in the autonomic nervous system and some of CNS Neurons that release acetylcholine are said to be "cholinergic"

Small Neurotransmitters

Synthesized in the cytoplasm of the terminal button and packaged in the synaptic vesicle by the Golgi complex Vesicles stored in clusters next to the presynaptic membrane

Reuptake and Enzymatic Degradation

Terminate synaptic messages and keep neurotransmitter molecules from clogging the synapse Reuptake (more common): Once released, neurotransmitters almost immediately drawn back into presynaptic buttons by transporter mechanisms Enzymatic Degradation: Enzymes break down neurotransmitters in the synapse Ex. Acetylcholinestrerase breaks down neurotransmitter acetylcholine

Membrane Potential

The difference in electrical charge between the inside and the outside of a cell

Receptor Subtypes

The different types of receptors to which a particular neurotransmitter can bind Enable one neurotransmitter to transmit different kinds of messages to different parts of the brain

Exocytosis

The process of neurotransmitter release Small-molecule neurotransmitters congregate around sections of the membrane rich in voltage-activated calcium channels When stimulated by action potentials, these channels open and Ca2+ ions enter the button This entry causes synaptic vesicles to fuse with the presynaptic membrane and empty their contents into the synaptic cleft

Ions

The salts in neural tissue separate into positively and negatively charged particles called ions

Microelectrodes

The tiny intracellular electrodes used to measure electrical activity of individual neurons, or record the membrane potential

Homogenizing Factors

Two factors that act to distribute ions equally throughout the intracellular and extracellular fluids of the nervous system: One is random motion, because particles in random motion tend to move down their concentration gradients (of high to low concentration) Second is electrostatic pressure, the opposite charges attract But still, two properties of the neural membrane counteract

Muscarinic antagonist

antagonist on muscarinic receptors -> blocking acetylcholine -> in ANS leads to pupil dilation -> in CNS to disruptive effects on memory

Nicotinic antagonist

antagonist on nictotinic receptors Curare - atropine blocks cholinergic synapses, thereby blocking transmission at neuromuscular junctions Botox - blocks the release of acetylcholine on neuromuscular junctions -> Lähmung

antagonists

decrease / inhibit activity

Astrocytes

glia cells that appear to communicate and modulate neuronal activity through gap junctions between cells

Agonists

increase / faciliate activity