Matering Biology notes about neural systems: chemical synapses, membrane potentials, action potentials, neuron structure, muscle weaknesses, steps for muscle contraction, electrocardiograph, causes of hypokalemia, functions of brain structures, parasympathetic and sympathetic, etc.
Signal transmission at a chemical synapse:
- When an action potential reaches the end of an axon, vesicles fuse with the plasma
membrane and release neurotransmitter into the synaptic cleft.
- Synaptic cleft is the space between an axon of one neuron and the dendrite of
another neuron.
- Vesicles within synaptic terminals contain neurotransmitters that may be released
into the synaptic cleft.
Membrane potentials
- Membrane potential is the difference in electrical charge across a membrane.
- Resting neurons are most permeable to K+ ions.
- Membrane potential comes both from the difference in electrical charge and from
the concentration gradient of ions across a membrane.
- Potassium leak channel is mainly responsible for the resting potential of a neuron. K+
ions flow along their concentration gradient to maintain the resting potential of a
neuron.
- An action potential is a rapid electrical signal generated by neurons.
- The sodium-potassium pump moving Na+ ions out and K+ ions in => maintains the
concentration gradients of ions
- If the voltage across a neuronal membrane is set to -20 mV, Na+ ions flow into the
cell (depolarization).
Action potentials:
- Myelin sheath is not part of neuron. Layer of Schwann cells wrapped around a
neuron.
- Action potentials are: They are identical in duration, identical in magnitude, occur
after the threshold potential is reached, propagated down the length of the axon.
- Unidirectional because sodium channels in the neuron are refractory (in inactive
state).
- Action potential created when membrane depolarizes above a certain threshold
potential due to influx of Na+ ions.
- Inhibitory signals hyperpolarize the membrane and make the membrane potential
even more negative than normal.
- Axon hillock is the region where voltage-gated channels begin in a neuron, near the
cell body => where the action potential begins
- How is action potential propagated down axon? The entry of sodium ions into the
neuron and their diffusion to adjacent areas of the membrane causes those portions
of the membrane to become depolarized and results in the opening of voltage-gated
sodium channels farther down the axon, which release potassium ions to the
outside, returning the charge to its previous state.
Nerve signals: action potentials
- Resting potential = -70mV. The charge difference found across the plasma membrane
of a “resting” neuron.
, - Action potential moves along axon. Only axon is capable of generating action
potential.
- At rest, the sodium-potassium pump moves more sodium ions out of the cell than
potassium ions into the cell; this net loss of positive ions establishes a charge
difference across the plasma membrane.
- Depolarization: influx of Na+ ions into neuron. Opening of voltage-gated sodium
channels and the diffusion of sodium ions into the neuron.
- A stimulus has opened the voltage-gated sodium channels in an area of a neuron's
plasma membrane. As a result, SODIUM rushes into the neuron and diffuses to
adjacent areas; this in turn results in the VOLTAGE GATED SODIUM CHANNELS in the
adjacent areas.
Neuron structure:
- Nucleus is located in cell body.
- Dendrites conduct an impulse from a synapse toward the cell body.
- Axons conduct a nerve impulse away from the cell body.
- In myelinated neurons the impulse jumps from node of Ranvier to node of Ranvier.
- Myelin sheaths allow neurons to conduct impulses more rapidly.
- Myelin sheaths are formed when Schwann cells wrap around the axons of motor
neurons.
- Synaptic terminals contain neurotransmitter molecules that relay the nerve impulse
across a synapse.
The three opiates blocked naloxone binding, whereas the three non-opiates did not block
naloxone binding. These results indicate that the receptors for naloxone in the brain are
specific for opiates.
Muscle weakness
Myasthenia gravis: affects postsynaptic nerve. Antibodies that bind to Acetylcholine
receptors => no binding to receptors. No depolarization. No muscle contraction.
Botulism: affects presynaptic nerve. Bacterial toxin prevents Acetylcholine from being
released. No vesicle transport. Paralysis.
Hyper and Hypokalemia: K+ important for maintaining membrane potential.
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