Nervous System Overview

Sensory nerves send information to the central nervous system about the internal and external environment.

Motor nerves primarily send information to sensory organs.

A synapse is the junction between one neurone and the next cell.

Neuromuscular junctions are a type of synapse between nerve and gland cells.

Motor response to sensory input depends on integration of information through reflex arcs.

Neurotransmitters are typically large, slow-acting molecules.

Electrical impulses are converted to chemical signals at synapses.

Interconnections between nerves are not necessary for motor response.

The central nervous system consists of the brain and spinal cord.

Efferent neurons transmit information towards the central nervous system.

Acetylcholinesterase has a role in neurotransmission at the neuromuscular junction.

Sensory nerves are also known as efferent nerves.

Nissl bodies are found in the presynaptic cell.

The primary role of motor neurons is to transmit sensory stimuli.

Dendrites receive input signals in a neuron.

Bi-polar neurons have multiple projections from the cell body.

The role of the axon is to propagate output signals in the form of action potentials.

Smooth muscle is primarily controlled by the somatic nervous system.

Binding of Ach opens Na+ channels in the synaptic cleft.

Graded potentials can travel long distances without dying out.

The resting membrane potential is typically around -70 mV.

Action potentials are triggered when graded potentials reach threshold voltage.

When sodium ions flood into the cell, it causes repolarization.

Graded potentials have a magnitude that varies with the triggering event.

Voltage-gated channels open when the membrane potential is around -70 mV.

Graded potentials can be integrated to generate an action potential.

Action potentials involve large changes in membrane potential of about ≅100mV.

Action potentials decrease in strength as they travel through the cell.

Voltage-gated Na+ channels allow Na+ to move out of the cell during an action potential.

The resting membrane potential is approximately -70mV.

After the opening of voltage-gated Na+ channels, the membrane potential becomes more negative.

Voltage-gated K+ channels open after Na+ channels to return the membrane potential towards resting level.

Action potentials involve only a small portion of the total excitable cell membrane at a time.

The process of action potential generation requires the influx of Ca2+ ions.

Acetylcholinesterase breaks down the neurotransmitter ACh at the neuromuscular junction.

Curare is known to enhance the binding of ACh to nicotinic receptors.

Botulinum toxin prevents muscles from responding to nerve impulses.

Myasthenia gravis is a condition where there is an excess of ACh at the neuromuscular junction.

Ingesting a small amount of botulinum toxin can be lethal to an adult.

Acidic food products are a primary source of botulinum toxin poisoning.

AChE inhibitors increase the duration of ACh action at the neuromuscular junction.

D-Tubocurarine is used to block neuromuscular junction activity.

Dopamine is an example of a neurotransmitter that depolarises the postsynaptic membrane.

The binding of acetylcholine to its receptors causes the efflux of Na+ ions from the postsynaptic cell.

Acetylcholine serves as a neurotransmitter at both excitatory and inhibitory synapses.

The end plate potential is created by hyperpolarization of the muscle fiber.

Acetylcholine (ACh) binds to receptors on the muscle fiber to initiate contraction.

When the postsynaptic membrane reaches a threshold due to depolarisation, an action potential is generated.

Voltage-gated Na+ channels are triggered to open by the resting membrane potential of -80 mV.

Neurons release more than one type of major neurotransmitter at a synapse.

The action potential in a muscle fiber travels down the axon towards the neuromuscular junction.

Acetylcholinesterase is responsible for stopping the action of ACh in the synaptic cleft.

Motor nerves primarily control the activity of the body by managing muscle and gland functions.

Sensory nerves do not send information to the central nervous system.

A synapse is the junction where an electrical impulse becomes a chemical signal for communication between cells.

Neuromuscular junctions are specialized connections between nerve cells and other nerve cells.

Neurotransmitters are typically large, slow-acting molecules.

Interconnections between nerves are essential for reflex actions.

Efferent neurons carry information away from the central nervous system.

The synaptic terminal is involved in converting chemical signals back into electrical impulses.

Curare is a drug that enhances the binding of ACh to nicotinic receptors.

Botulinum toxin can lead to muscle paralysis by blocking the release of ACh.

Myasthenia gravis is caused by an overproduction of ACh at the neuromuscular junction.

D-Tubocurarine is a neuromuscular blocking agent used to induce muscle relaxation.

Acetylcholinesterase inhibitors are used to shorten the effects of ACh on muscles.

Ingesting a large amount of botulinum toxin can be lethal to an adult.

The primary treatment for myasthenia gravis involves increasing the production of ACh.

Nicotinic cholinergic receptors are found exclusively at the neuromuscular junction.

The peripheral nervous system includes both sensory and motor nerves.

Neurons that transmit information away from the central nervous system are called afferent neurons.

The action potential is primarily propagated along the axon by the influx of potassium ions.

Acetylcholine (ACh) is released at the neuromuscular junction to stimulate muscle contraction.

Dendrites are responsible for sending signals away from the neuron.

Botulinum toxin causes muscles to contract more strongly.

Acetylcholinesterase (AChE) breaks down acetylcholine after its release at the neuromuscular junction.

Myasthenia gravis is caused by an excess of acetylcholine at the neuromuscular junction.

Nissl bodies are composed of rough endoplasmic reticulum and are found in the postsynaptic cell.

Graded potentials can travel short distances and can vary in magnitude.

Sensory nerves primarily activate gland functions by sending information to muscles.

Synapses facilitate communication between nerves and muscles by converting electrical impulses into chemical signals.

Neuromuscular junctions are specifically required for nerve-nerves communication.

The integration of information in the nervous system does not involve interconnections between neurons.

Acetylcholine is the only neurotransmitter involved in synaptic transmission at neuromuscular junctions.

Chemical signals transmitted at synapses are typically slow-acting molecules.

Efferent nerves are responsible for sending information towards the sensory organs.

Repolarization occurs when sodium ions leave the cell, restoring the membrane potential.

Graded potentials die out quickly over short distances within excitable cell membranes.

If graded potentials summate and reach a threshold voltage, it results in the opening of voltage-gated calcium channels.

A nerve impulse constitutes an action potential that moves down the axon.

During depolarization, potassium ions flood into the cell.

The magnitude of a graded potential is independent of the magnitude of the triggering event.

The resting membrane potential is typically less negative than -80 mV.

Action potentials involve only a small and localized change in membrane potential.

After the activation of voltage-gated Na+ channels, the influx of K+ ions initiates depolarization.

Action potentials involve a change in membrane potential of approximately ≅150mV.

During an action potential, Na+ channels open due to hyperpolarization.

Voltage-gated K+ channels close immediately after action potentials, leading to sustained depolarization.

The resting membrane potential is less negative than the threshold potential required for action potential initiation.

The influx of Na+ ions during an action potential is a key factor that contributes to depolarization.

Action potentials decrease in strength as they propagate along the axon.

After opening voltage-gated Na+ channels, Ca2+ influx is responsible for repolarization of the membrane potential.

The threshold potential is the membrane potential level at which voltage-gated sodium channels are triggered to open.

Ingestion of 0.001 mg of botulinum toxin can cause death in adults.

Myasthenia gravis leads to an excess of ACh at the neuromuscular junction.

Curare is a drug that enhances the binding of ACh to nicotinic receptors.

Neostigmine is used to prolong the effect of ACh at the neuromuscular junction.

Botulinum toxin prevents the release of neurotransmitters from synaptic vesicles.

D-Tubocurarine is effective in enhancing neuromuscular transmission.

The muscle contraction process is initiated by the decrease of ACh in the synaptic cleft.

Curare is derived from the skins of South American frogs.

Nicotinic receptors are ionotropic and mediate slow responses in muscle fibers.

The receptors for ACh at the neuromuscular junction are known as NM or N2 receptors.

ACh can be taken up by the muscle fiber when it is attached to its receptor.

Calcium ions (Ca2+) play a crucial role in muscle contraction following excitation-contraction coupling.

ACh is always cleared from the synaptic cleft by slowly diffusing away.

Voltage-gated sodium channels (VGSCs) open in response to depolarization at the postsynaptic membrane.

Nicotine inhibits the activation of nicotinic receptors at the neuromuscular junction.

Excitation-contraction coupling involves the binding of ACh at the presynaptic membrane.