3.2.2: Neurons, Neurotransmitters and Neuromodulators

Definition: Neural Synapse

The region that includes the axon terminals of the presynaptic neuron, the synaptic gap, and the dendrites of the postsynaptic neuron.

Definition: Presynaptic Neuron

The neuron that releases neurochemicals into the neural synapse

Axon Terminal (also known as terminal button)

The end of a neuron that releases neurochemicals into the neural synapse.

Definition: Synaptic Gap

The space between the presynaptic neuron and the postsynaptic neuron.

Postsynaptic Neuron

The neuron that receives neurochemicals from the neural synapse.

Dendrite

A branched extension of a neuron on which receptor sites are located.

Receptor Site

A protein molecule on the dendrites of a neuron that receives neurochemicals.

Neurochemical

A chemical substance that transmits neural information within the nervous system.

Synaptic Transmission

The chemical conveyance of neural information between two neurons across a neural synapse.

Action Potential

An electrical impulse that travels down the axon of a neuron.

Function of Neuron Components: Cell body & Dendrites

• Dendrites: Receive neurochemicals from the presynaptic neuron.

• Cell body: Contains the nucleus.

Function of Neuron Components: Axon, Myelin Sheath, & Axon Terminals

• Axon: Once the neuron fires, electrical impulses travel down this to reach the axon terminals.

• Myelin sheath: Protects/insulates the axon and speeds up the transmission of signals.

• Axon terminals: When electrical impulses reach these, they release neurochemicals into the synapse (which then activate postsynaptic neurons).

The Three Steps of Neural Transmission

• he presynaptic ("sending") cell sends an electrical signal down its axon called an action potential.

• Neurochemicals are released from the axon terminals into the synapse/synaptic gap.

• The postsynaptic ("receiving") cell receives the neurochemicals at specific receptors on the postsynaptic dendrite and acts accordingly.

The Lock & Key Model of Neurochemicals

• Each neurochemical has a specific receptor on the postsynaptic neuron.

• Neurotransmitter = key

• Receptor = lock

• The neurochemical can only bind to this specific receptor (active site), which "unlocks" a response.

Neurotransmitter

• A chemical molecule that has an effect on one or two postsynaptic neurons. They allow rapid communication across the synapse.

Definition & Mechanism: Excitatory Effect

• When the neurotransmitter increases the likelihood of the postsynaptic neuron firing an action potential (sending an electrical signal down its axon). They stimulate or activate postsynaptic neurons to enhance transmission along pathways. (Think: excitatory = excited = heightened).

Definition & Mechanism: Inhibitory Effect

• When the neurotransmitter decreases the likelihood of the postsynaptic neuron firing an action potential. They suppress or slow down postsynaptic neuron activity to regulate and prevent transmission along pathways. (Think: inhibitory = inhibit = stop/prevent).

Core Facts: Glutamate

• The main/primary excitatory neurotransmitter in the Central Nervous System (CNS).

• Activates or stimulates neural activity in the brain.

• Plays an important role in neural plasticity, learning, and the formation/storing of memories.

Example of Glutamate Pathway Activation

Reading text forms a memory about excitatory neurotransmitters, releasing glutamate in that neural pathway. Each time you retrieve, revise, do homework, or discuss the concept, this pathway will probably be strengthened.

Core Facts: GABA (gamma-aminobutyric acid)

• The main/primary inhibitory neurotransmitter in the Central Nervous System (CNS).

• Suppresses or slows down neural activity in the brain.

• Functions to stop your brain from firing completely out of control.

Consequences of Low GABA Levels / Unbalanced Glutamate

• Without sufficient GABA counterbalancing glutamate, neural activation gets out of control (hyperactivity in brain regions and increased sympathetic nervous system arousal), potentially leading to:

  • Mental disorders such as anxiety and specific phobias

  • Hyperactivity

  • Seizures

Useful Tip: The Misconception of Inhibitory Effects

• It is a common misconception that inhibitory effects are negative because they slow transmission. Both are critical for optimal functioning:

  • Without GABA: Neurons fire uncontrollably, causing anxiety and seizures.

  • Without Glutamate: Neurons are under-stimulated, causing learning/concentration difficulties and mental exhaustion.

Neuromodulator

• A chemical molecule that has an effect on multiple postsynaptic neurons. They are a subclass of neurotransmitters that alter the strength of neural transmission by increasing or decreasing the responsiveness of neurons to neurotransmitter signals. (Modulate = to keep in proper measure or proportion).

Neurotransmitters vs. Neuromodulators

• Neurotransmitters: Smaller molecules with rapid, direct effects on one or two postsynaptic neurons across a single synapse.

• Neuromodulators: Larger molecules with slower, longer-lasting, and more widespread effects across entire regions of the brain. They are released outside the synapse directly into brain tissue.

How do Neuromodulators alter the way neurons work?

• Change the cell itself: Causing neurons to grow more dendrites or release MORE neurotransmitters.

• Alter responsiveness (Sensitivity): Enhancing the existing inhibitory or excitatory effects of neurotransmitters.

Core Functions: Dopamine

• Responsible for voluntary motor movement, the experience of pleasure/well-being, and reward-based learning.

• Involved in CNS functions: pleasure, movement, attention, mood, cognition, and motivation.

• Reinforces neural activity by targeting structures in the reward pathway.

Dopamine Origins & Postsynaptic Effects

• Origins: Brain pathways originating from midbrain regions: the substantia nigra and the ventral tegmental area.

• Effects: Can have both excitatory and inhibitory effects depending on the type of receptor sites present at that specific brain location.

Substantia Nigra vs. Ventral Tegmental Area (Dopamine Roles)

• Substantia Nigra: Transmits neural information that enables smooth, coordinated voluntary muscle movement.

• Ventral Tegmental Area: Releases dopamine associated with pleasure during a rewarded behavior, powering motivation and reward-based learning.

Dopamine Textbook Roles: Thirst, Hunger, and Addiction

• Thirst (pp. 128-129): Released by the act of swallowing water, motivating us to drink when dehydrated (no dopamine release via IV drip hydration).

• Hunger (p. 130): Food consumption releases dopamine to reinforce eating. Dopamine makes us want to eat; mice without dopamine starved to death surrounded by food.

• Addiction (pp. 131-132): Addictive stimuli (gambling, drug use, smartphone use) cause intense dopamine release, motivating repetition regardless of difficulty or harm.

Core Functions: Serotonin

• Primarily responsible for the regulation and stabilization of mood and sleep.

• An inhibitory neurotransmitter acting as a neuromodulator that influences virtually all behavioral processes (mood, perception, reward, anger, aggression, appetite, memory, sexuality, attention).

Serotonin Pathways & Location

• Location: Over 90% is found in the gut (regulating bowel function and reducing appetite).

• Brain Pathway Origin: Originates from the raphe nuclei, which are masses of neurons located in the brainstem.

Serotonin Textbook Roles: Mood, Sleep, and Aggression

• Mood (p. 133): Balanced levels lead to calm, focused, happy, stable moods. Low levels cause depression/anxiety.

• Sleep (p. 134): Regulates the sleep-wake cycle (24-hour period) and dictates sleep quality, night quantity, and daytime alertness. Low levels disrupt circadian rhythms.

• Aggression (pp. 134-135): Regulates impulsive and aggressive behaviors. Adequate serotonin = less aggression.

Clinical Relevance: Depression & SSRIs (pp. 120-121)

• Depression is linked to low levels of serotonin and impairments in its pathway system.

• SSRIs (Selective Serotonin Reuptake Inhibitors): Common medications that treat depression by preventing the reuptake (reabsorption) of serotonin back into the presynaptic nerve ending.

• Note: SSRIs do not make more serotonin; they leave higher levels in the synapse to continue activating postsynaptic receptors.