BPP - midterms

Resting potential

The neuron is polarized, maintaining a

charge of about –70 mV inside

relative to the outside.

Resting potential

This is due to the sodium-potassium

pump, which actively moves Na⁺ out

and K⁺ in.

Resting potential

The neuron is stable but ready to

respond to a stimulus.

Resting potential

Think of this as the ready state, the

neuron is primed but inactive

Threshold reached

When a stimulus depolarizes the

membrane enough to reach the

threshold (~–55 mV), voltage-gated

Na⁺ channels open.

Threshold reached

This marks the point where the neuron

commits to firing an impulse.

Threshold reached

This is the trigger, once the threshold is

reached, the process becomes

unstoppable

Action potential

A rapid influx of Na⁺ ions causes a

sharp spike in voltage.

Action potential

The inside of the neuron becomes

positively charged for a brief moment.

Action potential

This is the nerve impulse, the electrical

signal that travels along the axon.

Action potential

This is the firing stage, the neuron

sends its message

Refractory period

After the spike, Na⁺ channels close and

K⁺ channels open, allowing K⁺ to exit.

Refractory period

The neuron repolarizes and briefly

becomes hyperpolarized.

Refractory period

During the absolute refractory period,

no new impulse can occur; during the

relative refractory period, a stronger

stimulus is needed.

Refractory period

This is the reset, the neuron recovers and

prevents overlap of signals

Propagation

The action potential moves along the

axon, regenerating at each segment.

Propagation

In myelinated axons, the impulse jumps

between nodes of Ranvier in a process

called saltatory conduction.

saltatory conduction

This makes transmission faster and

more efficient.

Propagation

This is the transmission, the signal travels

to the next neuron or target

Neurotransmitters

are the

chemical messengers of the

nervous system

Neurotransmitters

Released at synapses to

influence other neurons,

muscles, or glands

Behavior shaped by balance of

excitatory & inhibitory signals

Acetylcholine (ACh):

muscle movement,

memory, learning

Dopamine (DA):

reward, motivation, motor

control

Serotonin (5-HT)

mood, sleep, appetite

Norepinephrine (NE)

arousal, alertness,

stress response

GABA

main inhibitory transmitter, calming

effect

Glutamate

main excitatory transmitter,

learning & plasticity

Acetylcholine (ACh), Dopamine (DA), Serotonin (5-HT), Norepinephrine (NE), GABA, Glutamate

Major neurotransmitters

Presynaptic neuron

Neurotransmitter synthesis, Storage in vesicles, Action potential arrival

Neurotransmitter synthesis

Chemical

messengers are produced in the neuron’s cell

body or terminal

Storage in vesicles

These neurotransmitters are

packaged into synaptic vesicles, ready for

release

Action potential arrival

When an electrical

impulse reaches the presynaptic terminal,

voltage-gated calcium channels open. The

influx of calcium triggers vesicles to fuse with the

presynaptic membrane, releasing

neurotransmitters into the synaptic cleft.

Synaptic Cleft

Diffusion across the gap, Binding to receptors, Excitatory vs. inhibitory signals

Diffusion across the gap

Neurotransmitters

move across the tiny space separating

neurons.

Binding to receptors

They attach to specific

receptor sites on the postsynaptic

membrane

Excitatory:

Increase likelihood of

postsynaptic firing (glutamate)

Inhibitory

Decrease likelihood of firing

(GABA)

Postsynaptic Neuron

Receptor activation, Signal continuation, Integration of inputs

Receptor activation

Binding changes ion

flow in the postsynaptic cell, altering its

electrical state.

Signal continuation

If threshold is

reached, a new action potential is

generated, propagating the signal

downstream

Integration of inputs

The postsynaptic

neuron sums excitatory and inhibitory

inputs, deciding whether to fire.

Termination of Signal

Reuptake transporters, Enzymatic breakdown, Diffusion

Reuptake transporters

Specialized proteins

pull neurotransmitters back into the

presynaptic neuron for reuse.

, Enzymatic breakdown,

Enzymes degrade

neurotransmitters into inactive components.

Diffusion

Excess neurotransmitters drift away

from the synaptic cleft.

Drug Actions

Agonists, Antagonists, Reuptake Inhibitors, Enzyme Inhibitors

Agonists

Mimic neurotransmitters, stimulating

receptors (morphine acting on opioid

receptors)

Antagonists

Block receptors, preventing

activation (antipsychotics blocking

dopamine receptors)

Reuptake inhibitors

Prolong neurotransmitter

action by blocking reuptake to linger longer

in the sypnaptic cleft (SSRIs for serotonin).

Enzyme inhibitors

Prevent breakdown,

increasing neurotransmitter availability (MAO

inhibitors).

DANGS SAMAD PDM

acronym for neurotransmitter and disorder

Agonist

Mimics neurotransmitter . example Nicotine → ACh (Stimulates alertness)

Antagonist

Blocks receptor , example Antipsychotics → DA (Reduces psychotic

symptoms)

Reuptake Inhibitor

Prolongs neurotransmitter action, example SSRIs → 5-HT (Improves mood)

Enzyme Inhibitor

Prevents breakdown, example MAOIs → monoamines (Elevates mood)

Release Enhancer/Blocker

Alters release, example Amphetamines ↑ DA (Boosts energy or sedation)

DA

Dopamine short term

5-HT

Serotonin short term

MAOI

Monoamine Oxidase Inhibitor short term

Dopamine

Reward, motivation,

motor control

Dopamine

Target in

antipsychotics,

Parkinson’s treatment,

addiction

Serotonin

Mood, sleep, appetite

Serotonin

Target in

antidepressants (SSRIs)

Monoamine Oxidase Inhibitor

Prevents breakdown of monoamines (DA, 5-HT, NE)

Monoamine Oxidase Inhibitor

Antidepressant, boosts neurotransmitter levels

Brain injury

is the destruction or degeneration of

brain cells.

Tumors

Strokes

Closed-head injuries

Infections

Neurotoxins

Genetic Factors

Apoptosis

Brain injury

also known as brain damage or

neurotrauma,

Tumors

are abnormal growths disrupting

neural tissue

Benign (Non-cancerous)

These growths

do not invade nearby tissues or spread to

other parts of the body, though they can

still cause issues if they press on organs.

Malignant (Cancerous)

These growths

can invade surrounding tissues and

spread to distant areas of the body

through the blood or lymph systems, a

process called metastasis

Strokes

are also known as cerebrovascular disorders

Ischemic stroke

A blood clot blocks an artery that leads to the brain.

Hemorrhagic stroke

A blood vessel in the brain leaks or bursts open.

Transient ischemic attack (TIA)

A mini-stroke or brief blockage that does not cause lasting damage, but acts as a

warning sign

Face drooping, Arm weakness, Speech difficulty, Time to call for help

Key Symptoms (FAST)

High blood pressure: (The single

biggest modifiable risk factor.)

Smoking and tobacco use.

Diabetes and high cholesterol.

Obesity and physical inactivity

Major risk factors of stroke include

closed head injury

is a type of traumatic

brain injury where the brain sustains damage

from an external force, but the skull and dura

mater remain unbroken.

closed head injury

Falls, Motor vehicle accidents, Sports injuries, Physical violence, Concussion, Cerebral contusion, Diffuse axonal injury, Intracranial hematoma:

Falls

Slipping or tripping.

Motor vehicle accidents

Sudden stops or impacts causing violent head movement.

Sports injuries

High-impact collisions in

contact sports.

Physical violence

Direct blows to the head

Concussion

A temporary disruption of normal

brain function caused by a jolt or blow

Cerebral contusion

A bruise on the brain

tissue itself, often accompanied by local

swelling.

Diffuse axonal injury

Widespread tearing of

axons caused by rapid shaking or rotational

forces

Intracranial hematoma

Bleeding inside the

skull, such as a subdural or epidural

hematoma, which increases pressure on the

brain