• Synthesized in neuron
• Present in pre-synaptic terminal and causes action on post-synaptic
• Exogenous activity mimics endogenous activity if released.
• Mechanism exists to remove it from active site(e.g synaptic cleft)

• Cause most of acute responses of nervous system.
• Example- transmission of sensory signals to brain and motor signals back to the muscles.
• "Classical"

• Neuropeptides
• Cause more prolonged activity
• Example- long term changes in numbers of receptors, long term opening or closure of certain ion channels.

Inhibitory effect(vagus nerve)

• Parasympathetic NS: pre/postganglionic
• Sympathetic NS: preganglionic

Acetylcholinesterase (AChE)

Located on the pre and post synaptic membranes.

Adrenaline

• CNS: plays role in regulation of Blood Pressure
• Peripheral NS: (sympathetic) main excitatory transmitter released during "fight or flight" reactions.
• Comes from Tyrosine

Noradrenaline

• CNS: alertness and wakefulness
• Sympathetic NS: postganglionic neurons with excitotory influence
• Released by internal organs(gut, spleen, heart)

Bipolar and Schizoprenia

Regulation of mood

Responsible for symptoms of depression

Epi

Norepi

Dop

• certain regions of the midbrain
• Parkinson's Disease

stops MAO from working.

Increases neurotransmitters

Stop Epi, Norepi, and Dop from getting reabsorbed.

More neurotransmitters available.

Blocks packaging of Epi, Norepi, and Dop.

Depletes levels

Tranquilizer

Drug that is used to increase dopamine levels to treat Parkinson's Disease.

Can penetrate membrane and bypass Tyrosine precursor. Gets carboxylated into Dopamine.

Pre-Synaptic membrane.

Decreases outflow of neurotransmitters.

Sympathetic NS

Postsynaptic neuron.

Will break down Epi, Norepi, Dop

• Brain
• Mostly inhibitory effects on postsynapses
• Involved in control of eating, sleeping, and arousal.

What is the result of a Serotonin (5-HT) dysfunction?

• implicated in Bipolar dissorder, depression.

It blocks (Na cotransport) reabsorption of Serotonin(5-HT) back into the presynapse

Leads to increased levels being near postsynapse.

Leads to more inhibition of postsynapse usually

• Priciple excitatory transmitter in the brain.
• Plays a role in learning and memory.

• Brain and Spinal cord
• IPSP necessary for stabilizing electrical activity.
• Plays a role in learning and memory

• Activation increases Cl^- influx
• Produces ISPS at postsynapses

• Anticonvulsants (anti seizure)
• Sedatives
• Attaches to GABA at GABA_A and increases the influx of Cl^-. Acting as an IPSP

• Activation increases conductance of K (outward flux)
• produces IPSP
• G protein helps

• Spinal cord and Brain stem
• Inhibitory
• If blocked u will have locked jaw

• smaller # but very potent.
• Prolonged actions
• most are neuromodulators
• Synthesized by neural cell body. Then transferred to the axon
• No uptake system. Once they are released, they are out until they are used.

associated with neuromuscular junction.

area that presynapse and postsynapse meet.

Choline

the transmitter (Acetate) is left out

Caused by 1 quanta randomly hitting the receptor.

(remember NM transmitters dont have a reuptake mechanism so they hang around)

2 ACh bind to α subunits.

Non-specific cation channel.

Net Na influx

• Nueralmuscular Disease
• Junction fold are smaller, can hold less ACh
• Few receptors, and they dont work well
• Eyes taunt, droopy eye lids.

• Immediate paralysis
• Na channels(not TTX sensitive) appear
• ACh receptors appear out NM junction
• Hypersensitive to ACh-spontaneous twitching
• Muscle atrophy. Gets replaced with fat and CT

BLOCKS

Raises the threshold of the nerve action potential.

BLOCK

• blocks nerve and muscle action potential

BLOCK

Stops vesicle (Quanta) exocytosis

STIMULATES

stimulates vesicle exocitosis

BLOCKS

Less Ca to enter.

BLOCK

goes through Ca channels and no transmitters are released.

• Curare
• Succinycholine

• Curare
• α-bungarotoxin

• Methacholine
• Nicotine

mimics action of ACL

• Physostigmine and other anticolinergics.

Used by asmatics

Hemicholinium