Pharmacology of Neurotransmitters: Biological Psychology Lecture Notes | Study notes Cognitive Psychology

LESSON: PHARMACOLOGY OF

NEUROTRANSMITTERS

Biological Psychology| PSYCHOLOGY

4.0 Pharmacology of

Neurotransmitters

What are Neurotransmitters?

Neurotransmitters (NTs)

○Are chemical messengers that

neurons use to communicate across

synapses. Their pharmacology

studies how drugs affect their

synthesis, release, receptor binding,

and inactivation.

Key Steps in Neurotransmitter

Pharmacology

1. Synthesis

oNTs are made inside neurons from

precursors (e.g., dopamine from

tyrosine, serotonin from tryptophan).

oDrugs can enhance or block

synthesis.

oExample: L-DOPA is given in

Parkinson’s disease to increase

dopamine synthesis.

2. Storage

oNTs are packed into synaptic vesicles.

oSome drugs block this step.

oExample: Reserpine prevents storage of

monoamines (dopamine,

norepinephrine, serotonin).

3. Release

oAction potential triggers vesicle fusion -

NTs released into synaptic cleft.

oDrugs can enhance or inhibit release.

oExample: Amphetamines increase

dopamine and norepinephrine release.

oExample: Botulinum toxin blocks

acetylcholine release.

4. Receptor Binding

oNTs bind to postsynaptic receptors

oDrugs can mimic (agonists) or block

(antagonists) this action.

oExample: Nicotine = acetylcholine

receptor agonist.

oExample: Haloperidol = dopamine

receptor antagonist (antipsychotic).

5. Inactivation

oNTs are cleared by reuptake or

enzymatic breakdown.

oDrugs can prolong NT action by

blocking these.

oExample: SSRIs (fluoxetine) block

serotonin reuptake.

4.1 The Roles and Functions of

Neurotransmitters

1) Amino Acid Neurotransmitters

oThe four most widely studied amino

acid neurotransmitters are glutamate,

aspartate, glycine, and gamma-

aminobutyric acid (GABA).

oAmino acid transmitters provide the

majority of excitatory and

inhibitory neurotransmission in the

nervous system.

Glutamate - prevalent excitatory

neurotransmitter

GABA - prevalent inhibitory

neurotransmitter

2) Monoamine Neurotransmitters

oMonoamines are another class of

small-molecule neurotransmitters.

oMonoamine neurotransmitters are

slightly larger than amino acid

neurotransmitters, and their effects

tend to be more diffuse.

Types of monoamines:

a. Dopamine, norepinephrine, and

epinephrine (Catecholamines-

synthesized from amino acid

tyrosine which is converted to L-

dopa (converted to dopamine)

b. Serotonin (Indolamine)

3) Acetylcholine Neurotransmitters

oAcetylcholine is the neurotransmitter

at neuromuscular junctions, at

many of the synapses in the

autonomic nervous system, and at

synapses in several parts of the

central nervous system.

BIOLOGICAL PSYCHOLOGY NOTES LECTURE 1

Partial preview of the text

Download Pharmacology of Neurotransmitters: Biological Psychology Lecture Notes and more Study notes Cognitive Psychology in PDF only on Docsity!

NEUROTRANSMITTERS

Biological Psychology| PSYCHOLOGY 4.0 Pharmacology of Neurotransmitters What are Neurotransmitters?  Neurotransmitters (NTs) ○ Are chemical messengers that neurons use to communicate across synapses. Their pharmacology studies how drugs affect their synthesis, release, receptor binding, and inactivation. Key Steps in Neurotransmitter Pharmacology

1. Synthesis o NTs are made inside neurons from precursors (e.g., dopamine from tyrosine, serotonin from tryptophan). o Drugs can enhance or block synthesis. o Example: L-DOPA is given in Parkinson’s disease to increase dopamine synthesis. 2. Storage o NTs are packed into synaptic vesicles. o Some drugs block this step. o Example: Reserpine prevents storage of monoamines (dopamine, norepinephrine, serotonin). 3. Release o Action potential triggers vesicle fusion - NTs released into synaptic cleft. o Drugs can enhance or inhibit release. o Example: Amphetamines increase dopamine and norepinephrine release. o Example: Botulinum toxin blocks acetylcholine release. 4. Receptor Binding o NTs bind to postsynaptic receptors o Drugs can mimic (agonists) or block (antagonists) this action. o Example: Nicotine = acetylcholine receptor agonist. o Example: Haloperidol = dopamine receptor antagonist (antipsychotic). 5. Inactivation o NTs are cleared by reuptake or enzymatic breakdown. o Drugs can prolong NT action by blocking these. o Example: SSRIs (fluoxetine) block serotonin reuptake. **4.1 The Roles and Functions of Neurotransmitters

Amino Acid Neurotransmitters** o The four most widely studied amino acid neurotransmitters are glutamate, aspartate, glycine, and gamma- aminobutyric acid (GABA). o Amino acid transmitters provide the majority of excitatory and inhibitory neurotransmission in the nervous system.  Glutamate - prevalent excitatory neurotransmitter  GABA - prevalent inhibitory neurotransmitter 2) Monoamine Neurotransmitters o Monoamines are another class of small-molecule neurotransmitters. o Monoamine neurotransmitters are slightly larger than amino acid neurotransmitters , and their effects tend to be more diffuse. Types of monoamines: **a. Dopamine, norepinephrine, and epinephrine (Catecholamines- synthesized from amino acid tyrosine which is converted to L- dopa (converted to dopamine) b. Serotonin (Indolamine)
Acetylcholine Neurotransmitters** o Acetylcholine is the neurotransmitter at neuromuscular junctions , at many of the synapses in the autonomic nervous system, and at synapses in several parts of the central nervous system.

NEUROTRANSMITTERS

Biological Psychology| PSYCHOLOGY o Neurons that release acetylcholine are said to be **cholinergic

Unconventional Neurotransmitters o Nitric oxide and carbon monoxide (soluble-gas neurotransmitters)** o They are produced in the neural cytoplasm and immediately diffuse through the cell membrane into the extracellular fluid and then into nearby cells. They easily pass- through cell membranes because they are soluble in lipids. o Once inside another cell, they stimulate the production of a second messenger and in a few seconds are deactivated by being converted to other molecules. o Soluble-gas neurotransmitters have been shown to be involved in retrograde transmission. At some synapses, they transmit feedback signals from the postsynaptic neuron back to the presynaptic neuron. The function of retrograde transmission seems to be to regulate the activity of presynaptic neurons o Endocannabinoids (another type of soluble-gas neurotransmitter) are neurotransmitters that are similar to delta-9-tetrahydrocannabinol (main psychoactive constituent of marijuana) o Endocannabinoids are synthesized from fatty compounds in the cell membrane; they tend to be released from the dendrites and cell body; and they tend to have most of their effects on presynaptic neurons, inhibiting subsequent synaptic transmission. 5) Neuropeptides Neurotransmitters o About 100 neuropeptides have been identified. The actions of each neuropeptide depend on its amino acid sequence. Has five categories: a. pituitary peptides b. hypothalamic peptides c. brain-gut peptides d. opiod peptides e. miscellaneous peptides 4.2 The Pharmacology of Neurotransmitters Drugs have two fundamentally different kinds of effects on synaptic transmission : They facilitate it or they inhibit it. o Drugs that facilitate the effects of a particular neurotransmitter are said to be agonists of that neurotransmitter. o Drugs that inhibit the effects of a particular neurotransmitter are said to be its antagonists. 7 Steps on How Drugs Influence Synaptic Transmission
Synthesis of the neurotransmitter
Storage in vesicles
Breakdown in the cytoplasm of any neurotransmitter that leaks from the vesicles
Exocytosis
Inhibitory feedback via autoreceptors
Activation of postsynaptic receptors
Deactivation

NEUROTRANSMITTERS

Biological Psychology| PSYCHOLOGY started to produce mild Parkinsonian symptoms (e.g., tremor-at-rest). Researchers put this result together with two then-recent findings: (1) Parkinson’s disease is associated with the degeneration of a main dopamine pathway in the brain, and (2) dopamine agonists—cocaine and amphetamines— produce a transient condition that resembles schizophrenia. Together, these findings suggested that schizophrenia is caused by excessive activity at dopamine synapses and thus that potent dopamine antagonists would be effective in its treatment.  It was ultimately discovered that one particular dopamine receptor, the D receptor, plays a key role in schizophrenia and that drugs that most effectively block it are the most effective antischizophrenic drugs.  Depression – SSRIs (Selective Serotonin Reuptake Inhibitors) ○ Problem : In many depressed patients, serotonin activity is low. ○ Drug Example : Fluoxetine (Prozac) ○ How it Works : Blocks serotonin reuptake → more serotonin stays in the synaptic cleft → mood improves. Real-Life Impact: A patient who felt hopeless and withdrawn gradually regains energy, interest in daily activities, and improved sleep after consistent SSRI use.  Schizophrenia – Antipsychotics ○ Problem : Excess dopamine activity in certain brain areas is linked to hallucinations and delusions. ○ Drug Example: Haloperidol or Risperidone ○ How it Works : Blocks dopamine (D2) receptors → reduces psychotic symptoms. Real-Life Impact: A patient who used to hear voices daily can now focus, engage in conversations, and live more independently.  Anxiety Disorders – Benzodiazepines ○ Problem : Overactive brain circuits due to low GABA (the main calming neurotransmitter). ○ Drug Example: Diazepam (Valium) ○ How it Works: Enhances GABA’s effect → “turns down the volume” of brain activity → relaxation. Real-Life Impact: A student with panic attacks finds relief from constant fear and is able to attend classes without overwhelming anxiety.  Parkinson’s Disease (not a mental disorder, but important for dopamine link) ○ Problem : Dopamine neurons die , leading to tremors, stiffness, slow movement. ○ Drug Example: L-DOPA (dopamine precursor) ○ How it Works: Converts into dopamine in the brain → restores movement control. Real-Life Impact : An elderly patient who struggled to walk regains smoother movement and independence after treatment.  Bipolar Disorder – Mood Stabilizers ○ Problem : Extreme mood swings between mania (too much activity) and depression. ○ Drug Example: Lithium ○ How it Works: Modulates neurotransmitter release (serotonin, dopamine, glutamate) → stabilizes mood. Real-Life Impact: A person who once spent recklessly during manic phases and couldn’t get out of bed during depression is now living a steady, balanced life.

NEUROTRANSMITTERS

Biological Psychology| PSYCHOLOGY Other examples: Major Neurotransmitter Systems & Drug Targets  Acetylcholine (ACh) → memory, muscle contraction  Drugs: Atropine (antagonist), Neostigmine (AChE inhibitor)  Dopamine (DA) → reward, movement, psychosis  Drugs: L-DOPA (precursor), Cocaine (blocks reuptake), Haloperidol (antagonist)  Norepinephrine (NE) → alertness, stress  Drugs: Amphetamines (increase release), Propranolol (β-blocker)  Serotonin (5-HT) → mood, sleep, appetite  Drugs: SSRIs (increase serotonin), LSD (receptor agonist)  GABA → main inhibitory NT  Drugs: Benzodiazepines (enhance GABA action), Barbiturates (agonists)  Glutamate → main excitatory NT  Drugs: Ketamine (NMDA receptor antagonist), Memantine (used in Alzheimer’s) Summary:  The pharmacology of neurotransmitters is about how drugs:  Change their production (synthesis & storage),  Control their release,  Affect their receptors, and  Modify their removal (reuptake or breakdown). This explains how medicines for depression, anxiety, schizophrenia, Parkinson’s, and many other conditions work.

Pharmacology of Neurotransmitters: Biological Psychology Lecture Notes, Study notes of Cognitive Psychology

Related documents

Partial preview of the text

Download Pharmacology of Neurotransmitters: Biological Psychology Lecture Notes and more Study notes Cognitive Psychology in PDF only on Docsity!

NEUROTRANSMITTERS

NEUROTRANSMITTERS

NEUROTRANSMITTERS

NEUROTRANSMITTERS