Biopsychology 3

Classical Neurotransmitters

Include amino acids, monoamines, acetylcholine; significant for synaptic communication

Nonclassical Neurotransmitters

Include neuropeptides, lipid neurotransmitters, gas neurotransmitters

Neurotransmitter Precursors

Chemicals used to synthesize neurotransmitters

Acetylcholine Synthesis

Process including specific enzymes to produce ACh

Presynaptic vs Soma Synthesis

Some neurotransmitters made in presynaptic terminal, others in soma and transported

Neurotransmitters Not Stored in Vesicles

Example: nitric oxide (NO)

Neurotransmitter Release Role

Voltage-gated calcium channels and calmodulin trigger vesicle release

Protein/Neuropeptide Transport

From soma to presynaptic terminal along axon

Neurotransmitter Removal

Reuptake, enzymatic degradation, diffusion from synaptic cleft

Ionotropic Receptors

Open ion channels; can produce EPSPs or IPSPs depending on ion type

Metabotropic Receptors

Activate G-proteins; can indirectly affect postsynaptic cell

EPSP vs IPSP

Na⁺ influx = EPSP, K⁺ efflux or Cl⁻ influx = IPSP

Hormone vs Neurotransmitter

Hormones travel in blood; neurotransmitters are local synaptic signals

Posterior Pituitary Hormones

Include oxytocin and vasopressin

Anterior Pituitary Hormones

Controlled by hypothalamic releasing hormones; called "master gland"

Oxytocin Effects

Behavioral, psychological, and physiological roles in bonding and social behavior

Autoreceptors vs Heteroreceptors

Autoreceptors regulate same neuron; heteroreceptors regulate other neurons

Synaptic Plasticity

Changes in synapse strength due to over/underactivation or drugs

Denervation Supersensitivity

Enhanced receptor sensitivity after neuron loss

Lock-and-Key Model

Specific neurotransmitter binds specific receptor to create effect

Activating Systems

Acetylcholine, dopamine, norepinephrine, serotonin systems influence behavior and cognition

Dopamine Pathways

Nigrostriatal (movement) and mesolimbic (reward) pathways

Parkinson’s Disease

Caused by dopamine neuron degeneration in nigrostriatal pathway

Alzheimer’s Disease

Caused by neuron loss and plaques; affects memory and cognition

Agonist vs Antagonist

Agonist mimics neurotransmitter; antagonist blocks it

Acetylcholine Agonist/Antagonist

Substances that increase/decrease ACh effect

Alcohol & Sedative-Hypnotics

Depress CNS activity; affect GABAA receptors

Dopamine Hypothesis of Schizophrenia

Overactive dopamine leads to symptoms; antipsychotics reduce dopamine effects

Mood Stabilizers

Drugs primarily used to treat bipolar disorder

Antidepressants

MAOIs, tricyclics, SSRIs; affect monoamine neurotransmitter levels

SSRIs vs MAOIs/Tricyclics

SSRIs more selective, fewer side effects

Opioid Analgesics

Reduce pain and create euphoria; heroin more potent than morphine IV

Opioid Antagonist

Drugs that block opioid effects (e.g., naloxone)

Psychomotor Stimulants

Cocaine, amphetamines; increase dopamine/norepinephrine; can mimic schizophrenia symptoms

Cocaine Source

Derived from coca plant

Amphetamine vs Cocaine

Stronger, longer-lasting stimulant effects

Otto Loewi Frog Heart Experiment

Demonstrated chemical neurotransmission via acetylcholine

Acetylcholine Effects on Muscles

Same neurotransmitter has opposite effects on skeletal vs cardiac muscle

Opioid Overdose Treatment

Use antagonist (naloxone)

Opioid Analgesic Receptor

Mu opioid receptor mediates morphine pain relief

MAOIs, Tricyclics, SSRIs

Alter neurotransmitter levels; SSRIs fewer side effects