Comprehensive Neuroscience and Psychology: Consciousness, Brain Structures, and Behavior

What is consciousness?

Awareness of thoughts, perceptions, memories, and feelings; creates subjective experience.

How can brain damage affect consciousness?

It can disrupt perception and awareness without the person noticing.

What was the purpose of frontal lobotomy?

Mid-20th century treatment for mental disorders; removed frontal lobe connections.

Why did lobotomy fall out of use?

Antipsychotic medication was developed and made it unnecessary.

What is the corpus callosum?

A large bundle of ~200 million axons connecting the left and right hemispheres.

What happens in a split-brain surgery?

Corpus callosum is cut to reduce seizures; hemispheres cannot communicate.

What does each hemisphere control?

Left hemisphere → right side of body; Right hemisphere → left side of body.

How is visual information processed across hemispheres?

Left visual field → right hemisphere; Right visual field → left hemisphere.

What happens when a split-brain patient touches an object with the left hand?

They cannot verbally identify it (right hemisphere lacks language ability).

Why can't split-brain patients verbalize left-field stimuli?

Right hemisphere receives info but cannot speak.

Do split-brain patients notice their deficits?

No — they feel normal and unaware of missing information.

What is the 'interpreter theory'?

Left hemisphere creates narratives to explain behavior after it occurs.

What does Interpreter Theory say about free will?

Consciousness does not cause behavior; it explains behavior after the fact.

Where is consciousness located according to Interpreter Theory?

Left hemisphere (because consciousness requires language).

What is mind-body dualism?

Mind is immaterial; body follows physical laws.

What is the Cartesian impasse?

Immaterial mind shouldn't be able to control a physical body if physics is deterministic.

How does evolutionary theory explain consciousness?

Neural networks evolved to simulate future possibilities; thoughts guide behavior indirectly.

What are CHNOPS?

Carbon, hydrogen, nitrogen, oxygen, phosphorus, sulfur — six essential elements of life.

What is a molecule?

Two or more atoms covalently bonded.

What are the 5 major biological molecules?

Water, sugars, fats (lipids), nucleotides, amino acids.

What are macromolecules?

Chains of biological molecules: carbohydrates, lipids, proteins, nucleic acids.

Why is RNA important in early life?

Functions as a catalyst (ribozymes) and could both store and process information.

Why did proteins replace ribozymes as catalysts?

More stable and diverse; made from 20 amino acids.

What does a ribosome do?

Translates mRNA into proteins by joining amino acids.

What is a phospholipid?

Fatty acid chains with a phosphate head; form bilayers in water.

What is the difference between prokaryotes and eukaryotes?

Prokaryotes: no nucleus, small, simple; Eukaryotes: nucleus + mitochondria + organelles.

How did mitochondria evolve?

Endosymbiosis — a host cell engulfed a bacterium that became mitochondria.

What is a gene?

DNA sequence that is transcribed into RNA; may be translated into protein.

What percentage of the human genome codes for proteins?

~2%.

What regulates which genes a cell expresses?

Environmental cues + cell type.

Do all cells have the same genome?

Yes — differences arise from differential gene expression.

What does the Golgi stain show?

Randomly stains ~2% of neurons to reveal individual structure.

What are the main parts of a neuron?

Soma, dendrites, axon.

What is the resting membrane potential?

Voltage difference across neuron membrane: -40 to -90 mV.

What creates membrane potential?

Unequal ion distribution + selective permeability.

What ions are more concentrated outside neurons?

Na⁺, Cl⁻, Ca²⁺.

What ion is more concentrated inside neurons?

K⁺.

What two proteins establish the resting potential?

1. Na⁺/K⁺ pump — pumps 3 Na⁺ out, 2 K⁺ in; 2. K⁺ leak channels — allow K⁺ to move freely.

What is diffusion?

Movement of ions from high → low concentration.

What is electrostatic pressure?

Opposite charges attract; like charges repel.

What is depolarization?

Membrane potential becomes less negative (e.g., -70 → -60 mV).

Why are membrane changes brief?

K⁺ leak channels rapidly return cell to resting potential.

What activates voltage-gated ion channels?

Changes in membrane potential.

What is a voltage-gated Na⁺ channel?

Opens when membrane depolarizes; causes rapid Na⁺ influx.

Why does the Na⁺ channel inactivate?

Ball-and-chain mechanism blocks the pore after ~0.5 ms.

What is the threshold of excitation?

Voltage at which the first Na⁺ channel opens → triggers action potential.

What is an action potential?

Rapid, temporary depolarization that propagates along the axon.

Why can action potentials only move forward?

Inactivation of Na⁺ channels prevents backward flow.

What is the all-or-none law?

Action potentials do not vary in size; they either happen or don't.

What is the rate law?

Stronger stimuli cause more frequent action potentials.

What do voltage-gated K⁺ channels do?

Open later, repolarize the membrane quickly.

What is hyperpolarization?

Membrane becomes more negative than resting potential.

What are oligodendrocytes?

Glial cells that produce myelin in the CNS.

What is the function of myelin?

Insulates axons; speeds conduction ~20x.

What are nodes of Ranvier?

Gaps in myelin where Na⁺ channels cluster; regenerate action potentials.

What is saltatory conduction?

Action potential 'jumps' from node to node.

Which axons conduct fastest?

Thick, myelinated axons (up to 100 m/s).

Which sensations use unmyelinated axons?

Pain and temperature.

What triggers neurotransmitter release?

Ca²⁺ influx through voltage-gated Ca²⁺ channels.

What is the synaptic cleft?

Space between presynaptic and postsynaptic neurons.

What is an ionotropic receptor?

Ligand-gated ion channel; fast EPSPs or IPSPs.

What is a metabotropic receptor?

GPCR; activates G-proteins; slower, modulatory effects.

What is a G-protein?

Intracellular protein activated by GPCRs using GTP.

What do G-proteins do?

Open ion channels, modify gene expression, modulate signaling.

What is a g-protein-gated ion channel?

Channel opened indirectly after GPCR activation.

What is an axoaxonic synapse?

Axon → axon connection that regulates neurotransmitter release.

What is presynaptic inhibition?

Hyperpolarizes axon terminal → less Ca²⁺ entry → less NT release.

What is presynaptic facilitation?

Depolarizes axon terminal → more Ca²⁺ entry → more NT release.

What are the two main inhibitory effects?

Fast IPSP (Cl⁻ influx via ionotropic receptors) and Slow IPSP (metabotropic inhibition).

What are classical neurotransmitters?

Glutamate, GABA, dopamine, serotonin, norepinephrine, acetylcholine.

Where are classical NTs synthesized?

Axon terminals from modified amino acids.

What is glutamate?

Main excitatory NT; opens Na⁺ channels.

What is GABA?

Main inhibitory NT; opens Cl⁻ channels.

Why is blocking glutamate dangerous?

Can cause dissociation; high doses cause coma/anesthesia.

Why is blocking GABA dangerous?

Causes seizures due to runaway excitation.

What are neuropeptides?

Small proteins (10-30 aa); synthesized in soma; released once; diffuse far.

Do neuropeptides have ionotropic receptors?

No — only metabotropic.

What are endocannabinoids?

Lipid-based NTs that travel backward (postsynaptic → presynaptic).

What do endocannabinoids do?

Reduce neurotransmitter release (presynaptic inhibition).

What are monoamines?

Dopamine, serotonin, norepinephrine — share structural similarity.

What packages monoamines into vesicles?

VMAT — vesicular monoamine transporter.

What is an agonist?

Drug that activates a receptor.

What is an antagonist?

Drug that blocks a receptor.

What is competitive binding?

Drug binds to same site as NT.

What is non-competitive binding?

Drug binds to different site; modulates receptor activity.

What is a positive allosteric modulator?

Enhances receptor response (e.g., benzodiazepines on GABA_A).

What does black widow venom do?

Causes massive acetylcholine release → spasms.

What does botulinum toxin do?

Prevents acetylcholine release → paralysis.

What does neostigmine do?

Inhibits acetylcholinesterase → prolongs ACh action; treats myasthenia gravis.

What is biased agonism?

Ligand activates one signaling pathway more than another at the same receptor.

What causes neurotransmitter release?

Opening of voltage-gated Ca²⁺ channels at the axon terminal.

What do SNARE proteins do?

Mediate vesicle docking and neurotransmitter release.

How does botulinum toxin affect synapses?

Destroys SNARE proteins → prevents ACh release → paralysis.

How does black widow venom affect synapses?

Causes massive ACh release → muscle spasms.

What is reuptake?

Transporter proteins return neurotransmitters to the presynaptic terminal.

What is enzymatic degradation?

Enzymes (e.g., AChE) break down neurotransmitters in the synaptic cleft.

What does acetylcholinesterase (AChE) do?

Breaks down ACh into acetate + choline.

What is an autoreceptor?

A receptor on the presynaptic neuron that detects NT levels and inhibits further release.

What is the effect of blocking GABA signaling?

Seizures due to uncontrolled neural excitation.

What does alcohol do at synapses?

Enhances GABA_A and inhibits glutamate NMDA receptors → depressant effects.