Neuroscience and Biology Distinctions

CNS vs. PNS

• Central Nervous System. Brain + spinal cord.
• Peripheral Nervous System. Everything else (cranial nerves, spinal nerves, ganglia).

Key distinction: CNS does the thinking. PNS carries signals in and out.

Somatic vs. Autonomic Nervous System

• Somatic. VOLUNTARY control of skeletal muscle + conscious sensation. “I’ll lift my arm.”
• Autonomic. INVOLUNTARY control of smooth/cardiac muscle and glands. Heart rate, digestion.

Key distinction: somatic = voluntary, skeletal muscle. Autonomic = involuntary, internal organs.

Sympathetic vs. Parasympathetic (Review)

• Sympathetic. Fight or flight. Short pre-ganglionic axon, long post-ganglionic.
• Parasympathetic. Rest and digest. Long pre-ganglionic, short post-ganglionic.

Key distinction: sympathetic prepares for action; parasympathetic recovers. Opposite effects on the same organs.

Afferent vs. Efferent Neurons

• Afferent. ARRIVE at the CNS. Sensory. Mnemonic: “Afferent = Arrive.”
• Efferent. EXIT the CNS. Motor. Mnemonic: “Efferent = Exit.”

Key distinction: direction. In = afferent. Out = efferent.

Upper vs. Lower Motor Neuron Signs

• UMN damage (e.g., stroke). HYPERreflexia, hypertonia (spasticity), clonus, Babinski sign (toes fan UP).
• LMN damage (e.g., polio). HYPOreflexia, atrophy, fasciculations (twitches), flaccid paralysis.

Key distinction: UMN = hyper-everything (plus Babinski). LMN = hypo-everything (plus muscle wasting). Both cause weakness but differ elsewhere.

Gray vs. White Matter

• Gray matter. Cell bodies (somas) and dendrites.
• White matter. Myelinated axons (the fat makes it look white).

Locations flipped:

• Brain. Gray outside (cortex), white inside.
• Spinal cord. Gray inside (butterfly), white outside.

Key distinction: where the synapses happen (gray) vs. where signals travel fast (white).

Glutamate vs. GABA

• Glutamate. Main EXCITATORY neurotransmitter in the CNS.
• GABA. Main INHIBITORY neurotransmitter in the CNS.

Key distinction: opposite effects. Too much glutamate → seizures, excitotoxicity. Too little GABA → seizures. Alcohol/benzos enhance GABA (sedative).

Dopamine Pathways

• Nigrostriatal. Substantia nigra → striatum. MOTOR control. Damaged in Parkinson’s.
• Mesolimbic. VTA → nucleus accumbens. REWARD. Hyperactive → positive symptoms of schizophrenia.
• Mesocortical. VTA → prefrontal cortex. COGNITION. Hypoactive → negative symptoms of schizophrenia.
• Tuberoinfundibular. Hypothalamus → pituitary. Regulates PROLACTIN release.

Key distinction: four distinct pathways, four different jobs. Don’t confuse mesolimbic (reward) with mesocortical (cognition) - they’re opposite ends of the schizophrenia picture.

Acetylcholine: CNS vs. PNS

• CNS. Basal forebrain → cortex. Attention, memory. Declines in ALZHEIMER’S.
• PNS. All motor neurons at neuromuscular junction. All parasympathetic postganglionic synapses. All preganglionic sympathetic and parasympathetic.

Key distinction: acetylcholine is everywhere in the PNS. In the CNS it specifically matters for attention/memory.

Serotonin vs. Norepinephrine vs. Dopamine

• Serotonin. Raphe nuclei. Mood, sleep, appetite. LOW → depression. SSRIs boost it.
• Norepinephrine. Locus coeruleus. Alertness, attention. LOW → depression too.
• Dopamine. VTA + substantia nigra. Reward, motor. LOW → Parkinson’s. HIGH → positive symptoms of schizophrenia.

Key distinction: each has its own source nuclei and signature function. Some antidepressants (SNRIs) hit both serotonin and NE.

Anterior vs. Posterior Pituitary

• Anterior pituitary. MAKES AND RELEASES its own hormones (FLAT PEG: FSH, LH, ACTH, TSH, Prolactin, Endorphins, GH).
• Posterior pituitary. STORES AND RELEASES hormones made by the hypothalamus (ADH, oxytocin).

Key distinction: anterior = pituitary makes the hormones. Posterior = just a storage/release site.

Adrenal Medulla vs. Adrenal Cortex (Review)

• Medulla. Catecholamines (epinephrine, norepinephrine). Fast stress response.
• Cortex. Steroids (cortisol, aldosterone, sex steroids). Slow stress and metabolic regulation.

Key distinction: medulla fast, cortex slow.

Brain Imaging: Structure vs. Function

Structural (anatomy):

• CT. X-rays → fast, lower resolution. Good for urgent cases (bleeds, fractures).
• MRI. Magnetic fields → slower, higher resolution. Good for soft tissue.

Functional (activity):

• EEG. Electrical activity. Best TEMPORAL resolution (millisecond). Poor spatial.
• MEG. Magnetic signals. Better spatial than EEG, similar temporal.
• PET. Radioactive glucose. Metabolic activity. Low spatial and temporal resolution. Invasive.
• fMRI. Blood oxygenation (BOLD). Best SPATIAL resolution for function. Moderate temporal.

Key distinction: if you need anatomy → MRI or CT. If you need millisecond timing → EEG. If you need precise location of activity → fMRI. If you need metabolic activity → PET.

Gyrus vs. Sulcus

• Gyrus. RIDGE of the cortex (the bump).
• Sulcus. GROOVE of the cortex (the valley).

Key distinction: gyri stick out; sulci dip in. Deep sulci are fissures (central fissure divides frontal and parietal lobes).

Ectoderm vs. Mesoderm vs. Endoderm

• Ectoderm. OUTER layer. Skin, hair, nails, sensory organs, NERVOUS SYSTEM.
• Mesoderm. MIDDLE layer. Muscle, bone, cardiovascular, reproductive, kidneys.
• Endoderm. INNER layer. GI tract lining, lungs, liver, pancreas.

Key distinction: ectoderm = outside + nervous system (outside the body → sensors → brain). Mesoderm = middle (muscle/bone). Endoderm = inside (guts).

Fight-or-Flight vs. Tend-and-Befriend

• Fight-or-flight. Sympathetic mobilization for action. Both sexes.
• Tend-and-befriend. Alternative stress response. Social bonding, care of offspring. More common in women, driven partly by oxytocin.

Key distinction: fight-or-flight = act. Tend-and-befriend = affiliate. Both are adaptive responses to stress but produce opposite social behavior.

Parkinson’s vs. Huntington’s Disease

• Parkinson’s. Dopamine neurons die (substantia nigra). Tremor, rigidity, slowness. Late-life onset. Treated with L-DOPA.
• Huntington’s. Genetic (autosomal dominant, CAG repeat). Basal ganglia + cortex degeneration. Uncontrolled movements (chorea) + cognitive decline. Mid-life onset. No cure.

Key distinction: Parkinson’s = too little dopamine, hypokinetic. Huntington’s = different degeneration, HYPERkinetic. Parkinson’s rare genetic; Huntington’s genetic disease.

Adolescent Brain Changes

• Synaptic pruning. Unused synapses ELIMINATED. Used ones strengthened.
• Myelination. Axons get MORE myelin. Faster communication.

Key distinction: pruning removes connections. Myelination speeds up existing connections. Both continue into early 20s and explain adolescent changes.