Structure and function of the nervous and endocrine systems

Most organs receive both inputs and respond to their balance. Sympathetic activation mobilizes the body for stress: ↑ heart rate, dilated pupils and bronchioles, inhibited digestion, and adrenal release of epinephrine. Parasympathetic activation conserves and restores: ↓ heart rate, constricted pupils, stimulated digestion and salivation. A useful chemical anchor: most parasympathetic effects use acetylcholine, while most sympathetic target effects use norepinephrine.

The knee-jerk reflex is monosynaptic (sensory neuron synapses directly onto a motor neuron); most reflexes are polysynaptic, routing through interneurons. Reflexes act before the brain consciously registers the stimulus (you pull your hand off a hot stove first, feel pain after), which is the whole point — speed and protection.

Each receptor type transduces one kind of stimulus into a signal carried inward on afferent (sensory) neurons. Mechanoreceptors respond to physical deformation — skin touch/pressure, the auditory hair cells of the cochlea, and baroreceptors (a mechanoreceptor subtype that senses arterial stretch to monitor blood pressure). Chemoreceptors detect dissolved molecules — taste buds, olfactory neurons, and the central/peripheral chemoreceptors that track blood CO₂, O₂, and pH. Photoreceptors (rods and cones) detect light; thermoreceptors sense warm vs. cold; nociceptors signal pain from harmful stimuli. Proprioceptors (in muscles/tendons/joints) are mechanoreceptors that report body position. Sensory neurons exhibit adaptation — a steady stimulus produces fewer impulses over time.

Myelin insulates the axon so the action potential regenerates only at the nodes of Ranvier, effectively leaping the myelinated stretches — fast and energy-efficient. Demyelinating diseases (e.g., multiple sclerosis) slow or block conduction. Bigger-diameter axons conduct faster too, which is why some invertebrates use giant axons for escape reflexes.

• Acetylcholine (ACh) — the transmitter at the neuromuscular junction (excites skeletal muscle) and across the parasympathetic system; broken down by acetylcholinesterase.
• Glutamate — the main excitatory transmitter in the CNS (learning and memory).
• GABA — the main inhibitory transmitter in the CNS.
• Dopamine — movement and reward (depleted in Parkinson's, implicated in schizophrenia and addiction).
• Serotonin — mood, sleep, and appetite (a target of antidepressants).
• Norepinephrine — the sympathetic transmitter; arousal and alertness.

Whether a transmitter excites or inhibits ultimately depends on the receptor it binds, not the molecule alone — the same transmitter can do either at different synapses.

• Peptide / amino-acid-derived (e.g., insulin, glucagon, ADH) — hydrophilic, so they can't cross the membrane; they bind a cell-surface receptor and trigger a second-messenger cascade (e.g., GPCR → cAMP). Effects are fast and short-lived, and these hormones don't need to be carried by plasma proteins.
• Steroid (e.g., cortisol, aldosterone, estrogen, testosterone) — lipophilic, made from cholesterol; they diffuse through the membrane, bind a cytoplasmic or nuclear receptor, and the complex acts as a transcription factor. Effects are slow to start but long-lasting, and steroids ride carrier proteins in the blood.

The hypothalamus links the nervous and endocrine systems: it releases factors that stimulate the anterior pituitary to secrete tropic hormones (TSH, ACTH, FSH/LH, etc.) that drive target glands (thyroid, adrenal cortex, gonads). The posterior pituitary instead stores and releases two hormones (ADH, oxytocin) made by the hypothalamus. Negative feedback closes the loop — e.g., rising thyroid hormone (T₃/T₄) inhibits both TRH and TSH, so output is self-limiting. Most endocrine axes work this way; positive feedback is rarer (oxytocin in labor, the LH surge before ovulation).

The adrenal gland has two parts: an outer cortex (steroids) and an inner medulla. The medulla is essentially a modified sympathetic ganglion — when the sympathetic nervous system fires, it releases epinephrine (adrenaline) and norepinephrine directly into the bloodstream. These catecholamines are amino-acid-derived (from tyrosine) and water-soluble, so they act on cell-surface receptors for fast, short-lived effects: ↑ heart rate and contractility, bronchodilation, pupil dilation, glycogenolysis and lipolysis to raise blood glucose and free fatty acids, and blood shunting from the gut/skin to skeletal muscle.

Cortisol is the body's main stress steroid, governed by the HPA axis: hypothalamic CRH → anterior-pituitary ACTH → adrenal cortex → cortisol, which then negatively feeds back on CRH and ACTH. Cortisol raises blood glucose by driving gluconeogenesis (and decreasing peripheral glucose uptake and protein synthesis), and it suppresses the immune/inflammatory response — why synthetic glucocorticoids are prescribed as anti-inflammatories. Aldosterone instead handles salt and blood pressure: it drives Na⁺ reabsorption (and K⁺/H⁺ secretion) in the distal nephron, with water following — see osmoregulation: ADH & aldosterone. All are lipophilic steroids made from cholesterol, so they act on intracellular receptors and change gene transcription.

The anterior pituitary is the bridge between the hypothalamus and downstream glands. Its tropic hormones stimulate target glands — TSH → thyroid, ACTH → adrenal cortex, FSH/LH → gonads (this is the axis machinery in the hypothalamic–pituitary axis). But it also secretes direct hormones that act on tissues themselves: prolactin (stimulates milk production), growth hormone (GH/somatotropin) (promotes growth, largely via liver IGF-1; excess causes acromegaly/gigantism), and endorphins (pain modulation). A common mnemonic is FLAT PEG — FSH, LH, ACTH, TSH are tropic (FLAT); Prolactin, Endorphins, GH are direct (PEG).

The thyroid follicular cells iodinate tyrosine to make T₄ (thyroxine) and the more active T₃, under the HPT axis (TRH → TSH → thyroid, with rising T₃/T₄ inhibiting both). Although it is amino-acid-derived, thyroid hormone is lipophilic and acts on intracellular receptors (the classic exception to the peptide/steroid split in peptide vs. steroid hormones). Its job is to set metabolic rate — O₂ consumption and heat production. Hyperthyroidism (e.g., Graves') → high metabolic rate, heat intolerance, weight loss, ↑ heart rate and respiratory rate, and faster fuel use. Hypothyroidism → the opposite: low metabolic rate, cold intolerance, weight gain, fatigue, and sluggish HR. Calcitonin (from thyroid C cells) is separate — it lowers blood Ca²⁺, opposing parathyroid hormone.