compare the features of the nervous system and the endocrine system

Control and Coordination in Mammals – Nervous vs Endocrine Systems

This set of notes follows the Cambridge International AS & A Level Biology (9700) syllabus – Topic 15 (Control and Coordination). It covers all required sub‑topics, provides clear comparisons, and includes examples, clinical links and practical ideas.

1. Overview

• Both the nervous and endocrine systems transmit information to maintain internal stability (homeostasis) and to produce rapid or sustained responses to external stimuli.
• Key differences lie in the nature of the signalling molecules, speed and duration of the response, transport routes and the way target cells are activated.

2. The Nervous System

2.1 Structure – Central and Peripheral Divisions

• Central nervous system (CNS)

  • Brain: cerebrum (higher‑order processing), cerebellum (coordination), brain‑stem (medulla, pons, mid‑brain – control of vital functions).
  • Spinal cord: dorsal (sensory) and ventral (motor) horns; conduit for impulses to and from the brain.

• Peripheral nervous system (PNS)

  • Cranial nerves, spinal nerves and peripheral ganglia.
  • Afferent (sensory) pathways – carry information from receptors to the CNS.
  • Efferent (motor) pathways – carry commands from the CNS to effectors (muscle or gland).

2.2 Reflex Arc (example)

1. Receptor detects stimulus.
2. Afferent neuron transmits impulse to spinal cord.
3. Integration centre (single‑segment spinal cord) processes the signal.
4. Efferent neuron carries impulse to an effector.
5. Effector (e.g., skeletal muscle) produces a rapid, involuntary response.

Reflexes operate without conscious brain involvement, providing the fastest protective responses.

2.3 Neuronal Signalling

• Resting membrane potential: ≈ –70 mV, maintained by Na⁺/K⁺‑ATPase (3 Na⁺ out, 2 K⁺ in).
• Action potential (all‑or‑none)

  1. Threshold reached (≈ –55 mV).
  2. Depolarisation – rapid Na⁺ influx.
  3. Repolarisation – K⁺ efflux.
  4. Brief hyper‑polarisation.

• Refractory periods

  • Absolute – no new AP can be generated.
  • Relative – a stronger stimulus can trigger an AP.

• Propagation speed depends on axon diameter and myelination (saltatory conduction up to 120 m s⁻¹).
• Synaptic transmission

  • AP reaches axon terminal → Ca²⁺ influx.
  • Neurotransmitter‑filled vesicles fuse with the presynaptic membrane and release contents into the synaptic cleft.
  • Neurotransmitter binds to postsynaptic receptors:

    • Ionotropic – ligand‑gated ion channels (fast, ≤ 1 ms).
    • Metabotropic – G‑protein‑coupled receptors → second‑messenger cascades (slower, longer‑lasting).

  • Signal terminated by enzymatic degradation, diffusion, or re‑uptake.

2.4 Neuro‑transmitter Classification & Examples

2.5 Autonomic Nervous System (ANS)

• Divides the efferent pathways that control involuntary smooth muscle, cardiac muscle and glands.
• Sympathetic division – “fight‑or‑flight”; releases norepinephrine from post‑ganglionic fibres, stimulates adrenal medulla (catecholamine release).
• Parasympathetic division – “rest‑and‑digest”; releases acetylcholine at post‑ganglionic synapses, promotes digestion and energy storage.
• ANS interacts closely with the endocrine system (e.g., sympathetic stimulation of adrenal medulla, hypothalamic control of pituitary hormone release).

3. The Endocrine System

3.1 Major Endocrine Glands and Their Principal Hormones

3.2 Hormone‑Receptor Mechanisms

3.3 Hypothalamic‑Pituitary Control

• The hypothalamus synthesises releasing (e.g., TRH, CRH, GnRH, GHRH) and inhibiting (e.g., somatostatin, dopamine) hormones.
• These hormones are secreted into the hypophyseal portal vessels – a specialised capillary network that carries them directly to the anterior pituitary.
• Anterior pituitary cells respond by secreting tropic hormones (GH, ACTH, TSH, LH, FSH, Prolactin) that act on peripheral endocrine glands.
• The posterior pituitary stores oxytocin and vasopressin, which are synthesised in hypothalamic neurones and released into the systemic circulation when required.

3.4 Endocrine Disorders (clinical links)

4. Direct Comparison of the Two Signalling Systems

5. Integration of Nervous and Endocrine Systems

• Neuro‑endocrine link: The hypothalamus receives neural inputs (sensory, limbic, higher cortical) and translates them into hormonal signals.
• Anterior pituitary: Responds to hypothalamic releasing/inhibiting hormones and secretes tropic hormones that act on peripheral endocrine glands.
• Posterior pituitary: Stores oxytocin and vasopressin produced by hypothalamic neurones; release is directly neural.
• Example – Stress response

  1. Perceived threat → hypothalamus activates the sympathetic division → adrenal medulla releases epinephrine (seconds).
  2. Simultaneously, hypothalamus secretes CRH → anterior pituitary releases ACTH → adrenal cortex secretes cortisol (minutes‑hours) to sustain the response.

6. Feedback Mechanisms

• Negative feedback (most common)

  • Elevated blood glucose → pancreas releases insulin → glucose uptake ↓ → insulin secretion reduced.
  • High cortisol → inhibits CRH (hypothalamus) and ACTH (pituitary) release.
  • Thyroid axis: ↑ T₃/T₄ → ↓ TRH and TSH.

• Positive feedback (rare)

  • Oxytocin surge during labour intensifies uterine contractions, which further stimulates oxytocin release.

• Both systems also use local autocrine/paracrine signalling (e.g., presynaptic inhibition, local release of prostaglandins).

7. Practical Investigation Ideas (AO3)

1. Reflex latency experiment: Measure the time between a tap on the patellar tendon and the resulting leg extension using a high‑speed camera or motion sensor. Relate latency to nerve conduction speed and myelination.
2. Hormone assay: Use ELISA kits to quantify insulin or cortisol levels in blood samples taken before and after a controlled stimulus (e.g., glucose drink, stress test).
3. Second‑messenger detection: Treat cultured cells with a peptide hormone (e.g., glucagon) and measure intracellular cAMP using a colourimetric assay.
4. Effect of myelination on conduction: Compare conduction velocities in isolated frog sciatic nerves before and after applying a demyelinating agent (e.g., lysolecithin).
5. Feedback disruption simulation: Use a computer model to alter set‑point values in the hypothalamic‑pituitary‑thyroid axis and observe predicted hormone concentrations.

8. Summary of Key Points

1. Neural signalling is fast, short‑lived and highly targeted; endocrine signalling is slower, longer‑lasting and can affect many different cells.
2. Neurons use electrical impulses and neurotransmitters; endocrine glands secrete hormones into the blood.
3. Hormone‑receptor interactions differ: peptide hormones act via cell‑surface receptors and second messengers; steroid hormones act via intracellular receptors and gene transcription.
4. The hypothalamus is the principal neuro‑endocrine hub, linking rapid neural information to sustained hormonal responses.
5. Both systems are regulated mainly by negative feedback, but endocrine loops often involve multi‑gland cascades (e.g., hypothalamus‑pituitary‑target gland).
6. Clinical disorders illustrate what happens when feedback fails or when hormone production is abnormal.