compare the features of the nervous system and the endocrine system

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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

Class Key examples Receptor type Typical effect
Excitatory, ionotropic Acetylcholine (muscle end‑plate), Glutamate Ligand‑gated Na⁺/Ca²⁺ channels Depolarisation → AP generation
Inhibitory, ionotropic γ‑Aminobutyric acid (GABA), Glycine Ligand‑gated Cl⁻ channels Hyper‑polarisation → reduced firing
Modulatory, metabotropic Dopamine, Norepinephrine, Serotonin G‑protein‑coupled receptors Alter intracellular cAMP, Ca²⁺; affect mood, arousal, autonomic tone

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

Gland (location) Major hormones (type) Principal target organs / actions
Hypothalamus (brain) Releasing & inhibiting hormones (TRH, CRH, GnRH, GHRH, somatostatin, etc.) Regulate anterior pituitary hormone secretion via portal vessels.
Anterior pituitary (sella turcica) GH, TSH, ACTH, FSH, LH, Prolactin Growth, thyroid activity, adrenal cortex, gonadal function, lactation.
Posterior pituitary (neuro‑hypophysis) Oxytocin, Vasopressin (ADH) Uterine contraction & milk ejection; water re‑absorption in kidneys.
Thyroid (neck) Thyroxine (T₄), Triiodothyronine (T₃), Calcitonin Regulate basal metabolic rate; calcium homeostasis.
Parathyroids (posterior thyroid) Parathyroid hormone (PTH) Increase blood Ca²⁺ (bone resorption, renal re‑absorption, activation of vitamin D).
Adrenal cortex (suprarenal) Glucocorticoids (cortisol), Mineralocorticoids (aldosterone), Androgens Stress response, Na⁺/K⁺ balance, secondary sex characteristics.
Adrenal medulla (inner adrenal) Epinephrine, Norepinephrine (catecholamines) Rapid “fight‑or‑flight” effects on heart, blood vessels, metabolism.
Pancreas (abdomen) Insulin, Glucagon (peptide hormones) Lower / raise blood glucose; regulate carbohydrate metabolism.
Gonads (testes & ovaries) Testosterone, Estrogen, Progesterone (steroid hormones) Sexual development, reproduction, secondary sexual characteristics.

3.2 Hormone‑Receptor Mechanisms

Hormone type Receptor location Signalling pathway Example
Peptide / amino‑acid (water‑soluble) Cell‑surface (plasma‑membrane) receptors Ligand binding → G‑protein activation → second messengers (cAMP, IP₃/DAG) → protein‑kinase cascades → rapid cellular response. Insulin → tyrosine‑kinase receptor → PI3K → GLUT‑4 translocation to membrane (↑ glucose uptake).
Steroid (lipid‑soluble) Intracellular receptors (cytoplasm or nucleus) Hormone diffuses through membrane → binds receptor → hormone‑receptor complex acts as transcription factor → altered gene expression (hours‑days). Cortisol → glucocorticoid receptor → ↑ expression of gluconeogenic enzymes.
Amine hormones (e.g., thyroid hormones) Intracellular receptors (often nuclear) Similar to steroids – hormone‑receptor complex regulates transcription of metabolic genes. T₃ → thyroid‑hormone receptor → ↑ basal metabolic rate.

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)

Disorder Primary defect Typical hormonal imbalance Key clinical features
Type 1 Diabetes Mellitus Autoimmune destruction of pancreatic β‑cells ↓ Insulin, ↑ Glucose Polyuria, polydipsia, weight loss; requires exogenous insulin.
Hyperthyroidism (e.g., Graves’ disease) Autoantibodies stimulating TSH receptors ↑ T₃/T₄, ↓ TSH Weight loss, tachycardia, heat intolerance, exophthalmos.
Hypothyroidism (e.g., Hashimoto’s thyroiditis) Autoimmune destruction of thyroid tissue ↓ T₃/T₄, ↑ TSH Fatigue, weight gain, cold intolerance, bradycardia.
Addison’s disease Adrenal cortex insufficiency ↓ Cortisol & aldosterone, ↑ ACTH Hypotension, hyper‑K⁺, hyponatremia, hyperpigmentation.
Cushing’s syndrome Excess cortisol (pituitary adenoma, ectopic ACTH, or adrenal tumour) ↑ Cortisol, ↓ ACTH (if adrenal cause) Central obesity, moon face, hypertension, glucose intolerance.

4. Direct Comparison of the Two Signalling Systems

Feature Nervous System Endocrine System
Primary signalling molecules Neurotransmitters (e.g., ACh, dopamine, GABA) Hormones (e.g., insulin, cortisol, thyroxine)
Mode of transport Electrical impulse along axon → diffusion across synaptic cleft Bloodstream (circulatory system)
Speed of transmission 0.5–120 m s⁻¹ (milliseconds) 0.01–0.1 m s⁻¹ (seconds to hours)
Duration of action Very brief – seconds to minutes Prolonged – minutes to weeks
Target specificity Highly specific – one synapse per target cell Less specific – any cell with the appropriate receptor can respond
Typical physiological effects Rapid control of muscles, glands and sensory processing Metabolic regulation, growth, development, long‑term stress responses, reproduction
Feedback control Predominantly negative feedback via reflex arcs; limited hormonal involvement Extensive negative (and occasional positive) feedback loops, often involving the hypothalamus‑pituitary axis

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.
Suggested diagram: (1) a sensory reflex arc, (2) the hypothalamus‑pituitary‑target gland axis, (3) points of negative feedback, and (4) the sympathetic link to the adrenal medulla.

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