a) Explain why the effort of hormonal (Endocrine ) control tends to be slow whereas nervous control is usually very fast.
Endocrine control is normally slower when compared to nervous control majorly because hormones once released by the endocrine gland have to travel via the circulation to reach their target receptors on the effector organ which generally takes more time. Meanwhile, information relayed by nerves is in form of impulses (that is, action potentials generated due to electrical excitation produced by a change in the charge across the surface membrane of the neuron evoked by the stimuli) that simply travel along the axons of neurons by initiating action potentials along the surface membrane of the axon.The speed of nervous impulses in myelinated nerve fibres that is those surrounded by a material composed of lipids and proteins commonly termed lipoprotein ranges from 3-15 m/sec and as fast as 200µ/sec in nerves with wide diameters whilst that in unmyelinated fibres ranges from 0.5 to 2.0m/sec (Willam 2005, p.109).
b) In both cases, the system of control requires: Stimulus--receptor--co-ordinator--effector—response. For a specific hormone and reflex action, explain the sequence of events.
The autonomic blood pressure control reflex and the anti-diuretic hormone (ADH) will be used to explain the sequence of events involved in the stimulus-receptor-co-ordinator-effector-response. For the autonomic (involuntary) blood pressure control reflex; an increase in blood pressure (stimulus) stimulates baroreceptors (receptors) located in the carotid arteries and the aorta to transmit impulses through the glossopharyngeal nerve to the medulla oblongata (co-ordinator). The medulla oblongata sends impulses back to the heart (effector) via the vagus nerve which cause a decrease in the heart rate and hence lower the blood pressure (response) (Saladin 2007, p.457). For ADH; any increase in the osmotic concentration of the blood (stimulus) is detected by receptors in the hypothalamus (receptor), the hypothalamus in turn stimulates the posterior lobe of the pituitary (coordinator normally located in the brain) to produce ADH which travels via the blood stream to the kidneys (effector) and increases the permeability of the distal convoluted tubules and the collecting ducts to water resulting in an increase in tubular reabsorption of water (response). The net effect of the latter is to increase the blood volume while reducing the osmotic pressure and amount of urine (Chiras 2010, p.178).
c) The nerve impulse can be described as an all or nothing response. Explain what this mean in terms of changes in the membrane's permeability to Sodium and potassium.
The fibers of nerve cells are believed to posess sodium gated channels at the surface of their membranes. Reception of a stimulus by a nerve cell which was previously in the resting state/phase causes these gated sodium channels to open. Normally, a concentration gradient exists between the inside and the outside of the surface membrane of the nerve fiber during its resting phase with the outside of the membrane being positively charged due to a high concentration of sodium ions, Na+ and the cytosol enclosed within the surface membrane being negatively charged due to a low concentration of potassium ions, K+ as shown in the diagram 1 below.
The resting membrane potential is -80Mv. Opening of the sodium gated channels therefore is marked by rapid entry of sodium ions into the cytoplasm of the nerve cell a process termed depolarization of the cell membrane since the relative permeability of potassium is lower than that of sodium. For the depolarization to result in an action potential, the depolarization must reach a critical level otherwise known as the threshold normally -65Mv.In essence therefore, stimuli whose level of depolarization is lower than the critical level does not result in an action potential whilst those that rise beyond the critical level initiate an action potential a concept termed the ‘all or nothing response’ of nervous impulses as shown in diagram 2 below (Bear et al. 2007, p.77).
D) How does this impulse connect to the next nerve in the sequence, i.e across the synapse.
Once the nerve impulse reaches the post synaptic membrane, it causes the opening of calcium voltage-gated channels and the subsequent release of calcium ions in the presynaptic node. In turn calcium initiates the release of a neurotransmitter acetylcholine into the synaptic cleft which then diffuses across the cleft to bind to sodium ligand-gated ion channels in the post-synaptic membrane. The latter causes the sodium ligand-gated ion channels to open. Consequently, the postsynaptic membrane becomes depolarized due to the entry of sodium ions following the opening of the ligand-gated Na+ channels. An action potential is generated once the depolarization exceeds the threshold level and hence transmission of the impulse effectively occurs. These events are captured in diagram 3 below.
E) The nerve impulse also travels only in one direction, using your answers to 4 and 5, explain why this is the case.
The synaptic junction is structured in a manner that the release of the neurotransmitter that evokes an action potential on the post-synaptic membrane can only be from the pre-synaptic membrane. In effect therefore, impulses at a synaptic junction can only travel in one direction. On the other hand, action potentials travel across the nerve axon by initiating another action potential on the next section of the nerve axon as previously mentioned, the section that transmitted the action potential then goes into a repolarization phase whereby the membrane potential drops to less than the resting membrane potential due to an increased efflux of potassium, K+ ions from the neuron secondary to the opening of voltage-gated k+ channels. During this period the neuronal section cannot transmit any impulses as depicted in the diagram 4 below on action potential propagation.
Bibliography
Bear, M.F., Connors, B.W. and Paradiso, M.A., 2007. Neuro-science: Exploring the brain. Baltimore: Lippincott, Williams & Wilkins.
Chiras, D.D., 2010. Human biology.7th ed. Ontario: Jones and Barlett Learning Canada.
Saladin, K., 2007. Human anatomy. New York: McGraw-Hill companies, Inc.
Seeley, R.R., Stephens, T.D. and Tate, P., 2008. Anatomy and physiology.8th ed. Boston: McGraw-Hill companies, Inc.
William, K.J., 2005. Krause’s essential Human Histology for medical students.3rd ed. Florida: Universal publishers.
