The central nervous system (CNS) is equipped with various specialized sensory receptors to gather information about the world. These receptors detect specific types of energy, known as stimuli. When a stimulus activates a sensory receptor, it triggers a process called sensory transduction. This process converts information about the stimulus, such as its intensity and duration, into local electrical signals. These signals are referred to as action potentials.

Comparison of action potential conduction in unmyelinated and myelinated axons reveals differences in their behavior. In an unmyelinated axon, an action potential generated at one point depolarizes the adjacent portion. On the other hand, in a myelinated axon, the inward current depolarizes the entire membrane up to the next node. This distinction is illustrated in Figure 5.11, which compares the conduction of action potentials in these two types of axons.

Certain diseases, referred to as demyelinating disorders, involve the deterioration of the myelin sheath. Multiple sclerosis is an example of such a disorder, characterized by progressive demyelination of axons in the CNS. This condition leads to a loss of motor control and sensory deficits. Similarly, in severe cases of diabetes mellitus, neuropathy occurs due to the demyelination of peripheral axons. Loss of myelin causes a significant reduction in the length constant, resulting in a decrease in action potential amplitude as it is electrotonically conducted from one node of Ranvier to the next. In severe demyelination, the action potential may not reach the next node with enough strength to trigger another action potential, resulting in propagation failure.

Myelinated axons possess distinct characteristics compared to unmyelinated axons. They may lack a hyperpolarizing afterpotential or an extended relative refractory period due to the displacement of their K+ channels from the nodes into the partly exposed flanking paranodes. This displacement increases the firing rate of these fast-conducting axons. Additionally, myelinated axons are more metabolically efficient than unmyelinated axons. The Na+,K+-ATPase helps in extruding the Na+ that enters the cell and accumulating the K+ that leaves the cell during action potentials. Ionic currents in myelinated axons are confined to the small fraction of the membrane surface at the nodes of Ranvier. As a result, fewer ions traverse a unit length of fiber membrane, reducing the amount of ion pumping and energy expenditure needed to maintain the gradients.
To receive information about the world, the CNS contains a wide variety of sensory receptors, each of which is specialized •Fig. 5.11 Comparison of Action Potential Conduction in an Unmyelinated Axon and in a Myelinated Axon. Attheinitialtime(A andC),anactionpotentialisbeinggeneratedattheleftsideofeachaxon.Notethattheinwardcurrentintheunmyelinatedaxon(A) isdepolarizinganadjacentportion,whereastheinwardcurrentinthemyelinatedaxon(C) isdepolarizingallofthemembranetothenextnode.Atthesecondinstantintime(B andD),theactionpotentialintheunmyelinatedaxon(B) hasbeengeneratedintheadjacentportion,whereastheactionpotentialinthemyelinatedaxon(D) hasbeengeneratedatsubsequentnodesandisalreadydepolarizingthelastnodetotheright.(RedrawnfromCastroA,etal:Neuroscience: An Outline Approach. Philadelphia:Mosby;2002.)
Insomediseasesknownasdemyelinating disorders, themyelinsheathdeteriorates.Inmultiple sclerosis, scatteredprogressivedemyelinationofaxonsintheCNSresultsinlossofmotorcontrolandsensorydeficits.Theneuropathycommoninseverecasesofdiabetesmellitusiscausedbythedemyelinationofperipheralaxons.Whenmyelinislost,thelengthconstantbecomesmuchshorter.Hence,theactionpotentiallosesamplitudeasitiselectrotonicallyconductedfromonenodeofRanviertothenext.Ifdemyelinationissufficientlysevere,theactionpotentialmayarriveatthenextnodeofRanvierwithinsufficientstrengthtofireanactionpotentialatthatnode,leadingtopropagationfailure.
to detect a particular type of energy (stimulus). When a stimulus activates a sensory receptor, it initiates a process called sensory transduction by which information about the stimulus (e.g., its intensity and duration) is converted into local electrical signals. These local signals are called
TheactionpotentialsofmyelinatedaxonsmaynothaveahyperpolarizingafterpotentialoranextendedrelativerefractoryperiodbecausetheirK+ channelsaredisplacedfromthenodesintothepartlyexposedflankingparanodes.Thatincreasestherateatwhichthesefast-conductingaxonscanfire.Myelinatedaxonsarealsomoremetabolicallyefficientthanunmyelinatedaxons.Na+,K+-ATPaseextrudestheNa+ thatentersthecellandcausestheK+ thatleavesthecelltoreaccumulateduringactionpotentials.Inmyelinatedaxons,ioniccurrentsarerestrictedtothesmallfractionofthemembranesurfaceatthenodesofRanvier.Forthisreason,farfewerionstraverseaunitlengthoffibermembrane,andmuchlessionpumping—andenergyexpenditure—isnecessarytomaintainthegradients.