Theaxon hillockis a specialized part of the cell body (orsoma) of aneuronthat connects to theaxon.It can be identified usinglight microscopyfrom its appearance and location in a neuron and from its sparse distribution ofNissl substance.[1]
| Axon hillock | |
|---|---|
 Red labeled is pointing directly at the axon hillock. | |
| Details | |
| Part of | Axonof anerve |
| System | Nervous system |
| Identifiers | |
| Latin | colliculus axonis |
| TH | H2.00.06.1.00006 |
| Anatomical terminology | |
The axon hillock is the last site in the soma wheremembrane potentialspropagated fromsynaptic inputsaresummatedbefore being transmitted to the axon.[2]For many years, it was believed that the axon hillock was the usual site of initiation ofaction potentials—thetrigger zone.It is now thought that the earliest site of action potential initiation is at theaxonal initial segment:just between the peak of the axon hillock and the initial (unmyelinated) segment of theaxon.[3]However, the positive point, at which the action potential starts, varies between cells.[citation needed]It can also be altered by hormonal stimulation of the neuron, or bysecond messengereffects of neurotransmitters.[citation needed]
The axon hillock also delineates separate membrane domains between the cell body and axon.[4] This allows for localization ofmembrane proteinsto either the axonal or somal side of the cell.
Structure
editThe axon hillock and initial segment have a number of specialized properties that make them capable of action potential generation, including adjacency to the axon and a much higher density ofvoltage-gated ion channelsthan is found in the rest of the cell body.[5] Indorsal root ganglioncells, the cell body is thought to have approximately 1voltage-gated sodium channelper square micrometre, while the axon hillock and initial segment of theaxonhave about ~100–200voltage-gated sodium channelsper square micrometre; in comparison, thenodes of Ranvieralong the axon are thought to have ~1000–2000 such channels per square micrometre.[6] This clustering of voltage-gated ion channels is a consequence of plasma-membrane and cytoskeletal associating proteins such asankyrin.[7]
In electrophysiological models, the axon hillock is included with theinitial segmentof the axon wheremembrane potentialspropagated fromsynaptic inputsto the dendrites or cell body aresummed.[citation needed]
Function
editBoth inhibitory postsynaptic potentials (IPSPs) and excitatory postsynaptic potentials (EPSPs) are summed in the axon hillock and once a triggering threshold is exceeded, anaction potentialpropagates through the rest of the axon (and "backwards" towards the dendrites as seen inneural backpropagation). The triggering is due topositive feedbackbetween highly crowdedvoltage-gated sodium channels,which are present at the critical density at the axon hillock (and nodes of ranvier) but not in the soma.
In its resting state, a neuron is polarized, with its inside at about −70 mV relative to its surroundings. When anexcitatory neurotransmitteris released by thepresynaptic neuronand binds to the postsynaptic dendritic spines,ligand-gated ion channelsopen, allowing sodium ions to enter the cell. This may make the postsynaptic membrane depolarized (less negative). Thisdepolarizationwill travel towards the axon hillock, diminishing exponentially with time and distance. If several such events occur in a short time, the axon hillock may become sufficiently depolarized for the voltage-gatedsodium channelsto open. This initiates an action potential that then propagates down the axon.
As sodium enters the cell, the cell membrane potential becomes more positive, which activates even more sodium channels in the membrane. The sodium influx eventually overtakes the potassium efflux (via thetwo-pore-domain potassium channelsorleak channels,initiating a positive feedback loop (rising phase). At around +40 mV, the voltage-gated sodium channels begin to close (peak phase) and the voltage-gated potassium channels begin to open, moving potassium down its electrochemical gradient and out of the cell (falling phase).
The potassium channels exhibit a delayed reaction to the membrane repolarisation, and, even after theresting potentialis achieved, some potassium continues to flow out, resulting in an intracellular fluid that is more negative than the resting potential, and during which no action potential can begin (undershoot phase/refractory period). This undershoot phase ensures that the action potential propagates down the axon and not back up it.
Once this initial action potential is initiated, principally at the axon hillock, it propagates down the length of the axon. Under normal conditions, the action potential would attenuate very quickly due to the porous nature of the cell membrane. To ensure faster and more efficient propagation of action potentials, the axon ismyelinated.Myelin, a derivative of cholesterol, acts as an insulating sheath and ensures that the signal cannot escape through the ion or leak channels. There are, nevertheless, gaps in the insulation (nodes of Ranvier), which boost the signal strength. As the action potential reaches a node of Ranvier, it depolarises the cell membrane. As the cell membrane is depolarised, the voltage-gated sodium channels open and sodium rushes in, triggering a fresh new action potential.
References
edit- ^Palay, Sanford L.; Sotelo, Constantino; Peters, Alan; Orkand, Paula M. (1968)."The Axon Hillock and the Initial Segment".The Journal of Cell Biology.38(1): 193–201.doi:10.1083/jcb.38.1.193.PMC2107452.PMID5691973.
- ^Hemmings, Hugh C.; Egan, Talmage D. (2012-12-06).Pharmacology and Physiology for Anesthesia E-Book: Foundations and Clinical Application.Elsevier Health Sciences.ISBN9781455737932.
- ^Clark BD, Goldberg EM, Rudy B (December 2009)."Electrogenic Tuning of the Axon Initial Segment".Neuroscientist.15(6): 651–668.doi:10.1177/1073858409341973.PMC2951114.PMID20007821.
- ^Kobayashi, Toshihide; Storrie, Brian; Simons, Kai; Dotti, Carlos (15 October 1992)."A functional barrier to movement of lipids in polarized neurons".Nature.359(6396): 647–650.Bibcode:1992Natur.359..647K.doi:10.1038/359647a0.PMID1406997.S2CID4325727.
- ^Wollner D, Catterall WA (November 1986)."Localization of sodium channels in axon hillocks and initial segments of retinal ganglion cells".Proceedings of the National Academy of Sciences of the United States of America.83(21): 8424–28.Bibcode:1986PNAS...83.8424W.doi:10.1073/pnas.83.21.8424.PMC386941.PMID2430289.
- ^Safronov BV, Wolff M, Vogel W (February 1, 1999)."Axonal expression of sodium channels in rat spinal neurones during postnatal development".J. Physiol.514(3): 729–34.doi:10.1111/j.1469-7793.1999.729ad.x.PMC2269106.PMID9882745.
- ^Zhou D, Lambert S, Malen PL, Carpenter S, Boland LM, Bennett V (November 30, 1998)."AnkyrinG Is Required for Clustering of Voltage-gated Na Channels at Axon Initial Segments and for Normal Action Potential Firing".The Journal of Cell Biology.143(5): 1295–304.doi:10.1083/jcb.143.5.1295.PMC2133082.PMID9832557.
External links
edit- Histology image: 3_09at the University of Oklahoma Health Sciences Center - "Slide 3Spinal cord"
