Some Special Characteristics of Synaptic Transmission

Fatigue of Synaptic Transmission. When excitatory synapses are repetitively stimulated at a rapid rate, the number of discharges by the postsynaptic neuron is at first very great, but the firing rate becomes progressively less in succeeding milliseconds or seconds. This is called fatigue of synaptic transmission.

Fatigue is an exceedingly important characteristic of synaptic function because when areas of the nervous system become overexcited, fatigue causes them to lose this excess excitability after awhile. For example, fatigue is probably the most important means by which the excess excitability of the brain during an epileptic seizure is finally subdued so that the seizure ceases. Thus, the development of fatigue is a protective mechanism against excess neuronal activity. This is discussed further in the description of reverberating neuronal circuits in Chapter 46.

The mechanism of fatigue is mainly exhaustion or partial exhaustion of the stores of transmitter substance in the presynaptic terminals. The excitatory terminals on many neurons can store enough excitatory transmitter to cause only about 10,000 action potentials, and the transmitter can be exhausted in only a few seconds to a few minutes of rapid stimulation. Part of the fatigue process probably results from two other factors as well: (1) progressive inactivation of many of the postsynaptic membrane receptors and (2) slow development of abnormal concentrations of ions inside the postsynaptic neuronal cell.

Effect of Acidosis or Alkalosis on Synaptic Transmission. Most neurons are highly responsive to changes in pH of the surrounding interstitial fluids. Normally, alkalosis greatly increases neuronal excitability. For instance, a rise in arterial blood pH from the 7.4 norm to 7.8 to 8.0 often causes cerebral epileptic seizures because of increased excitability of some or all of the cerebral neurons. This can be demonstrated especially well by asking a person who is predisposed to epileptic seizures to overbreathe. The overbreathing blows off carbon dioxide and therefore elevates the pH of the blood momentarily, but even this short time can often precipitate an epileptic attack.

Conversely, acidosis greatly depresses neuronal activity; a fall in pH from 7.4 to below 7.0 usually causes a comatose state. For instance, in very severe diabetic or uremic acidosis, coma virtually always develops.

Effect of Hypoxia on Synaptic Transmission. Neuronal excitability is also highly dependent on an adequate supply of oxygen. Cessation of oxygen for only a few seconds can cause complete inexcitability of some neurons. This is observed when the brain's blood flow is temporarily interrupted, because within 3 to 7 seconds, the person becomes unconscious.

Effect of Drugs on Synaptic Transmission. Many drugs are known to increase the excitability of neurons, and others are known to decrease excitability. For instance, caffeine, theophylline, and theobromine, which are found in coffee, tea, and cocoa, respectively, all increase neuronal excitability, presumably by reducing the threshold for excitation of neurons.

Strychnine is one of the best known of all agents that increase excitability of neurons. However, it does not do this by reducing the threshold for excitation of the neurons; instead, it inhibits the action of some normally inhibitory transmitter substances, especially the inhibitory effect of glycine in the spinal cord. Therefore, the effects of the excitatory transmitters become overwhelming, and the neurons become so excited that they go into rapidly repetitive discharge, resulting in severe tonic muscle spasms.

Most anesthetics increase the neuronal membrane threshold for excitation and thereby decrease synaptic transmission at many points in the nervous system. Because many of the anesthetics are especially lipid-soluble, it has been reasoned that some of them might change the physical characteristics of the neuronal membranes, making them less responsive to excitatory agents.

Synaptic Delay. During transmission of a neuronal signal from a presynaptic neuron to a postsynaptic neuron, a certain amount of time is consumed in the process of (1) discharge of the transmitter substance by the presy-naptic terminal, (2) diffusion of the transmitter to the postsynaptic neuronal membrane, (3) action of the transmitter on the membrane receptor, (4) action of the receptor to increase the membrane permeability, and (5) inward diffusion of sodium to raise the excitatory postsynaptic potential to a high enough level to elicit an action potential. The minimal period of time required for all these events to take place, even when large numbers of excitatory synapses are stimulated simultaneously, is about 0.5 millisecond. This is called the synaptic delay. Neurophysiologists can measure the minimal delay time between an input volley of impulses into a pool of neurons and the consequent output volley. From the measure of delay time, one can then estimate the number of series neurons in the circuit.


Albright TD, Jessell TM, Kandell ER, Posner MI: Progress in the neural sciences in the century after Cajal (and the mysteries that remain). Ann N Y Acad Sci 929:11, 2001.

Boehning D, Snyder SH: Novel neural modulators. Annu Rev Neurosci 26:105, 2003.

Brasnjo G, Otis TS: Glycine transporters not only take out the garbage, they recycle. Neuron 40:667, 2003.

Cowley MA, Cone RD, Enriori P, et al: Electrophysiological actions of peripheral hormones on melanocortin neurons. Ann N Y Acad Sci 994:175, 2003.

Engelman HS, MacDermott AB: Presynaptic inotropic receptors and control of transmitter release. Nat Rev Neu-rosci 5:135, 2004.

Girault JA, Greengard P: The neurobiology of dopamine signaling. Arch Neurol 61:641, 2004.

Haines DE: Fundamental Neuroscience. New York: Churchill Livingstone, 1997.

Haines DE, Lancon JA: Review of Neuroscience. New York: Churchill Livingstone, 2003.

Kandel ER: The molecular biology of memory storage: a dialogue between genes and synapses. Science 294:1030, 2001.

Kandel ER, Schwartz JH, Jessell TM: Principles of Neural Science, 4th ed. New York: McGraw-Hill, 2000.

Magee JC: Dendritic integration of excitatory synaptic input. Nat Rev Neurosci 1:181, 2000.

Migliore M, Shepherd GM: Emerging rules for the distributions of active dendritic conductances. Nat Rev Neurosci 3:362, 2002.

Muller D, Nikonenko I: Dynamic presynaptic varicosities: a role in activity-dependent synaptogenesis. Trends Neu-rosci 26:573, 2003.

Nicholls DG, Budd SL: Mitochondria and neuronal survival. Physiol Rev 80:315, 2000.

Nimchinsky EA, Sabatin BL, Svoboda K: Structure and function of dendritic spines. Annu Rev Physiol 64:313, 2002.

Prast H, Philippu A: Nitric oxide as modulator of neuronal function. Prog Neurobiol 64:51, 2001.

Reid CA, Bekkers JM, Clements JD: Presynaptic Ca2+ channels: a functional patchwork.Trends Neurosci 26:683,2003.

Robinson RB, Siegelbaum SA: Hyperpolarization-activated cation currents: from molecules to physiological function. Annu Rev Physiol 65:453, 2003.

Ruff RL: Neurophysiology of the neuromuscular junction: overview. Ann N Y Acad Sci 998:1, 2003.

Schmolesky MT, Weber JT, De Zeeuw CI, Hansel C: The making of a complex spike: ionic composition and plasticity. Ann N Y Acad Sci 978:359, 2002.

Semyanov A, Walker MC, Kullmann DM, Silver RA: Tonically active GABA A receptors: modulating gain and maintaining the tone. Trends Neurosci 27:262, 2004.

Stern JE: Nitric oxide and homeostatic control: an intercellular signaling molecule contributing to autonomic and neuroendocrine integration? Prog Biophys Mol Biol 84: 197, 2004.

Timofeev I, Steriade M: Neocortical seizures: initiation, development and cessation. Neuroscience 123:299, 2004.

Tsay D, Yuste RL: On the electrical function of dendritic spines. Trends Neurosci 27:77, 2004.

West AR, Floresco SB, Charara A, et al: Electrophysiologi-cal interactions between striatal glutamatergic and dopaminergic systems. Ann N Y Acad Sci 1003:53, 2003.

Williams SR, Stuart GJ: Role of dendritic synapse location in the control of action potential output. Trends Neurosci 26:147, 2003.

Zucker RS, Regehr WG: Short-term synaptic plasticity. Annu Rev Physiol 64:355, 2002.

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  • maximilian
    How alkalosis increases neuronal excitability?
    5 years ago
  • justiina
    How alkolosis increase synaptic transmission?
    5 years ago
  • Severi
    How does acidosis affect synaptic transmission?
    4 years ago
  • furio
    How tea increases synaptic transmission?
    4 years ago
  • marvin
    How does alkalosis affect neuronal excitability?
    4 years ago
  • edward
    How acidiosis and alkaliosis change excitablity of neurons?
    4 years ago
  • thomas
    What is the charactrestics of synaptic transmission?
    4 years ago
    How tea increase excitement to neuron?
    4 years ago
  • ellis baugh
    What is the effect of ph on synaptic transmission?
    4 years ago
  • sebastian
    What are the characteristic of synapses?
    4 years ago
  • teodros
    Why alkalosis cause excitation?
    4 years ago
  • doderic
    How acidosis decreases excitability of neurons?
    3 years ago
  • Cedivar
    What are characteristics of synaptic transmission?
    3 years ago
  • Cillian
    How alkalosis causes increased neuronal activity?
    3 years ago
  • michael
    What are the characterstic of synaptuc transmition?
    3 years ago
  • bellisima
    What is the mecanism by which acidosis decrease excitability in synapse?
    3 years ago
  • Luca Ricci
    What is the characterise of synaptic transmision un darectly?
    2 years ago
  • bildad
    What is the characters of synapse?
    1 year ago
  • christian k
    Does caffeine increase synaptic transmission?
    3 months ago
  • christin
    What is the effect of acidosis or alkalosis on synaptictransmission?
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