Tripartite synapse

Tripartite synapse refers to the functional integration and physical proximity of the presynaptic membrane, postsynaptic membrane, and their intimate association with surrounding glia as well as the combined contributions of these three synaptic components to the production of activity at the chemical synapse.[1] Tripartite synapses occur at a number of locations in the central nervous system with astrocytes[1] and may also exist with Muller glia of retinal ganglion cells[2] and Schwann cells at the neuromuscular junction.[3] The term was first introduced in the late 1990s to account for a growing body of evidence that glia are not merely passive neuronal support cells but, instead, play an active role in the integration of synaptic information through bidirectional communication with the neuronal components of the synapse as mediated by neurotransmitters and gliotransmitters.[4]

Evidence of the Tripartite Synapse

Evidence for the role of astrocytes in the integration and processing of synaptic integration presents itself in a number of ways:

  • Astrocytes are excitable cells: In response to stimuli from any of the three components of the tripartite synapse, astrocytes are capable of producing transient changes in their intracellular calcium concentrations through release of calcium stores from the endoplasmic reticulum[5]
  • Astrocytes communicate bidirectionally with neurons: Through changes in their calcium concentration excitability, astrocytes are able to detect neurotransmitters and other signals released from neurons at the synapse[5] and can release their own neurotransmitters or gliotransmitters[6] that are, in turn, capable of modifying the electrophysiological excitability of neurons.[7]
  • Astrocytes are capable of responding selectively to stimuli: Astrocytes of the hippocampal stratum oriens form tripartite synapses with axonal projections from the alveus. The alveus projections can form either glutamatergic or cholinergic synapses with the stratum oriens, but the astrocytes of this region respond with changes in calcium concentration only to cholinergic activation of alveus projections.[8] This is not merely due to a sensitivity of these astrocytes exclusive to acetylcholine, as they will also respond to glutamatergic synaptic activity originating from a different brain region, the Schaffer collateral.[9]
  • Astrocytes integrate and modulate information from their synaptic inputs: Astrocytic calcium concentration changes in response to simultaneous stimulation by two neurotransmitter types is not always a linear summation (a linear summation being an increase in intracellular calcium concentration in the astrocyte in response to two simultaneous stimuli that would be the equivalent of adding the calcium concentration changes that would occur in response to each stimulation individually) of the effects of each individual input but varies by the transmitter combinations as well as frequency of stimulation. The hippocampal stratum oriens astrocytes, which respond to synaptic activity from glutamatergic neurons originating in the Schaffer collateral and cholinergic neurons originating in the alveus, produce changes in their intracellular calcium concentrations that is non-linear with the strength of synaptic input.[9] Additionally, these same stimuli are capable of producing either a potentiated calcium concentration response at low frequencies of stimulation or a depressed calcium concentration response at high frequencies of stimulation.[9]

References
  1. Araque, A (22 May 1999). "Tripartite synapses: glia, the unacknowledged partner". Trends in Neurosciences. 22 (5): 208–215. doi:10.1016/s0166-2236(98)01349-6. PMID 10322493.
  2. Newman, EA (1 June 1998). "Modulation of neuronal activity by gliaal cells in the retina". The Journal of Neuroscience. 18 (11): 4022–4028.
  3. Rochon, D (1 June 2001). "Synapse-glia interactions at the mammalian neuromuscular junction". The Journal of Neuroscience. 21 (11): 3819–3829.
  4. Perea, Gertrudis (15 July 2009). "Tripartite synapses: astrocytes process and control synaptic information". Trends in Neurosciences. 32 (8): 421–431. doi:10.1016/j.tins.2009.05.001. PMID 19615761.
  5. Perea, Gertrudis (September 2005). "Glial calcium signaling and neuron–glia communication". Cell Calcium. 38 (3–4): 375–382. doi:10.1016/j.ceca.2005.06.015. hdl:10261/154079.
  6. Volterra, A. The Tripartite Synapse: Glia in Synaptic Transmission. Chapter 13: Release of transmitters from glial cells.: Oxford University Press. pp. 164–184.CS1 maint: location (link)
  7. Newman, E.A. (2003). "New roles for astrocytes: regulation of synaptic transmission". Trends in Neurosciences. 26: 536–542. doi:10.1016/s0166-2236(03)00237-6. PMID 14522146.
  8. Araque, Alfonso (1 April 2002). "Synaptically released acetylcholine evokes Ca2+ elevations in astrocytes in hippocampal slices". The Journal of Neuroscience. 22 (7): 2443–2450. PMID 11923408.
  9. Perea, Gertrudis (16 March 2005). "Properties of Synaptically Evoked Astrocyte Calcium Signal Reveal Synaptic Information Processing by Astrocytes". The Journal of Neuroscience. 25 (9): 2192–2203. doi:10.1523/jneurosci.3965-04.2005. PMID 15745945.
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