Glutamate-induced glutamate release: A proposed mechanism for calcium bursting in astrocytes

Abstract

Here we present a new model for the generation of complex calcium-bursting patterns in astrocytes, a type of brain cell recently implicated in a variety of neural functions including memory formation. The model involves two positive feedback processes, in which the key feedback species are calcium ion and glutamate. The latter is the most abundant excitatory neurotransmitter in the brain and has been shown to be involved in bidirectional communication between astrocytes and nearby neurons. The glutamate feedback process considered here is shown to be critical for the generation of complex bursting oscillations in the astrocytes and to, perhaps, code for information which may be passed from neuron to neuron via the astrocyte. These processes may be involved in memory storage and formation as well as in mechanisms which lead to dynamical diseases such as epilepsy.

Spinal Astrocyte Glutamate Receptor 1 Overexpression after Ischemic Insult Facilitates Behavioral Signs of Spasticity and Rigidity

“…These data are consistent with our in vitro experiments showing AMPA-evoked glutamate release using pure astrocyte cultures. Together, these data support a theorized positive-feedback system whereby glutamate released by astrocytes autoactivates glutamate receptors found on astrocyte membranes, further triggering Ca 2ϩ oscillations and maintaining an increased glutamate concentration in the local milieu (Carmignoto, 2000;Parri et al, 2001;Larter and Craig, 2005).…”

Diffuse TBI-induced expression of anxiety-like behavior coincides with altered glutamatergic function, TrkB protein levels and region-dependent pathophysiology in amygdala circuitry

“…Reduced glutamate release indicates less stores available for potential neuronal communication between those located in presynaptic neurons, interneurons, and astrocytic processes. The second peak within the biphasic profile of KCl-evoked glutamate release ( Figure 2G) provides evidence that glial transmission could be contributing to glutamate overflow whereas the first peak is thought to primarily be the response of presynaptic neurons 55,56 . While the amplitude of the first peaks was significantly decreased at 28DPI compared to shams (data not shown), area under the curve was used to evaluate all aspects of glutamate neurotransmission.…”

On the Integration of Physiological Mechanisms in the Nervous Tissue Using the Mtip: Synaptic Plasticity Depending on Neurons-Astrocytes-Capillaries Interactions

“…We believe that our present methods can decrease this incertitude. For example, in the proposed illustration of learning and memory function, we know that some potential component models are not yet included in our system; some examples are: (i) in the presynaptic bouton: calcium dependent mechanism of glutamate release [6], endogenous and exogenous calcium buffers, and voltage dependent calcium channel [20], full glutamate synthesis mechanism [23,32], ATP-driven plasma membrane calcium pumps [21] Na + /Ca 2+ exchanger [29] (also see Refs. 23 and 32).…”

“…23 and 32). (ii) In the dendritic spine: metabotropic glutamate receptor [7], endogenous and exogenous calcium buffers [20], ATP-driven plasma membrane calcium pumps [21], Na + /Ca 2+ exchanger [29]. (iii) In the astrocyte: full glutamate synthesis mechanism [23,32] and glutamate induced glutamate release [30].…”