Activity-Dependent Release of Adenosine Contributes to Short-Term Depression at CA3-CA1 Synapses in Rat Hippocampus

Brager, Darrin H.; Thompson, Scott M.

doi:10.1152/jn.00554.2002

Cited by 20 publications

(18 citation statements)

References 27 publications

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“…Previous studies have shown that activity-dependent increases in adenosine and activation of presynaptic A1 receptors can inhibit transmitter release at Schaffer collateral fiber inputs onto CA1 pyramidal cells, although only during much higher frequencies of synaptic stimulation than those used in our experiments (Brager and Thompson 2003;Manzoni et al 1994;Mitchell et al 1993). We find, however, that monosynaptic EPSPs elicited by Schaffer collateral fiber stimulation are not inhibited by short trains of 1-Hz stimulation.…”

Section: Activity-dependent Modulation Of Recurrent Synaptic Connecticontrasting

confidence: 59%

Activity-Dependent Depression of Local Excitatory Connections in the CA1 Region of Mouse Hippocampus

Fink

Sariñana²,

Gray³

et al. 2007

Journal of Neurophysiology

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Fink AE, Sarinana J, Gray EE, O'Dell TJ. Activity-dependent depression of local excitatory connections in the CA1 region of mouse hippocampus. J Neurophysiol 97: 3926 -3936, 2007. First published April 4, 2007 doi:10.1152/jn.00213.2007. The existence of recurrent excitatory synapses between pyramidal cells in the hippocampal CA1 region has been known for some time yet little is known about activity-dependent forms of plasticity at these synapses. Here we demonstrate that under certain experimental conditions, Schaffer collateral/commissural fiber stimulation can elicit robust polysynaptic excitatory postsynaptic potentials due to recurrent synaptic inputs onto CA1 pyramidal cells. In contrast to CA3 pyramidal cell inputs, recurrent synapses onto CA1 pyramidal cells exhibited robust pairedpulse depression and a sustained, but rapidly reversible, depression in response to low-frequency trains of Schaffer collateral fiber stimulation. Blocking GABA B receptors abolished paired-pulse depression but had little effect on low-frequency stimulation (LFS)-induced depression. Instead, LFS-induced depression was significantly attenuated by an inhibitor of A1 type adenosine receptors. Blocking the postsynaptic effects of GABA B and A1 receptor activation on CA1 pyramidal cell excitability with an inhibitor of G-protein-activated inwardly rectifying potassium channels had no effect on either pairedpulse depression or LFS-induced depression. Thus activation of presynaptic GABA B and adenosine receptors appears to have an important role in activity-dependent depression at recurrent synapses. Together, our results indicate that CA3-CA1 and CA1-CA1 synapses exhibit strikingly different forms of short-term synaptic plasticity and suggest that activity-dependent changes in recurrent synaptic transmission can transform the CA1 region from a sparsely connected recurrent network into a predominantly feedforward circuit.

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Section: Activity-dependent Modulation Of Recurrent Synaptic Connecticontrasting

confidence: 59%

Activity-Dependent Depression of Local Excitatory Connections in the CA1 Region of Mouse Hippocampus

Fink

Sariñana²,

Gray³

et al. 2007

Journal of Neurophysiology

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“…1) indicates that the local synthesis/replenishment of ATP can occur at sites of high activity and independently of mitochondria, at least in the short-term, and may permit the "on-demand" nature of synaptic adenosine release which dampens presynaptic excitation [85][86][87][88]. This local, extra-mitochondrial, generation of ATP has an important additional advantage in the context of brain injury due to the mitochondrial dysfunction that can follow.…”

Section: The Purine Salvage Pathway As the Vehicle For Atp Replenishmentmentioning

confidence: 99%

The Purine Salvage Pathway and the Restoration of Cerebral ATP: Implications for Brain Slice Physiology and Brain Injury

Frenguelli

2017

Neurochem Res

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Brain slices have been the workhorse for many neuroscience labs since the pioneering work of Henry McIlwain in the 1950s. Their utility is undisputed and their acceptance as appropriate models for the central nervous system is widespread, if not universal. However, the skeleton in the closet is that ATP levels in brain slices are lower than those found in vivo, which may have important implications for cellular physiology and plasticity. Far from this being a disadvantage, the ATP-impoverished slice can serve as a useful and experimentally-tractable surrogate for the injured brain, which experiences similar depletion of cellular ATP. We have shown that the restoration of cellular ATP in brain slices to in vivo values is possible with a simple combination of d-ribose and adenine (RibAde), two substrates for ATP synthesis. Restoration of ATP in slices to physiological levels has implications for synaptic transmission and plasticity, whilst in the injured brain in vivo RibAde shows encouraging positive results. Given that ribose, adenine, and a third compound, allopurinol, are all separately in use in man, their combined application after acute brain injury, in accelerating ATP synthesis and increasing the reservoir of the neuroprotective metabolite, adenosine, may help reduce the morbidity associated with stroke and traumatic brain injury.

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“…The antagonist eliminated age differences in theta-burst facilitation, suggesting that adenosine build-up during the train either (1) disrupts the facilitation process itself or (2) simply depresses release and thereby offsets the effects of facilitation. It is likely that TBS elevates extracellular adenosine levels given evidence that afferent activity releases adenosine in hippocampus (Schubert et al, 1976;Dunwiddie and Masino, 2001) to a degree sufficient to cause homosynaptic and heterosynaptic depression (Mitchell et al, 1993;Brager and Thompson, 2003). These physiological effects appear within 50 ms and are generated by short afferent bursts (Mitchell et al, 1993), conditions that fall well within the parameters of TBS.…”

Section: Discussionmentioning

confidence: 97%

Long-Term Potentiation Is Impaired in Middle-Aged Rats: Regional Specificity and Reversal by Adenosine Receptor Antagonists

Rex¹,

Kramár²,

Colgin³

et al. 2005

J. Neurosci.

126

106

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Memory loss in humans begins early in adult life and progresses thereafter. It is not known whether these losses reflect the failure of cellular processes that encode memory or disturbances in events that retrieve it. Here, we report that impairments in hippocampal long-term potentiation (LTP), a form of synaptic plasticity associated with memory, are present by middle age in rats but only in select portions of pyramidal cell dendritic trees. Specifically, LTP induced with theta-burst stimulation in basal dendrites of hippocampal field CA1 decayed rapidly in slices prepared from 7-to 10-month-old rats but not in slices from young adults. There were no evident age-related differences in LTP in the apical dendrites. Both the adenosine A 1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine and a positive AMPA receptor modulator (ampakine) offset age-related LTP deficits. Adenosine produced greater depression of synaptic responses in middle-aged versus young adult slices and in basal versus apical dendrites. These results were not associated with variations in A 1 receptor densities and may instead reflect regional and age-related differences in adenosine clearance. Pertinent to this, brief applications of A 1 receptor antagonists immediately after theta stimulation fully restored LTP in middle-aged rats. We hypothesize that the build-up of extracellular adenosine during theta activity persists into the postinduction period in the basal dendrites of middle-aged slices and thereby activates the A 1 receptor-dependent LTP reversal effect. Regardless of the underlying mechanism, the present results provide a candidate explanation for memory losses during normal aging and indicate that, with regard to plasticity, different segments of pyramidal neurons age at different rates.

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Activity-Dependent Release of Adenosine Contributes to Short-Term Depression at CA3-CA1 Synapses in Rat Hippocampus

Cited by 20 publications

References 27 publications

Activity-Dependent Depression of Local Excitatory Connections in the CA1 Region of Mouse Hippocampus

Activity-Dependent Depression of Local Excitatory Connections in the CA1 Region of Mouse Hippocampus

The Purine Salvage Pathway and the Restoration of Cerebral ATP: Implications for Brain Slice Physiology and Brain Injury

Long-Term Potentiation Is Impaired in Middle-Aged Rats: Regional Specificity and Reversal by Adenosine Receptor Antagonists

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