Brain, Vol. 125, No. 4, 844-860,
April 2002
© 2002 Guarantors of Brain
Post-ischaemic long-term synaptic potentiation in the striatum: a putative mechanism for cell type-specific vulnerability
1 Clinica Neurologica, Dipartimento di Neuroscienze, Università di Tor Vergata and IRCCS Fondazione Santa Lucia, Rome, Italy
Correspondence to: Paolo Calabresi, Clinica Neurologica, Dipartimento di Neuroscienze, Università di Tor Vergata, Via di Tor Vergata 135, 00133 Rome, Italy E-mail: calabre{at}uniroma2.it
In the present in vitro study of rat brain, we report that transient oxygen and glucose deprivation (in vitro ischaemia) induced a post-ischaemic long-term synaptic potentiation (i-LTP) at corticostriatal synapses. We compared the physiological and pharmacological characteristics of this pathological form of synaptic plasticity with those of LTP induced by tetanic stimulation of corticostriatal fibres (t-LTP), which is thought to represent a cellular substrate of learning and memory. Activation of N-methyl-D-aspartate (NMDA) receptors was required for the induction of both forms of synaptic plasticity. The intraneuronal injection of the calcium chelator BAPTA [bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetate] and inhibitors of the mitogen-activated protein kinase pathway blocked both forms of synaptic plasticity. However, while t-LTP showed input specificity, i-LTP occurred also at synaptic pathways inactive during the ischaemic period. In addition, scopolamine, a muscarinic receptor antagonist, prevented the induction of t-LTP but not of i-LTP, indicating that endogenous acetylcholine is required for physiological but not for pathological synaptic potentiation. Finally, we found that striatal cholinergic interneurones, which are resistant to in vivo ischaemia, do not express i-LTP while they express t-LTP. We suggest that i-LTP represents a pathological form of synaptic plasticity that may account for the cell type-specific vulnerability observed in striatal spiny neurones following ischaemia and energy deprivation.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  I. Galea, F. Norwood, M. J. Phillips, C. Shearman, P. McMonagle, and W. R. Gibb Pearls & Oy-sters: Resolution of hemichorea following endarterectomy for severe carotid stenosis Neurology, December 9, 2008; 71(24): e80 - e82. [Full Text] [PDF]
|
|
|
|
 |
|
 N.-W. Hu, I. M. Smith, D. M. Walsh, and M. J. Rowan Soluble amyloid-{beta} peptides potently disrupt hippocampal synaptic plasticity in the absence of cerebrovascular dysfunction in vivo Brain, September 1, 2008; 131(9): 2414 - 2424. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Zhang, P. Deng, Y. Ruan, and Z. C. Xu Dopamine D1-Like Receptors Depress Excitatory Synaptic Transmissions in Striatal Neurons After Transient Forebrain Ischemia Stroke, August 1, 2008; 39(8): 2370 - 2376. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Tortiglione, B. Picconi, I. Barone, D. Centonze, S. Rossi, C. Costa, M. Di Filippo, A. Tozzi, M. Tantucci, G. Bernardi, et al. Na+/Ca2+ Exchanger Maintains Ionic Homeostasis in the Peri-Infarct Area Stroke, May 1, 2007; 38(5): 1614 - 1620. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Costa, G. Martella, B. Picconi, C. Prosperetti, A. Pisani, M. Di Filippo, F. Pisani, G. Bernardi, and P. Calabresi Multiple Mechanisms Underlying the Neuroprotective Effects of Antiepileptic Drugs Against In Vitro Ischemia Stroke, May 1, 2006; 37(5): 1319 - 1326. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Zhang, P. Deng, Y. Li, and Z. C. Xu Enhancement of Excitatory Synaptic Transmission in Spiny Neurons After Transient Forebrain Ischemia J Neurophysiol, March 1, 2006; 95(3): 1537 - 1544. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Costa, G. Leone, E. Saulle, F. Pisani, G. Bernardi, and P. Calabresi Coactivation of GABAA and GABAB Receptor Results in Neuroprotection During In Vitro Ischemia Stroke, February 1, 2004; 35(2): 596 - 600. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z.-P. Pang, P. Deng, Y.-W. Ruan, and Z. C. Xu Depression of Fast Excitatory Synaptic Transmission in Large Aspiny Neurons of the Neostriatum after Transient Forebrain Ischemia J. Neurosci., December 15, 2002; 22(24): 10948 - 10957. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Saulle, D. Centonze, A. B. Martin, R. Moratalla, G. Bernardi, and P. Calabresi Endogenous Dopamine Amplifies Ischemic Long-Term Potentiation via D1 Receptors Stroke, December 1, 2002; 33(12): 2978 - 2984. [Abstract] [Full Text] [PDF]
|
|