Increased long‐term potentiation in the surround of experimentally induced focal cortical infarction

Abstract

Functional recovery after stroke is partly due to cortical reorganization on a structural as well as a functional level. Recent investigations have shown that the excitability of brain areas surrounding cortical ischemic lesions is increased, probably due to a down-regulation of gamma-aminobutyric acid-receptor activity. There is some evidence that these changes might increase the susceptibility of the lesioned brain for adaptive changes and recovery. Here, we investigated the propensity for the induction of long-term potentiation (LTP) in the surround of experimentally induced focal cortical infarcts in rat somatosensory cortex in vitro. By using standard paradigms, LTP induction was found to be facilitated ipsilaterally in slices of lesioned animals 1 week after lesion induction. In homotopic contralateral areas, LTP was not different from control values. As LTP is commonly associated with plasticity and learning, the results provide further evidence for the lesion-induced amplification of network plasticity, as it is required for the reshaping of cortical circuits by timely training procedures.

Reorganization of Visual Cortical Maps after Focal Ischemic Lesions

“…Axonal sprouting has been correlated with functional recovery (Stroemer et al, 1995) and has also been linked to enhanced synchronous neuronal activity in perilesion cortex (Carmichael and Chesselet, 2002). Another mechanism likely to contribute to the observed reorganization of functional maps is the increased propensity for synaptic long-term potentiation at the border of focal cortical lesions both in the somatosensory cortex (Hagemann et al, 1998) and in the visual cortex (Mittmann and Eysel, 2001). Experiments addressing modifications in cytoskeletal proteins and in the excitatory/inhibitory balance in our lesion model are currently being undertaken in our laboratory (A.Z.…”

Rodent models of focal stroke: Size, mechanism, and purpose

“…Witte and colleagues 122,123 have used the precise localization of these lesions for both in vivo and slice electrophysiological experiments that have shown increased baseline neuronal firing rates, diminished recurrent neuronal inhibition, and enhanced longterm potentiation after stroke. Diminished GABA␣ receptor binding and subunit expression, and increased NMDA receptor expression may underlie these physiological changes, and occur within a large region of cortex both ipsi-and contralateral to photothrombotic stroke.…”

Repetitive Task Practice: A Critical Review of Constraint-Induced Movement Therapy in Stroke

“…Suggested mechanisms for these map changes can be summarized to include the following: (1) resolution of edema and removal of necrotic tissue after CNS injury (62); (2) (77); (6) substitution from ipsilesional parallel pathways (77,91); (7) activation of ipsilateral (contralesional) pathways (88); (8) short-term potentiated responses after terminating repetitive stimulation (87); and (10) long-term potentiation (75,92).…”