Synaptic plasticity in hippocampal CA1 neurons and learning behavior in transient ischemia-loaded gerbils

Abstract

We studied the synaptic plasticity of hippocampal CA1 neurons and spatial learning behavior in gerbils that had been loaded with a transient cerebral ischemia caused by 5 min or 10 min occlusion of the bilateral carotid arteries. The stimulus threshold to elicit the field responses after a transient cerebral ischemia was not different from that in controls, but there was a significant decrease in the magnitude of synaptic responses, which might result from the observed loss of neurons. Long-term potentiation (LTP) and depotentiation after a 10 min cerebral ischemia expressed as a percentage of the pre-tetanus or pre-low frequency stimulation value were almost the same as those in controls, although the actual magnitude of the LTP and depotentiation was lower than in controls. Gerbils that were loaded with a 10 min cerebral ischemia showed impairment in a spatial learning test when this was started 10 days after the cerebral ischemia, but not when it was started 20 days after the same cerebral ischemia. These results suggest that the changes in electrophysiological properties of hippocampal CA1 neurons seen at 10 days after a 10 min cerebral ischemia contribute to the impairment of spatial learning of gerbils seen at this time, and that the extra-CA1 regions might be involved in the recovery of spatial learning seen at 20 days after cerebral ischemia.

Increasing small conductance Ca2+‐activated potassium channel activity reverses ischemia‐induced impairment of long‐term potentiation

“…We observe rapid and sustained loss of synaptic plasticity (LTP) in the CA1 synapses of mice following CA‐induced cerebral ischemia, consistent with the extensive literature indicating that global cerebral ischemia causes selective CA1 injury. The data remain unclear regarding the effects of global cerebral ischemia on hippocampal synaptic plasticity, with studies demonstrating no impairment (Li et al ., ) and several studies reporting impaired LTP during the first week following global ischemia (Mori et al ., ; Gillardon et al ., ; Kiprianova et al ., ; Dai et al ., ; Nagy et al ., ). Our data are consistent with the large number of reports demonstrating deficits in synaptic plasticity following global cerebral ischemia and provide important new information regarding the timing of onset and duration of impaired synaptic plasticity.…”

Ischemic LTP: NMDA‐dependency and dorso/ventral distribution within the hippocampus

“…Ischemia involving oxygen deprivation can cause catastrophic, persistent damage in brain tissue (Calabresi et al, ; Di Filippo et al, ). One of the earliest events that follow oxygen/glucose deprivation (OGD) in the brain is a massive release of glutamate (Wahl et al, ) associated with a marked reduction in the evoked responses to afferent stimulation both in vivo (Miyamoto et al, ; Li et al, ) and in vitro (Crepel et al, ; Ai and Baker, ). Surprisingly, following termination of a brief OGD (3min) in vitro and replacement of normal recording medium, afferent reactivity rises persistently above baseline level, to produce what is known as ischemic LTP (iLTP; Crepel et al, ).…”

The importance of neuronal plasticity in the prognosis of cases of cerebral ischemia: a systematic review

“…Li J et al [92] 2013 Biomedical Research (Japan) Male mongolian gerbils, aged 13 to 16 weeks with a body weight of 60 to 80 g, were housed one to a cage in the Animal Center of our university on a 12-h/12-h light/dark cycle at a room temperature of about 23ºC with free access to rodent food.…”

“…It was shown that the hippocampal synaptic plasticity is considered to be the cellular basis of learning and memory in the brain. [90,92] For example, in relation to the Gabaergic receptor, altered receptor binding in the hippocampus would contribute to spatial learning deficits. [22] There are findings indicating, also, that a different function for HCN1 channels is found in hippocampal CA1 neurons.…”

“…Chronic cerebral ischemia is the common pathological process of the development of various diseases, such as Vascular Dementia, Alzheimer's disease and Binswanger's disease, and eventually cause cognitive impairment [1,33]. It was also noticed that the cerebral ischemia resulting from an inadequate supply of blood and oxygen to the brain due to cerebrovascular disease, cardiac arrest, or traumatic brain injury is often accompanied by neuropsychiatric symptoms [2,3,4,92]. In an attempt to mitigate these negative consequences, the body develops some defenses, such as motor cortex neuronal changes within motor cortex that include up regulation of trophic factors, like BDNF, attacking increase in protein synthesis, synaptogenesis, and map reorganization [5,120], because recovery might be enhanced not only by dampening inflammation, but also by increasing synaptic and structural plasticity [6].…”