Abstract
There is growing realization that the relationship between memory and stress/emotionality is complicated, and may include both memory enhancing and memory impairing aspects. It has been suggested that the underlying mechanisms involve amygdala modulation of hippocampal synaptic plasticity, such as long-term potentiation (LTP). We recently reported that while in CA1 basolateral amygdala (BLA) priming impaired theta stimulation induced LTP, it enhanced LTP in the dentate gyrus (DG). However, emotional and stressfull experiences were found to activate synaptic plasticity within the BLA, raising the possibility that BLA modulation of other brain regions may be altered as well, as it may depend on the way the BLA is activated or is responding. In previous studies BLA priming stimulation was relatively weak (1 V, 50 μs pulse duration). In the present study we assessed the effects of two stronger levels of BLA priming stimulation (1 V or 2 V, 100 μs pulse duration) on LTP induction in hippocampal DG and CA1, in anesthetized rats. Results show that 1V-BLA priming stimulation enhanced but 2V-BLA priming stimulation impaired DG LTP; however, both levels of BLA priming stimulation impaired CA1 LTP, suggesting that modulation of hippocampal synaptic plasticity by amygdala is dependent on the degree of amygdala activation. These findings suggest that plasticity-induced within the amygdala, by stressful experiences induces a form of metaplasticity that would alter the way the amygdala may modulate memory-related processes in other brain areas, such as the hippocampus.
Highlights
It is generally accepted that memory is organized in multiple brain systems that can functionally interact with each other (Squire and Zola, 1996; Thompson and Kim, 1996)
We examined the effects of two levels of basolateral amygdala (BLA) priming activation on synaptic plasticity in the perforant path (PP) input to the granule cells in the dentate gyrus (DG), and the ventral hippocampal commisure (vHC) input to the CA1 pyramidal cells of the hippocampus
The results show that 1V-BLA priming stimulation enhanced but 2V-BLA priming stimulation impaired DG long-term potentiation (LTP), whereas both levels of BLA priming stimulation impaired CA1 LTP
Summary
It is generally accepted that memory is organized in multiple brain systems that can functionally interact with each other (Squire and Zola, 1996; Thompson and Kim, 1996). It has been suggested that emotional arousal/stress activates the amygdala and that this activation, that of the basolateral amygdala (BLA), results in modulation of memory-related processes in the hippocampus (McGaugh, 2000; Richter-Levin and Akirav, 2000; Roozendaal, 2000; Packard and Cahill, 2001; Richter-Levin, 2004; LaBar and Cabeza, 2006). These two structures form a functional system relevant to the complicated effects of emotionality and stress on learning and memory (Kim and Diamond, 2002; Roozendaal, 2002; Prickaerts and Steckler, 2005; Lupien et al, 2007). Amygdala activation is suggested to mediate stress-induced impairment of hippocampusdependent memory (Akirav and Richter-Levin, 2006; Hurlemann et al, 2007a,b; Maroun and Akirav, 2008)
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