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ABSTRACT Hippocampal long-term potentiation (LTP) is a cellular model of learning and memory. An early form of LTP (E-LTP) can be reinforced into its late form (L-LTP) by various behavioral interactions within a specific time window ('behavioral LTP-reinforcement'). Depending on the type and procedure used, various studies have shown that stress differentially affects synaptic plasticity. Under low stress, such as novelty detection or mild foot shocks, E-LTP can be transformed into L-LTP in the rat dentate gyrus (DG). A reinforcing effect of a 2-min swim, however, has only been shown in (Korz and Frey (2003) J Neurosci 23:7281-7287; Korz and Frey (2005) J Neurosci 25:7393-7400; Ahmed et al. (2006) J Neurosci 26:3951-3958; Sajikumar et al., (2007) J Physiol 584.2:389-400) so far. We have reinvestigated these studies using the same as well as an improved recording technique which allowed the recording of field excitatory postsynaptic potentials (fEPSP) and the population spike amplitude (PSA) at their places of generation in freely moving rats. We show that acute swim stress led to a long-term depression (LTD) in baseline values of PSA and partially fEPSP. In contrast to earlier studies a LTP-reinforcement by swimming could never be reproduced. Our results indicate that 2-min swim stress influenced synaptic potentials as well as E-LTP negatively. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Well known as the center for learning and memory, hippocampus is the crucial brain region to study synaptic plasticity in the context of cellular fundamental mechanisms such as long‐term depression (LTD) and long‐term potentiation (LTP). However, despite years of extensive research, the key to our LTD queries and their induction mechanisms has not been fully understood. Previously, we reported the induction of late‐LTD (L‐LTD) in the distally located synapses of apical branch of hippocampal CA1 dendrites using strong low‐frequency stimulation (SLFS). In contrast synapses at the proximal site could not express L‐LTD. Thus, in the present study, we wanted to investigate whether or not synapses of apical dendritic branch at the proximal location could induce and maintain LTD and its related properties in in vitro rat hippocampal slices. Results indicated that the SLFS in the distal and proximal region triggered the plasticity related proteins (PRP) synthesis in both regions, as evident by the induction and maintenance of L‐LTD in the distal region by virtue of synaptic and cross‐tagging. In addition, the application of emetine at the time of proximal input stimulation prevented the transition of early‐LTD (E‐LTD) into L‐LTD at the distal region, proving PRP synthesis at the proximal site. Further, it was observed that weak low‐frequency stimulation (WLFS) could induce E‐LTD in the proximal region along with LTD‐specific tag‐setting at the synapses. In conclusion, the current study suggests unique findings that the synaptic and cross‐tagging mediate L‐LTD expression is maintained in the proximal location of hippocampus apical CA1 dendrites. [ABSTRACT FROM AUTHOR]