Long‐term depression induction and maintenance across regions of the apical branch of CA1 dendrites

Author:

Parvez Suhel12ORCID,Ramachandran Binu23ORCID,Kaushik Medha1,Tabassum Heena24,Frey Julietta U.5

Affiliation:

1. Department of Toxicology, School of Chemical and Life Sciences Jamia Hamdard New Delhi India

2. Department of Neurophysiology Leibniz‐Institute for Neurobiology Magdeburg Germany

3. Neuronal Plasticity Group, Department of Zoology University of Calicut Malappuram Kerala India

4. Division of Basic Medical Sciences Indian Council of Medical Research New Delhi India

5. Department of Neuroloy, Medical College of Georgia, Brain & Behavior Discovery Institute Georgia Regents University Augusta GA USA

Abstract

AbstractWell 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.

Publisher

Wiley

Subject

Cognitive Neuroscience

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