TRPV1 regulates excitatory innervation of OLM neurons in the hippocampus

Joaquin I. Hurtado-Zavala, Binu Ramachandran, Saheeb Ahmed, Rashi Halder, Christiane Bolleyer, Ankit Awasthi, Markus A. Stahlberg, Robin J. Wagener, Kristin Anderson, Ryan M. Drenan, Henry A. Lester, Julie M. Miwa, Jochen F. Staiger, Andre Fischer and Camin Dean ()
Additional contact information
Joaquin I. Hurtado-Zavala: Trans-synaptic Signaling Group, European Neuroscience Institute
Binu Ramachandran: Trans-synaptic Signaling Group, European Neuroscience Institute
Saheeb Ahmed: Trans-synaptic Signaling Group, European Neuroscience Institute
Rashi Halder: German Center for Neurodegenerative Disease, University Medical Center Goettingen
Christiane Bolleyer: Trans-synaptic Signaling Group, European Neuroscience Institute
Ankit Awasthi: Trans-synaptic Signaling Group, European Neuroscience Institute
Markus A. Stahlberg: Trans-synaptic Signaling Group, European Neuroscience Institute
Robin J. Wagener: Institute for Neuroanatomy, University Medical Center Goettingen
Kristin Anderson: Lehigh University
Ryan M. Drenan: Purdue University
Henry A. Lester: California Institute of Technology
Julie M. Miwa: Lehigh University
Jochen F. Staiger: Institute for Neuroanatomy, University Medical Center Goettingen
Andre Fischer: German Center for Neurodegenerative Disease, University Medical Center Goettingen
Camin Dean: Trans-synaptic Signaling Group, European Neuroscience Institute

Nature Communications, 2017, vol. 8, issue 1, 1-20

Abstract: Abstract TRPV1 is an ion channel activated by heat and pungent agents including capsaicin, and has been extensively studied in nociception of sensory neurons. However, the location and function of TRPV1 in the hippocampus is debated. We found that TRPV1 is expressed in oriens-lacunosum-moleculare (OLM) interneurons in the hippocampus, and promotes excitatory innervation. TRPV1 knockout mice have reduced glutamatergic innervation of OLM neurons. When activated by capsaicin, TRPV1 recruits more glutamatergic, but not GABAergic, terminals to OLM neurons in vitro. When TRPV1 is blocked, glutamatergic input to OLM neurons is dramatically reduced. Heterologous expression of TRPV1 also increases excitatory innervation. Moreover, TRPV1 knockouts have reduced Schaffer collateral LTP, which is rescued by activating OLM neurons with nicotine—via α2β2-containing nicotinic receptors—to bypass innervation defects. Our results reveal a synaptogenic function of TRPV1 in a specific interneuron population in the hippocampus, where it is important for gating hippocampal plasticity.

Date: 2017
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms15878 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15878

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms15878

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().