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Development of Brainstem 5-HT1A Receptor Binding Sites in Serotonin-Deficient Mice
Journal article   Open access   Peer reviewed

Development of Brainstem 5-HT1A Receptor Binding Sites in Serotonin-Deficient Mice

Caitlin A Massey, Gloria Kim, Andrea E Corcoran, Robin L Haynes, David S Paterson, Kevin J Cummings, Susan M Dymecki, George B Richerson, Eugene E Nattie, Hannah C Kinney, …
Journal of neurochemistry, Vol.126(6), pp.749-757
09/2013
DOI: 10.1111/jnc.12311
PMCID: PMC3987866
PMID: 23692315
url
https://doi.org/10.1111/jnc.12311View
Published (Version of record) Open Access

Abstract

The sudden infant death syndrome (SIDS) is associated with a reduction in brainstem serotonin (5-hydroxytryptamine, 5-HT) and 5-HT 1A receptor binding, yet it is unknown if and how these findings are linked. In this study, we used quantitative tissue autoradiography to determine if postnatal development of brainstem 5-HT 1A receptors is altered in two mouse models where the development of 5-HT neurons is defective, the Lmx1b f/f/p , and the Pet-1 -/- mouse. 5-HT 1A receptor agonist-binding sites were examined in both 5-HT-source nuclei (autoreceptors) and in sites that receive 5-HT innervation (heteroreceptors). In control mice between postnatal day (P) 3 and 10, 5-HT 1A receptor binding increased in several brainstem sites; by P25, there were region-specific increases and decreases, refining the overall binding pattern. In the Lmx1b f/f/p and Pet-1 -/- mice, 5-HT 1A -autoreceptor binding was significantly lower than in control mice at P3, and remained low at P10 and P25. In contrast, 5-HT 1A heteroreceptor levels were comparable between control and 5-HT-deficient mice. These data define the postnatal development of 5-HT 1A receptor binding in the mouse brainstem. Furthermore the data suggest that 5-HT 1A heteroreceptor deficits detected in SIDS are not a direct consequence of a 5-HT neuron dysfunction nor reduced brain 5-HT levels.
sudden infant death syndrome autoreceptors raphe Lmx1b heteroreceptors Pet1

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