Genetic identity of thermosensory relay neurons in the lateral parabrachial nucleus

Joel C Geerling; Minjee Kim; Carrie E Mahoney; Stephen B G Abbott; Lindsay J Agostinelli; Alastair S Garfield; Michael J Krashes; Bradford B Lowell; Thomas E Scammell

doi:10.1152/ajpregu.00094.2015

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Genetic identity of thermosensory relay neurons in the lateral parabrachial nucleus

Journal article

Open access

Peer reviewed

Genetic identity of thermosensory relay neurons in the lateral parabrachial nucleus

Joel C Geerling, Minjee Kim, Carrie E Mahoney, Stephen B G Abbott, Lindsay J Agostinelli, Alastair S Garfield, Michael J Krashes, Bradford B Lowell and Thomas E Scammell

American journal of physiology. Regulatory, integrative and comparative physiology, Vol.310(1), pp.R41-R54

01/01/2016

DOI: 10.1152/ajpregu.00094.2015

PMCID: PMC4747895

PMID: 26491097

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Abstract

The parabrachial nucleus is important for thermoregulation because it relays skin temperature information from the spinal cord to the hypothalamus. Prior work in rats localized thermosensory relay neurons to its lateral subdivision (LPB), but the genetic and neurochemical identity of these neurons remains unknown. To determine the identity of LPB thermosensory neurons, we exposed mice to a warm (36°C) or cool (4°C) ambient temperature. Each condition activated neurons in distinct LPB subregions that receive input from the spinal cord. Most c-Fos+ neurons in these LPB subregions expressed the transcription factor marker FoxP2. Consistent with prior evidence that LPB thermosensory relay neurons are glutamatergic, all FoxP2+ neurons in these subregions colocalized with green fluorescent protein (GFP) in reporter mice for Vglut2, but not for Vgat. Prodynorphin (Pdyn)-expressing neurons were identified using a GFP reporter mouse and formed a caudal subset of LPB FoxP2+ neurons, primarily in the dorsal lateral subnucleus (PBdL). Warm exposure activated many FoxP2+ neurons within PBdL. Half of the c-Fos+ neurons in PBdL were Pdyn+, and most of these project into the preoptic area. Cool exposure activated a separate FoxP2+ cluster of neurons in the far-rostral LPB, which we named the rostral-to-external lateral subnucleus (PBreL). These findings improve our understanding of LPB organization and reveal that Pdyn-IRES-Cre mice provide genetic access to warm-activated, FoxP2+ glutamatergic neurons in PBdL, many of which project to the hypothalamus.

Parabrachial Nucleus - metabolism

Enkephalins - metabolism

Fever - metabolism

Neuroanatomical Tract-Tracing Techniques

Male

Green Fluorescent Proteins - genetics

Fever - physiopathology

Internal Ribosome Entry Sites

Thermosensing

Enkephalins - genetics

Forkhead Transcription Factors - metabolism

Hypothermia - metabolism

Integrases - metabolism

Neurons - metabolism

Genes, Reporter

Repressor Proteins - metabolism

Skin Temperature

Disease Models, Animal

Green Fluorescent Proteins - metabolism

Protein Precursors - genetics

Vesicular Glutamate Transport Protein 2 - metabolism

Gene Expression Regulation

Proto-Oncogene Proteins c-fos - metabolism

Genotype

Mice, Transgenic

Protein Precursors - metabolism

Phenotype

Animals

Vesicular Inhibitory Amino Acid Transport Proteins - metabolism

Fever - genetics

Glutamic Acid - metabolism

Parabrachial Nucleus - physiopathology

Hypothermia - physiopathology

Integrases - genetics

Hypothermia - genetics

Details

Title: Subtitle: Genetic identity of thermosensory relay neurons in the lateral parabrachial nucleus
Creators: Joel C Geerling - Department of Neurology, Beth Israel Deaconess Medical Center; Harvard Medical School, Boston, Massachusetts; jgeerlin@bidmc.harvard.edu
Minjee Kim - Department of Neurology, Beth Israel Deaconess Medical Center; Harvard Medical School, Boston, Massachusetts
Carrie E Mahoney - Department of Neurology, Beth Israel Deaconess Medical Center; Harvard Medical School, Boston, Massachusetts
Stephen B G Abbott - Department of Neurology, Beth Israel Deaconess Medical Center; Harvard Medical School, Boston, Massachusetts
Lindsay J Agostinelli - Department of Neurology, Beth Israel Deaconess Medical Center; Harvard Medical School, Boston, Massachusetts
Alastair S Garfield - Division of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center; Harvard Medical School, Boston, Massachusetts; Centre for Integrative Physiology, University of Edinburgh, Edinburgh, Scotland
Michael J Krashes - Diabetes, Endocrinology and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland; and National Institute on Drug Abuse, National Institutes of Health, Bethesda, Maryland
Bradford B Lowell - Division of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center; Harvard Medical School, Boston, Massachusetts
Thomas E Scammell - Department of Neurology, Beth Israel Deaconess Medical Center; Harvard Medical School, Boston, Massachusetts
Resource Type: Journal article
Publication Details: American journal of physiology. Regulatory, integrative and comparative physiology, Vol.310(1), pp.R41-R54
DOI: 10.1152/ajpregu.00094.2015
PMID: 26491097
PMCID: PMC4747895
NLM abbreviation: Am J Physiol Regul Integr Comp Physiol
ISSN: 0363-6119
eISSN: 1522-1490
Publisher: American Physiological Society; United States
Grant note: T32 HL007901 / NHLBI NIH HHS R01 DK089044 / NIDDK NIH HHS NIH-T32 AG000222 / NIA NIH HHS R01 DK075632 / NIDDK NIH HHS P01 HL095491 / NHLBI NIH HHS T32 AG000222 / NIA NIH HHS R01 DE022912 / NIDCR NIH HHS R25 NS070682 / NINDS NIH HHS P30 DK057521 / NIDDK NIH HHS
Language: English
Date published: 01/01/2016
Academic Unit: Neurology; Iowa Neuroscience Institute
Record Identifier: 9984020761502771

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