Ontogeny of excitatory spinal neurons processing distinct somatic sensory modalities
Spatial and temporal cues govern the genesis of a diverse array of neurons located in the dorsal spinal cord, including dI1-dI6, dIL(A), and dIL(B) subtypes, but their physiological functions are poorly understood. Here we generated a new line of conditional knock-out (CKO) mice, in which the homeob...
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| Veröffentlicht in: | The Journal of neuroscience 2013-09, Vol.33 (37), p.14738-14748 |
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| creator | Xu, Yi Lopes, Claudia Wende, Hagen Guo, Zhen Cheng, Leping Birchmeier, Carmen Ma, Qiufu |
| description | Spatial and temporal cues govern the genesis of a diverse array of neurons located in the dorsal spinal cord, including dI1-dI6, dIL(A), and dIL(B) subtypes, but their physiological functions are poorly understood. Here we generated a new line of conditional knock-out (CKO) mice, in which the homeobox gene Tlx3 was removed in dI5 and dIL(B) cells. In these CKO mice, development of a subset of excitatory neurons located in laminae I and II was impaired, including itch-related GRPR-expressing neurons, PKCγ-expressing neurons, and neurons expressing three neuropeptide genes: somatostatin, preprotachykinin 1, and the gastrin-releasing peptide. These CKO mice displayed marked deficits in generating nocifensive motor behaviors evoked by a range of pain-related or itch-related stimuli. The mutants also failed to exhibit escape response evoked by dynamic mechanical stimuli but retained the ability to sense innocuous cooling and/or warm. Thus, our studies provide new insight into the ontogeny of spinal neurons processing distinct sensory modalities. |
| doi_str_mv | 10.1523/JNEUROSCI.5512-12.2013 |
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Here we generated a new line of conditional knock-out (CKO) mice, in which the homeobox gene Tlx3 was removed in dI5 and dIL(B) cells. In these CKO mice, development of a subset of excitatory neurons located in laminae I and II was impaired, including itch-related GRPR-expressing neurons, PKCγ-expressing neurons, and neurons expressing three neuropeptide genes: somatostatin, preprotachykinin 1, and the gastrin-releasing peptide. These CKO mice displayed marked deficits in generating nocifensive motor behaviors evoked by a range of pain-related or itch-related stimuli. The mutants also failed to exhibit escape response evoked by dynamic mechanical stimuli but retained the ability to sense innocuous cooling and/or warm. 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Thus, our studies provide new insight into the ontogeny of spinal neurons processing distinct sensory modalities.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Capsaicin - toxicity</subject><subject>Cell Count</subject><subject>Chloroquine - toxicity</subject><subject>Embryo, Mammalian</subject><subject>Ganglia, Spinal - cytology</subject><subject>Gastrin-Releasing Peptide - genetics</subject><subject>Gastrin-Releasing Peptide - metabolism</subject><subject>Gene Expression Regulation, Developmental - genetics</subject><subject>Gene Expression Regulation, Developmental - physiology</subject><subject>Homeodomain Proteins - genetics</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Muscle Proteins - genetics</subject><subject>Neurons - classification</subject><subject>Neurons - physiology</subject><subject>Oligopeptides - toxicity</subject><subject>Pain - chemically induced</subject><subject>Pain - genetics</subject><subject>Pain - metabolism</subject><subject>Physical Stimulation - adverse effects</subject><subject>Protein Kinase C - metabolism</subject><subject>Protein Precursors - genetics</subject><subject>Protein Precursors - metabolism</subject><subject>Pruritus - etiology</subject><subject>Pruritus - metabolism</subject><subject>Psychomotor Performance - drug effects</subject><subject>Psychomotor Performance - physiology</subject><subject>Sensation - genetics</subject><subject>Somatostatin - genetics</subject><subject>Somatostatin - metabolism</subject><subject>Tachykinins - genetics</subject><subject>Tachykinins - metabolism</subject><subject>Vesicular Glutamate Transport Protein 1 - metabolism</subject><issn>0270-6474</issn><issn>1529-2401</issn><issn>1529-2401</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkVtLAzEQhYMoWi9_QfbRl625bJLuiyDFS0UsaH0OaTZbI7tJzaRi_70p1qIwMA9nzplhPoTOCR4STtnlw9PN6_P0ZTwZck5oSeiQYsL20CCrdUkrTPbRAFOJS1HJ6ggdA7xjjCUm8hAdZZ1KKqsBmk19Cgvr10VoC_tlXNIpxHUBS-d1V3i7isFDsYzBWADnF0XjIDlvUgGh18mZAqyHjaUPje5cchZO0UGrO7Bn236CXm9vZuP78nF6NxlfP5aGE5ZKYkVT8ZEQvMUjimuCWdOKkTSUsYpjLjQRWtQN0cbqhsxb0ghhqOG1zQY8Zyfo6id3uZr3tjHWp6g7tYyu13Gtgnbqv-Ldm1qET8WkzMvqHHCxDYjhY2Uhqd6BsV2nvQ0rUCQ_VzBc1zyPip9REwNAtO1uDcFqg0TtkKgNEpVrgyQbz_8eubP9MmDfc6OLPw</recordid><startdate>20130911</startdate><enddate>20130911</enddate><creator>Xu, Yi</creator><creator>Lopes, Claudia</creator><creator>Wende, Hagen</creator><creator>Guo, Zhen</creator><creator>Cheng, Leping</creator><creator>Birchmeier, Carmen</creator><creator>Ma, Qiufu</creator><general>Society for Neuroscience</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>5PM</scope></search><sort><creationdate>20130911</creationdate><title>Ontogeny of excitatory spinal neurons processing distinct somatic sensory modalities</title><author>Xu, Yi ; 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Here we generated a new line of conditional knock-out (CKO) mice, in which the homeobox gene Tlx3 was removed in dI5 and dIL(B) cells. In these CKO mice, development of a subset of excitatory neurons located in laminae I and II was impaired, including itch-related GRPR-expressing neurons, PKCγ-expressing neurons, and neurons expressing three neuropeptide genes: somatostatin, preprotachykinin 1, and the gastrin-releasing peptide. These CKO mice displayed marked deficits in generating nocifensive motor behaviors evoked by a range of pain-related or itch-related stimuli. The mutants also failed to exhibit escape response evoked by dynamic mechanical stimuli but retained the ability to sense innocuous cooling and/or warm. 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| subjects | Animals Animals, Newborn Capsaicin - toxicity Cell Count Chloroquine - toxicity Embryo, Mammalian Ganglia, Spinal - cytology Gastrin-Releasing Peptide - genetics Gastrin-Releasing Peptide - metabolism Gene Expression Regulation, Developmental - genetics Gene Expression Regulation, Developmental - physiology Homeodomain Proteins - genetics Mice Mice, Transgenic Muscle Proteins - genetics Neurons - classification Neurons - physiology Oligopeptides - toxicity Pain - chemically induced Pain - genetics Pain - metabolism Physical Stimulation - adverse effects Protein Kinase C - metabolism Protein Precursors - genetics Protein Precursors - metabolism Pruritus - etiology Pruritus - metabolism Psychomotor Performance - drug effects Psychomotor Performance - physiology Sensation - genetics Somatostatin - genetics Somatostatin - metabolism Tachykinins - genetics Tachykinins - metabolism Vesicular Glutamate Transport Protein 1 - metabolism |
| title | Ontogeny of excitatory spinal neurons processing distinct somatic sensory modalities |
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