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GABAergic and glycinergic synapses onto neurokinin-1 receptor-immunoreactive neurons in the pre-Bötzinger complex of rats: light and electron microscopic studies.
Eur J Neurosci. 2002 Sep; 16(6):1058-66.EJ

Abstract

The pre-Bötzinger complex (preBötC) in the ventrolateral medulla is thought to be the kernel for respiratory rhythm generation. Neurons in the preBötC contain intense neurokinin-1 receptor (NK1R) immunoreactivity. Some of these neurons in the adult preBötC are presumed to be the pre-inspiratory interneurons that are essential for generating respiratory rhythm in the neonate. Chloride-mediated synaptic inhibition is critical for rhythmogenesis in the adult. The present study used immunofluorescence histochemistry and immunogold-silver staining to determine the inhibitory synaptic relationship between glutamic acid decarboxylase (GAD)- or glycine transporter 2 (GlyT2)-immunoreactive (ir) boutons and NK1R-ir neurons in the preBötC of adult rats. Under the confocal microscope, we found that GAD- and GlyT2-ir boutons were in close apposition to NK1R-ir somas and dendrites in the preBötC. Under the electron microscope, GAD- and GlyT2-ir terminals were in close apposition to NK1R-ir somas and dendrites. Symmetric synapses were identified between GAD- or GlyT2-ir terminals and NK1R-ir neurons. A total of 51.6% GAD-ir and 38.2% GlyT2-ir terminals were found to contact or make synapses with NK1R-ir profiles, respectively. GAD- and GlyT2-ir terminals synapsed not only upon NK1R-ir neurons but also upon NK1R immuno-negative neurons. NK1R-ir neurons received both symmetric (presumed inhibitory) and asymmetric (presumed excitatory) synapses. Thus, the present findings provide the morphological basis for inhibitory inputs to NK1R-ir neurons in the preBötC, consistent with the suggestion that chloride-mediated synaptic inhibition may contribute importantly to rhythm generation by controlling the membrane potential trajectory and resetting rhythmic bursting of the kernel neurons in the adult.

Authors+Show Affiliations

Institute of Neurosciences, The Fourth Military Medical University, Xi'an 710032, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12383234

Citation

Liu, Ying-Ying, et al. "GABAergic and Glycinergic Synapses Onto Neurokinin-1 Receptor-immunoreactive Neurons in the pre-Bötzinger Complex of Rats: Light and Electron Microscopic Studies." The European Journal of Neuroscience, vol. 16, no. 6, 2002, pp. 1058-66.
Liu YY, Wong-Riley MT, Liu JP, et al. GABAergic and glycinergic synapses onto neurokinin-1 receptor-immunoreactive neurons in the pre-Bötzinger complex of rats: light and electron microscopic studies. Eur J Neurosci. 2002;16(6):1058-66.
Liu, Y. Y., Wong-Riley, M. T., Liu, J. P., Jia, Y., Liu, H. L., Jiao, X. Y., & Ju, G. (2002). GABAergic and glycinergic synapses onto neurokinin-1 receptor-immunoreactive neurons in the pre-Bötzinger complex of rats: light and electron microscopic studies. The European Journal of Neuroscience, 16(6), 1058-66.
Liu YY, et al. GABAergic and Glycinergic Synapses Onto Neurokinin-1 Receptor-immunoreactive Neurons in the pre-Bötzinger Complex of Rats: Light and Electron Microscopic Studies. Eur J Neurosci. 2002;16(6):1058-66. PubMed PMID: 12383234.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - GABAergic and glycinergic synapses onto neurokinin-1 receptor-immunoreactive neurons in the pre-Bötzinger complex of rats: light and electron microscopic studies. AU - Liu,Ying-Ying, AU - Wong-Riley,Margaret T T, AU - Liu,Jin-Ping, AU - Jia,Yi, AU - Liu,Hui-Ling, AU - Jiao,Xi-Ying, AU - Ju,Gong, PY - 2002/10/18/pubmed PY - 2002/12/5/medline PY - 2002/10/18/entrez SP - 1058 EP - 66 JF - The European journal of neuroscience JO - Eur. J. Neurosci. VL - 16 IS - 6 N2 - The pre-Bötzinger complex (preBötC) in the ventrolateral medulla is thought to be the kernel for respiratory rhythm generation. Neurons in the preBötC contain intense neurokinin-1 receptor (NK1R) immunoreactivity. Some of these neurons in the adult preBötC are presumed to be the pre-inspiratory interneurons that are essential for generating respiratory rhythm in the neonate. Chloride-mediated synaptic inhibition is critical for rhythmogenesis in the adult. The present study used immunofluorescence histochemistry and immunogold-silver staining to determine the inhibitory synaptic relationship between glutamic acid decarboxylase (GAD)- or glycine transporter 2 (GlyT2)-immunoreactive (ir) boutons and NK1R-ir neurons in the preBötC of adult rats. Under the confocal microscope, we found that GAD- and GlyT2-ir boutons were in close apposition to NK1R-ir somas and dendrites in the preBötC. Under the electron microscope, GAD- and GlyT2-ir terminals were in close apposition to NK1R-ir somas and dendrites. Symmetric synapses were identified between GAD- or GlyT2-ir terminals and NK1R-ir neurons. A total of 51.6% GAD-ir and 38.2% GlyT2-ir terminals were found to contact or make synapses with NK1R-ir profiles, respectively. GAD- and GlyT2-ir terminals synapsed not only upon NK1R-ir neurons but also upon NK1R immuno-negative neurons. NK1R-ir neurons received both symmetric (presumed inhibitory) and asymmetric (presumed excitatory) synapses. Thus, the present findings provide the morphological basis for inhibitory inputs to NK1R-ir neurons in the preBötC, consistent with the suggestion that chloride-mediated synaptic inhibition may contribute importantly to rhythm generation by controlling the membrane potential trajectory and resetting rhythmic bursting of the kernel neurons in the adult. SN - 0953-816X UR - https://www.unboundmedicine.com/medline/citation/12383234/GABAergic_and_glycinergic_synapses_onto_neurokinin_1_receptor_immunoreactive_neurons_in_the_pre_Bötzinger_complex_of_rats:_light_and_electron_microscopic_studies_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0953-816X&date=2002&volume=16&issue=6&spage=1058 DB - PRIME DP - Unbound Medicine ER -