A population of large lamina I projection neurons with selective inhibitory input in rat spinal cord

Puskár, Zita; Polgár, Erika; Todd, Andrew

doi:10.1016/s0306-4522(00)00445-0

Cited by 74 publications

(69 citation statements)

References 37 publications

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“…Sections were viewed with epifluorescence illumination and 15 large gephyrin-coated lamina I neurons (Puskár et al, 2001; Polgár et al, 2008) were chosen (4–6 from each rat). Selected regions of dendritic trees, and in some cases also the soma, were scanned sequentially with the confocal microscope through a 60× oil-immersion lens, with a z-separation of 0.5 μm.…”

Section: Methodsmentioning

confidence: 99%

“…We have shown that GABAergic axons that contain NPY, and presumably originate from local interneurons, form numerous synapses on large NK1r-expressing projection neurons with cell bodies in lamina III and prominent dorsal dendrites, but form significantly fewer contacts on two other types of projection neuron: those in lamina I that express the NK1r and postsynaptic dorsal column cells in laminae III–V (Polgár et al, 1999b). In contrast, GABAergic axons that contain nNOS preferentially innervate a population of large lamina I projection neurons that lack the NK1r and have a very high density of inhibitory synapses that can be revealed with antibody against the glycine receptor-associated protein gephyrin (Puskár et al, 2001). Characterizing the inhibitory interneurons that are presynaptic to projection cells is important, as these may provide targets for the development of new analgesics.…”

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confidence: 99%

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Quantitative study of NPY‐expressing GABAergic neurons and axons in rat spinal dorsal horn

et al. 2011

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Between 25–40% of neurons in laminae I–III are GABAergic, and some of these express neuropeptide Y (NPY). We previously reported that NPY-immunoreactive axons form numerous synapses on lamina III projection neurons that possess the neurokinin 1 receptor (NK1r). The aims of this study were to determine the proportion of neurons and GABAergic boutons in this region that contain NPY, and to look for evidence that they selectively innervate different neuronal populations. We found that 4–6% of neurons in laminae I–III were NPY-immunoreactive and based on the proportions of neurons that are GABAergic, we estimate that NPY is expressed by 18% of inhibitory interneurons in laminae I–II and 9% of those in lamina III. GABAergic boutons were identified by the presence of the vesicular GABA transporter (VGAT) and NPY was found in 13–15% of VGAT-immunoreactive boutons in laminae I–II, and 5% of those in lamina III. For both the lamina III NK1r-immunoreactive projection neurons and protein kinase Cγ (PKCγ)-immunoreactive interneurons in lamina II, we found that around one-third of the VGAT boutons that contacted them were NPY-immunoreactive. However, based on differences in the sizes of these boutons and the strength of their NPY-immunoreactivity, we conclude that these originate from different populations of interneurons. Only 6% of VGAT boutons presynaptic to large lamina I projection neurons that lacked NK1rs contained NPY. These results show that NPY-containing neurons make up a considerable proportion of the inhibitory interneurons in laminae I–III, and that their axons preferentially target certain classes of dorsal horn neuron. J. Comp. Neurol. 519:1007–1023, 2011. © 2010 Wiley-Liss, Inc.

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Section: Methodsmentioning

confidence: 99%

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confidence: 99%

Quantitative study of NPY‐expressing GABAergic neurons and axons in rat spinal dorsal horn

et al. 2011

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“…Most evidence indicates that GlyRcs are efficiently removed from synapses that only release GABA (Levi et al, 1999a, Dumoulin et al, 2001; but see Puskar et al, 2001), whereas removal of GABA A receptors postsynaptic to glycine-only boutons has not been investigated thoroughly. Because receptor activation seems necessary to stabilize GlyRc clusters Levi et al, 1998), GlyRcs might be efficiently removed from postsynaptic sites opposite to boutons that do not release glycine.…”

Section: Mismatches Between Postsynaptic Gaba a Receptor Clusters Andmentioning

confidence: 99%

Glycine and GABA_A receptor subunits on Renshaw cells: Relationship with presynaptic neurotransmitters and postsynaptic gephyrin clusters

Geiman

Zheng

Fritschy

et al. 2002

J of Comparative Neurology

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Inhibitory synapses with large and gephyrin-rich postsynaptic receptor areas are likely indicative of higher synaptic strength. We investigated the presynaptic inhibitory neurotransmitter content (GABA, glycine, or both) and the presence and subunit composition of GABA(A) and glycine postsynaptic receptors in one example of gephyrin-rich synapses to determine neurochemical characteristics that could also contribute to enhance synaptic strength. Hence, we analyzed subunit receptor expression in gephyrin patches located on Renshaw cells, a type of spinal interneuron that receives powerful excitatory and inhibitory inputs and displays many large gephyrin patches on its surface. GABA(A) and glycine receptors were almost always colocalized inside Renshaw cell gephyrin clusters. According to the subunit-immunoreactivities detected, the composition of GABA(A) receptors was inferred to be either alpha(3)beta((2or3))gamma(2), alpha(5)beta((2or3))gamma(2), alpha(3)alpha(5)beta((2or3))gamma(2) or a combination of these. The types of neurotransmitters contained inside boutons presynaptic to Renshaw cell gephyrin patches were also investigated. The majority (60-75%) of terminals presynaptic to Renshaw cell gephyrin patches contained immunocytochemical markers for GABA as well as glycine, but a proportion contained markers only for glycine. Significantly, 40% of GABA(A) receptor clusters were opposed to presynaptic boutons that contained only glycinergic markers. We postulate that GABA and glycine corelease, and the presence of alpha3-containing GABA(A) receptors can enhance the postsynaptic current and contribute to strengthen inhibitory input on Renshaw cells. In addition, a certain degree of imprecision in the localization of postsynaptic GABA(A) receptors in regard to GABA release sites onto adult Renshaw cells was also found.

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“…CRF did not change the number of activated spinal neurons (Fos positive) in Lewis rats and increased the number in Fischer rats despite an antinociceptive effect. This finding does not entirely rule out the possibility of descending inhibition because there could be a discrepancy between c-fos expression and pain behavior (Harris, 1998) due to Fos expression in neurons such as GABAergic inhibitory interneurons not involved in nociceptive activation (Puskar et al, 2001).…”

Section: Other Substrates For the Antinociceptive Effect Of Crfmentioning

confidence: 96%

Mechanisms in Chronic Multisymptom Illnesses

Clauw¹

2008

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. 5e. TASK NUMBER 5f. WORK UNIT NUMBER REPORT DATE 01-06-2006 REPORT TYPE PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBERUniversity of Michigan Ann Arbor, MI 48106-0737 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTESOriginal contains colored plates: ALL DTIC reproductions will be in black and white. ABSTRACTThe overall objectives of this cooperative agreement are to conduct research in pursuit of identifying the physiologic mechanisms responsible for the symptoms of pain, fatigue, and memory difficulties commonly seen in patients with Chronic Multisymptom Illnesses (CMI) (i.e., fibromyalgia, chronic fatigue syndrome, Gulf War Illnesses, etc.); to identify the risk factors for developing these syndromes as well as programs aimed at both preventing these illnesses and treating established cases. These objectives will be achieved through multiple research studies using innovative, technologically advanced (e.g., functional MRI and telemedicine) methodologies in a multidisciplinary environment. Various studies will be conducted to explore all aspects of pain processing, the effects of exercise deprivation and sleep reduction on symptomatology, the ability of exercise and/or cognitive behavioral therapies to alter patients' locus of control for pain, the neurobiological mechanism(s) of acupuncture on analgesia, the presence of hypersensitivity to auditory stimuli, and the effectiveness of cognitive behavioral therapy delivered via telemedicine and the internet. These studies will be conducted on well-characterized cohorts of CMI subjects and healthy controls taken from our burgeoning subject registry. Research will occur over the next 3 years at the University of Michigan, Ann Arbor, MI and Avera Research Institute, Sioux Falls, SD. SUBJECT TERMS INTRODUCTION:Researchers in the Chronic Pain and Fatigue Research Center ...

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A population of large lamina I projection neurons with selective inhibitory input in rat spinal cord

Cited by 74 publications

References 37 publications

Quantitative study of NPY‐expressing GABAergic neurons and axons in rat spinal dorsal horn

Quantitative study of NPY‐expressing GABAergic neurons and axons in rat spinal dorsal horn

Glycine and GABA_A receptor subunits on Renshaw cells: Relationship with presynaptic neurotransmitters and postsynaptic gephyrin clusters

Mechanisms in Chronic Multisymptom Illnesses

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A population of large lamina I projection neurons with selective inhibitory input in rat spinal cord

Cited by 74 publications

References 37 publications

Quantitative study of NPY‐expressing GABAergic neurons and axons in rat spinal dorsal horn

Quantitative study of NPY‐expressing GABAergic neurons and axons in rat spinal dorsal horn

Glycine and GABAA receptor subunits on Renshaw cells: Relationship with presynaptic neurotransmitters and postsynaptic gephyrin clusters

Mechanisms in Chronic Multisymptom Illnesses

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Glycine and GABA_A receptor subunits on Renshaw cells: Relationship with presynaptic neurotransmitters and postsynaptic gephyrin clusters