Calbindin D28k expression in immunohistochemically identified Renshaw cells

Carr, Patrick A.; Álvarez, Francisco J.; Leman, Elizabeth E.; Fyffe, Robert E.W.

doi:10.1097/00001756-199808030-00043

Cited by 80 publications

(85 citation statements)

References 13 publications

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“…(i) They were characterized as being large neurons located in the ventral horn that could be activated antidromically from the ventral root. In accordance with classical criteria, the antidromic spike followed high stimulus frequencies (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) with no jitters in the activation latencies (see Fig. 1b).…”

Section: Methodssupporting

confidence: 80%

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Mammalian motor neurons corelease glutamate and acetylcholine at central synapses

Nishimaru

Restrepo

Ryge

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

220

201

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Motor neurons (MNs) are the principal neurons in the mammalian spinal cord whose activities cause muscles to contract. In addition to their peripheral axons, MNs have central collaterals that contact inhibitory Renshaw cells and other MNs. Since its original discovery >60 years ago, it has been a general notion that acetylcholine is the only transmitter released from MN synapses both peripherally and centrally. Here, we show, using a multidisciplinary approach, that mammalian spinal MNs, in addition to acetylcholine, corelease glutamate to excite Renshaw cells and other MNs but not to excite muscles. Our study demonstrates that glutamate can be released as a functional neurotransmitter from mammalian MNs.synaptic transmission ͉ spinal cord M otor neurons (MNs) are the output neurons from the central nervous system. Their activity directly leads to muscle contraction. By the 1940s, it was generally accepted that MNs release acetylcholine (ACh) at the neuromuscular junction (1). Shortly thereafter, it was shown that ACh also is released from MNs' central axonal branches contacting Renshaw cells (RCs) (2). As was found at the neuromuscular junction, this transmission was shown to be nicotinic (3, 4). The collaterals contacting other MNs (5) are also thought to be mediated by ACh, although this has not been shown directly (6). Since these initial discoveries and after many later investigations, it has been a general dogma that mammalian MNs contain and release one neurotransmitter, ACh, both centrally and peripherally. It has been suggested recently, based on anatomical data, that MNs might contain glutamate as a neurotransmitter (7,8). There has been, however, no direct electrophysiological evidence to support this. Here, we examine this question directly by investigating the transmission in central and peripheral MN synapses (Fig. 1a). Materials and MethodsRecordings from RCs and MNs. All procedures followed Swedish federal guidelines for animal care. Postnatal heterozygote glutamic acid decarboxylase (GAD) 67-GFP mice [postnatal day (P) 0 to P4] were anaesthetized with isoflurane and eviscerated, and spinal cords were removed with ventral laminectomy, as described in ref. 9. The spinal cord was placed in a recording chamber perfused with oxygenated Ringer's solution (128 mM NaCl͞4.69 mM KCl͞25 mM NaHCO 3 ͞1.18 mM KH 2 PO 4 ͞1.25 mM MgSO 4 ͞2.5 mM CaCl 2 ͞22 mM glucose aerated with 5% CO 2 in O 2 ) at room temperature. Whole-cell tight-seal recording of RCs and MNs were performed with patch electrodes pulled from thick-walled borosilicate glass (o.d. of 1.5 mm, i.d. of 1.0 mm; Harvard Instruments) to a final resistance of 5-8 M⍀. The electrode tips were filled with 138 mM K-gluconate, 10 mM Hepes, 0.0001 mM CaCl 2 , 5 mM ATP-Mg, and 0.3 mM GTP-Li. After filling of the tip, the electrodes were back-filled with the same solution, and to label the recorded cell, Alexa Fluor dye (0.15-0.20%; Molecular Probes) or neurobiotin (1-2%) was diluted into the electrode solution. Cells were filled during recording. Signals wer...

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Section: Methodssupporting

confidence: 80%

“…Recorded cells were filled intracellularly with Alexa Fluor dyes ( Fig. 1c; Alexa Fluor 488 or 588), which also allowed us to confirm their identity as RCs because of their expression of calbindin (13) (Fig. 1c).…”

Section: Resultsmentioning

confidence: 99%

Mammalian motor neurons corelease glutamate and acetylcholine at central synapses

Nishimaru

Restrepo

Ryge

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

220

201

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“…1 A). RCs also show specific calbindin 28k immunoreactivity (Carr et al, 1998), as shown in Figure 1, Ac and Ad. GFP-positive cells in the ventral cord were visually patched in the L2 (Fig.…”

Section: Identification Of Rcsmentioning

confidence: 71%

Activity of Renshaw Cells during Locomotor-Like Rhythmic Activity in the Isolated Spinal Cord of Neonatal Mice

Nishimaru¹,

Restrepo²,

Kiehn³

2006

J. Neurosci.

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In the present study, we examine the activity patterns of and synaptic inputs to Renshaw cells (RCs) during fictive locomotion in the newborn mouse using visually guided recordings from GABAergic cells expressing glutamic acid decarboxylase 67-green fluorescent protein (GFP). Among the GFP-positive neurons in the lumbar ventral horn, RCs were uniquely identified as receiving ventral rootevoked short-latency EPSPs that were markedly reduced in amplitude by nicotinic receptor blockers mecamylamine or tubocurarine. During locomotor-like rhythmic activity evoked by bath application of 5-HT and NMDA, 50% of the recorded RCs fired in-phase with the ipsilateral L2 flexor-related rhythm, whereas the rest fired in the extensor phase. Each population of RCs fired throughout the corresponding locomotor phase. All RCs received both excitatory and inhibitory synaptic inputs during the locomotor-like rhythmic activity. Blocking nicotinic receptors with mecamylamine markedly reduced the rhythmic excitatory drive, indicating that these rhythmic inputs originate mainly from motor neurons (MNs). Inhibitory synaptic inputs persisted in the presence of the nicotinic blocker. Part of this inhibitory drive and remaining excitatory drive could be from commissural interneurons because the present study also shows that RCs receive direct crossed inhibitory and excitatory synaptic inputs. However, rhythmic synaptic inputs in RCs were also observed in hemicord preparations in the presence of mecamylamine. These results show that, during locomotor activity, RC firing properties are modulated not only by MNs but also by the ipsilateral and contralateral locomotor networks.

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“…These nuclei are associated with the following muscles: soleus (SOL), medial gastrocnemius (MG), lateral gastrocnemius (LG) and tibialis anterior (TA). The total number of neurons simulated for these nuclei is shown in Table 1, based on estimates from human and cat literature (Feinstein et al 1955;Cooper 1966;Ariano et al 1973;Johnson et al 1973;Buchthal and Schmalbruch 1980;Dum and Kennedy 1980;McComas 1991;Jankowska 1992;Carr et al 1998;Banks 2006). Interneuron numbers are underestimated, in order to improve system performance.…”

Section: Methodsmentioning

confidence: 99%

Simulation system of spinal cord motor nuclei and associated nerves and muscles, in a Web-based architecture

2008

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Calbindin D28k expression in immunohistochemically identified Renshaw cells

Cited by 80 publications

References 13 publications

Mammalian motor neurons corelease glutamate and acetylcholine at central synapses

Mammalian motor neurons corelease glutamate and acetylcholine at central synapses

Activity of Renshaw Cells during Locomotor-Like Rhythmic Activity in the Isolated Spinal Cord of Neonatal Mice

Simulation system of spinal cord motor nuclei and associated nerves and muscles, in a Web-based architecture

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