The morphology and distribution of neurons containing choline acetyltransferase in the adult rat spinal cord: An immunocytochemical study

Barber, Robert P.; Phelps, Patricia E.; Houser, Carolyn R.; Crawford, G. D.; Salvaterra, Paul M.; Vaughn, James E.

doi:10.1002/cne.902290305

Cited by 426 publications

(242 citation statements)

References 63 publications

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“…We found that the YFP ϩ /NOS Ϫ neurons, which likely give rise to the C boutons, are lateral to the central canal and show strong ChAT immunoreactivity. This profile identifies them as belonging to the medial group of partition neurons (33). Interestingly, YFP was not present in all of the strongly ChAT ϩ neurons in this region, suggesting that the C boutons originate from a specific subpopulation of medial partition cells that express Dbx1 at some stage during their development.…”

Section: Discussionmentioning

confidence: 94%

“…Several groups of cholinergic interneurons have been identified in the spinal cord (33). In addition to autonomic neurons (which are present at thoraco-lumbar and sacral levels), there are scattered neurons in the dorsal horn, cells that surround the central canal (central canal cluster cells), and a population of neurons that occupy a region extending from lamina X to the lateral edge of the gray matter.…”

Section: Discussionmentioning

confidence: 99%

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Spinal cholinergic interneurons regulate the excitability of motoneurons during locomotion

Miles

Hartley

Todd

et al. 2007

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

268

365

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To effect movement, motoneurons must respond appropriately to motor commands. Their responsiveness to these inputs, or excitability, is regulated by neuromodulators. Possible sources of modulation include the abundant cholinergic ''C boutons'' that surround motoneuron somata. In the present study, recordings from motoneurons in spinal cord slices demonstrated that cholinergic activation of m 2-type muscarinic receptors increases excitability by reducing the action potential afterhyperpolarization. Analyses of isolated spinal cord preparations in which fictive locomotion was elicited demonstrated that endogenous cholinergic inputs increase motoneuron excitability during locomotion. Anatomical data indicate that C boutons originate from a discrete group of interneurons lateral to the central canal, the medial partition neurons. These results highlight a unique component of spinal motor networks that is critical in ensuring that sufficient output is generated by motoneurons to drive motor behavior.T o generate movement, it is necessary for motoneurons (MNs) to integrate the inputs (motor commands) they receive and produce an output sufficient to effect muscular contraction. The relationship of input to output is determined by neuronal excitability, which in the case of MNs is known to be regulated by identified descending modulatory systems (1). Given that these descending systems are disrupted after spinal cord injury, strategies aimed at restoring movement need to address not only premotor circuits that provide motor commands but also any modulatory systems that ensure MNs are sufficiently excitable to respond to these commands. Spinal premotor circuits for locomotion can be activated after spinal transection (2) and provide one clear target for treatments designed to produce functional recovery. Should an intrinsic spinal modulatory system exist, this would be an important additional target for such strategies.The somata and proximal dendrites of MNs are contacted by large cholinergic varicosities named ''C boutons'' (3-11). It has been known since 1972 (12) that C boutons originate from spinal cord neurons, but the location of these cells remains unknown (10). Although the C bouton synapse has been anatomically characterized and shown to be associated with postsynaptic type 2 muscarinic (m 2 ) receptors (8-10), neither the physiological effects of m 2 receptor activation on MNs nor the roles of C boutons in motor activity are known. In the absence of motor behavior, exogenous application of cholinergic agonists affects MN excitability via undefined mechanisms (13-17). We therefore studied the possibility that the intrinsic spinal neurons that give rise to the C boutons regulate MN excitability via activation of m 2 receptors, and that this system is used during motor behavior. ResultsThe Effects of Muscarinic Receptor Activation on Spinal MNs. Because C boutons are closely associated with postsynaptic m 2 receptors by the second postnatal week (8-10), we investigated the effects of muscarinic receptor activatio...

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Spinal cholinergic interneurons regulate the excitability of motoneurons during locomotion

Miles

Hartley

Todd

et al. 2007

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

268

365

View full text Add to dashboard Cite

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“…ChAT is a marker of cholinergic motoneurons and interneurons, 46 while HSP-27 labels motoneurons only. 47 There were approximately 30 neurons per section stained with HSP-27, whereas ChAT-labeled sections averaged around 60 neurons per section.…”

Section: Fos In Lamina IXmentioning

confidence: 99%

Use of c-fos to identify activity-dependent spinal neurons after stepping in intact adult rats

Ahn¹,

Guu²,

Tobin

et al. 2005

Spinal Cord

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Study design: An investigation of c-fos activation pattern in spinal neurons of intact adult rats after acute bouts of treadmill locomotion. Objectives: To map spinal neurons that are involved in quadrupedal treadmill stepping of intact adult rats by using c-fos as a marker. Settings: Los Angeles, CA, USA. Methods: Spinal cord sections of rats that were not stepped (n ¼ 4) were used to map the FOSpositive ( þ ) neurons under basal conditions. The stepped group (n ¼ 16) was placed on a treadmill to step quadrupedally for varying durations to induce c-fos activity. Spinal cord sections of thoracic and lumbar segments of Stp and Nstp rats were processed using a c-fos antibody, choline acetyl transferase and heat shock protein 27 for identifying motoneurons. Results: Stepping induced a greater number of FOS þ neurons than was observed in rats that did not step on the treadmill. There was a rostrocaudal and a dorsoventral gradient of FOS labeled neurons. The number of FOS þ neurons increased with the duration of treadmill stepping. Significant increases in FOS þ neurons were in the most medial parts of laminae IV, V, and VII. FOS þ motoneurons increased with treadmill stepping, particularly in large motoneurons (X700 mm 2 ). Conclusion: These data suggest that FOS can be used to identify activity-dependent neuronal pathways in the spinal cord that are associated with treadmill stepping, specifically in lamina VII and in alpha motoneurons. Sponsorship: NIH NS16333, NS40917, and the Christopher Reeve Paralysis Foundation (CRPF VEC 2002).

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“…SPNs and motoneurons are known to be cholinergic and contain the acetylcholine synthetizing enzyme ChAT. 25,55,56 One limitation of this study is the small number of cases that we were able to investigate. Although we examined only three human cases, we were able to detect degenerative changes within the speci®c neuronal population of the spinal cord.…”

Section: Discussionmentioning

confidence: 99%

The changes in human spinal sympathetic preganglionic neurons after spinal cord injury

Krassioukov¹,

Bunge

Pucket

et al. 1999

Spinal Cord

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We have applied conventional histochemical, immunocytochemical and morphometric techniques to study the changes within the human spinal sympathetic preganglionic neurons (SPNs) after spinal cord injury. SPNs are localized within the intermediolateral nucleus (IML) of the lateral horn at the thoraco-lumbar level of the spinal cord and are the major contributors to central cardiovascular control. SPNs in di erent thoracic segments in the normal spinal cord were similar in soma size. SPNs in the IML were also identi®ed using immunoreactivity to choline acetyltransferase. Soma area of SPNs was 400.7+15 mm 2 and 409.9+22 mm 2 at the upper thoracic (T3) and middle thoracic (T7) segments, respectively. In the spinal cord obtained from a person who survived for 2 weeks following a spinal cord injury at T5, we found a signi®cant decrease in soma area of the SPNs in the segments below the site of injury: soma area of SPNs at T8 was 272.9+11 mm 2 . At T1 the soma area was 418+19 mm 2 . In the spinal cord obtained from a person who survived 23 years after cord injury at T3, the soma area of SPNs above (T1) and below (T7) the site of injury was similar (416.2+19 and 425.0+20 mm 2 respectively). The ®ndings demonstrate that the SPNs in spinal segments caudal to the level of the lesion undergo a signi®cant decrease of their size 2 weeks after spinal cord injury resulting in complete transection of the spinal cord. The impaired cardiovascular control after spinal cord injury may be accounted for, in part, by the described changes of the SPNs. The SPNs in spinal segments caudal to the injury were of normal size in the case studied 23 years after the injury, suggesting that the atrophy observed at 2 weeks is transient. More studies are necessary to establish the precise time course of these morphological changes in the spinal preganglionic neurons.

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The morphology and distribution of neurons containing choline acetyltransferase in the adult rat spinal cord: An immunocytochemical study

Cited by 426 publications

References 63 publications

Spinal cholinergic interneurons regulate the excitability of motoneurons during locomotion

Spinal cholinergic interneurons regulate the excitability of motoneurons during locomotion

Use of c-fos to identify activity-dependent spinal neurons after stepping in intact adult rats

The changes in human spinal sympathetic preganglionic neurons after spinal cord injury

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