Organization of cortical projections to the medullary subnucleus reticularis dorsalis: A retrograde and anterograde tracing study in the rat

Desbois, Christophe; Bars, D. Le; Villanueva, Luis

doi:10.1002/(sici)1096-9861(19990726)410:2<178::aid-cne2>3.0.co;2-f

Cited by 59 publications

(16 citation statements)

References 73 publications

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“…To identify targets of the ectopic PLAP or GFP-labeled axons in the midbrain and hindbrain region of Tbr1 −/− ; Fezf2 +/− or Tbr1 −/− ; Golli-τ-GFP mice, we compared the PLAP staining pattern with the expression pattern of choline acetyltransferase (ChAT), a marker of midbrain and hindbrain motor nuclei that are targets of layer 5 corticobulbar projections (Valverde, 1962; Satoh et al, 1983; O'Leary and Koester, 1993; Desbois et al, 1999). We found that ectopic, mutant PLAP projections overlapped with ChAT immunostaining in what appeared to be the pedunculopontine tegmental nucleus (Figure 2K–M).…”

Section: Resultsmentioning

confidence: 99%

Tbr1andFezf2Regulate Alternate Corticofugal Neuronal Identities during Neocortical Development

McKenna¹,

Betancourt²,

Larkin³

et al. 2011

J. Neurosci.

231

293

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The molecular mechanisms regulating fate divergence of closely related, but distinct, layer 6 corticothalamic and layer 5 subcerebral projection neurons are largely unknown. We present evidence for central transcriptional mechanisms that regulate fate specification of corticothalamic (layer 6) and subcerebral (layer 5) projection neurons. We found that TBR1 promotes the identity of corticothalamic neurons and represses subcerebral fates through reducing expression of Fezf2 and CTIP2. These conclusions are based on: (1) In Tbr1−/− mice, the number of cells expressing layer 6 markers was reduced, and the number of cells expressing layer 5 markers was increased. Early-born (birthdated on E11.5) neurons ectopically expressed subcerebral neuronal markers, and extended their axons into subcerebral targets; (2) Ectopic Tbr1 expression in layer 5 neurons prevented them from extending axons into the brain stem and the spinal cord; (3) ChIP analysis using TBR1 antibodies showed that TBR1 bound to a conserved region in the Fezf2 gene; (4) Analysis of Fezf2 mutants and Tbr1−/−; Fezf2−/− compound mutants provided evidence that Fezf2 blocks corticothalamic fate in layer 5 by reducing Tbr1 expression in subcerebral neurons. All neocortical regions appear to use this core transcriptional program to specify corticothalamic (layer 6) and subcerebral (layer 5) projection neurons.

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Section: Resultsmentioning

confidence: 99%

Tbr1andFezf2Regulate Alternate Corticofugal Neuronal Identities during Neocortical Development

McKenna¹,

Betancourt²,

Larkin³

et al. 2011

J. Neurosci.

231

293

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“…The reticular zone just medial to the spinal nucleus of the trigeminal nerve (SpV) has been shown to be important for the coordination of pain and eye blink reflex pathways (Almeida and Lima, 1997; Almeida et al, 1999; Lima and Almeida, 2002; Leite-Almeida et al, 2006; Smit et al, 2006), and receives direct cortical and spinal input (Desbois et al, 1999). Lmx1b -derived neurons were present within the parvocellular reticular formation and dorsal medullary reticular nucleus (PCRt, MdD, Figures 2B–H).…”

Section: Resultsmentioning

confidence: 99%

“…Neurons within the region containing dorsal Lmx1b , PCRt population have been implicated in facilitating nociceptive behavior (Almeida et al, 1999). These neurons receive ascending innervation from dorsal horn projection neurons as well as descending input from multiple cortical areas (Almeida and Lima, 1997; Desbois et al, 1999). Previously, neurons within the MdD region been implicated in the eye blink reflex as they express cFos after supraorbital nerve stimulation and project to the orbicularis oculi muscle innervating VII motoneurons (Smit et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Transcription factors define the neuroanatomical organization of the medullary reticular formation

Gray¹

2013

Front. Neuroanat.

134

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The medullary reticular formation contains large populations of inadequately described, excitatory interneurons that have been implicated in multiple homeostatic behaviors including breathing, viserosensory processing, vascular tone, and pain. Many hindbrain nuclei show a highly stereotyped pattern of localization across vertebrates suggesting a strong underlying genetic organization. Whether this is true for neurons within the reticular regions of hindbrain is unknown. Hindbrain neurons are derived from distinct developmental progenitor domains each of which expresses distinct patterns of transcription factors (TFs). These neuronal populations have distinct characteristics such as transmitter identity, migration, and connectivity suggesting developmentally expressed TFs might identify unique subpopulations of neurons within the reticular formation. A fate-mapping strategy using perinatal expression of reporter genes within Atoh1, Dbx1, Lmx1b, and Ptf1a transgenic mice coupled with immunohistochemistry (IHC) and in situ hybridization (ISH) were used to address the developmental organization of a large subset of reticular formation glutamatergic neurons. All hindbrain lineages have relatively large populations that extend the entire length of the hindbrain. Importantly, the location of neurons within each lineage was highly constrained. Lmx1b- and Dbx1- derived populations were both present in partially overlapping stripes within the reticular formation extending from dorsal to ventral brain. Within each lineage, distinct patterns of gene expression and organization were localized to specific hindbrain regions. Rostro-caudally sub-populations differ sequentially corresponding to proposed pseudo-rhombomereic boundaries. Dorsal-ventrally, sub-populations correspond to specific migratory positions. Together these data suggests the reticular formation is organized by a highly stereotyped developmental logic.

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“…Within the spinal–supraspinal–spinal loop, not only the PAG but also the subnucleus reticularis dorsalis (SRD) of the medulla appears to be critically important for CPM [57,58]. The SRD not only plays an important part in the processing of ascending nociceptive information from peripheral tissues, but also signals back to dorsal horn neurons of the spinal cord [59]. Furthermore, the SRD appears to receive information from several cortical structures including the prefrontal cortex and anterior cingulate cortex, which might explain the influence of psychological factors on CPM [60–62].…”

Section: Endogenous Pain Modulationmentioning

confidence: 99%

Abnormal endogenous pain modulation is a shared characteristic of many chronic pain conditions

Staud¹

2012

Expert Review of Neurotherapeutics

246

176

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The intensity of acute and chronic pain depends on interactions between peripheral impulse input and CNS pain mechanisms, including facilitation and inhibition. Whereas tonic pain inhibition is a characteristic of most pain-free individuals, pain facilitation can be detected in many chronic pain patients. The capability to inhibit pain is normally distributed along a wide continuum in the general population and can be used to predict chronic pain. Accumulating evidence suggests that endogenous pain inhibition depends on activation of the prefrontal cortex, periaqueductal gray and rostral ventral medulla. Quantitative sensory test paradigms have been designed to acquire detailed information regarding each individual’s endogenous pain inhibition and facilitation. Such tests include: temporal summation of pain, which is mostly used to assess facilitatory pain modulation by measuring the change in pain perception during a series of identical nociceptive stimuli; and conditioned pain modulation, which tests pain inhibition by utilizing two simultaneously applied painful stimuli (the ‘pain inhibits pain’ paradigm). Considerable indirect evidence seems to indicate that not only increased pain facilitation but also ineffective pain inhibition represents a predisposition for chronic pain. This view is supported by the fact that many chronic pain syndromes (e.g., fibromyalgia, temporomandibular joint disorder, irritable bowel syndrome, headache and chronic fatigue syndrome) are associated with hypersensitivity to painful stimuli and reduced endogenous pain inhibition. However, future prospective studies will be necessary to provide definitive evidence for this relationship. Such research would not only provide important information about mechanisms relevant to chronic pain but would also permit identification of individuals at high risk for future chronic pain.

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Organization of cortical projections to the medullary subnucleus reticularis dorsalis: A retrograde and anterograde tracing study in the rat

Cited by 59 publications

References 73 publications

Tbr1andFezf2Regulate Alternate Corticofugal Neuronal Identities during Neocortical Development

Tbr1andFezf2Regulate Alternate Corticofugal Neuronal Identities during Neocortical Development

Transcription factors define the neuroanatomical organization of the medullary reticular formation

Abnormal endogenous pain modulation is a shared characteristic of many chronic pain conditions

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