Coordinated development of identified serotonergic neurons and their target ciliary cells in Helisoma trivolvis embryosKoss, Ron; Diefenbach, Thomas J.; Kuang, Shihuan; Doran, Shandra A.; Goldberg, Jeffrey I.
doi: 10.1002/cne.10512pmid: 12561073
Embryonic neuron C1s (ENC1s) are bilateral serotonergic neurons that function as cilioexcitatory motor neurons in embryonic development of the pond snail, Helisoma trivolvis. Recent experiments demonstrated that these neurons stimulate cilia‐driven embryo rotation in response to hypoxia. In the present study, a comprehensive anatomic analysis of these cells and their target ciliary structures was done to address the following questions: (1) Does ENC1 have a morphology consistent with an oxygen‐sensitive sensory cell; (2) Is the development of ENC1's neurite outgrowth pathway coordinated with the development of its target effectors, the pedal and dorsolateral ciliary bands; and (3) What is the anatomic basis of ENC1–ciliary communication? By using an array of microscopic techniques on live and serotonin‐immunostained embryos, we found that each ENC1 possessed an apical dendrite that was capped with an integral dendritic knob penetrating the embryo surface. The dendritic knobs contained both microvilli and nonmotile cilia that suggested a sensory transduction role. Each ENC1 also possessed a descending projection, whose development was characterized by the rapid formation of the primary neurite pathway between stages E13 and E15, with the primary neurite of the right ENC1 developing in advance of its contralateral homologue. Secondary neurite branches formed between stages E15 and E30 in a spatiotemporal pattern that closely matched the development of the dorsolateral and pedal bands of cilia. Both dorsolateral and pedal ciliated cells formed basal processes that contacted ENC1 neurites. Finally, gap junction profiles were observed at neurite–neurite, neurite–ciliary cell, and ciliary cell–ciliary cell apposition sites, whereas putative chemical synaptic profiles were observed at neurite–neurite and neurite–ciliary cell apposition sites. J. Comp. Neurol. 457:313–325, 2003. © 2003 Wiley‐Liss, Inc.
Retinotopic pathways providing motion‐selective information to the lobula from peripheral elementary motion‐detecting circuitsDouglass, John K.; Strausfeld, Nicholas J.
doi: 10.1002/cne.10575pmid: 12561074
Recordings from afferent channels from the medulla supplying deep neuropils of the fly's optic lobes reveal different filter properties among the three classes of afferent neurons: transmedullary cells, T2 neurons, and Y cells. Whereas transmedullary cells respond to local flicker stimuli without discriminating these from directional or oriented motion, the T2 afferent neurons show clear motion orientation selectivity, which corresponds closely with a morphological bias in the orientation of their dendrites and could also be influenced by systems of local recurrent neurons in the medulla. A Y cell having a clearly defined terminal in the lobula, but having dendrite‐like processes in the medulla and, possibly, the lobula plate, discriminates the direction of motion and its orientation. These results demonstrate unambiguously that the lobula receives information about motion and that the channels carrying it are distinct from those supplying wide‐field motion‐selective neurons in the lobula plate. Furthermore, recordings from a newly identified recurrent neuron linking the lobula back to the inner medulla demonstrate that the lobula discriminates nondirectional edge motion from flicker, thereby reflecting a property of this neuropil that is comparable with that of primary visual cortex in cats. The present findings support the proposal that elementary motion detecting circuits supply several parallel channels through the medulla, which segregate to, but are not shared by, the lobula and the lobula plate. The results are discussed in the context of other intracellular recordings from retinotopic neurons and with analogous findings from mammalian visual systems. J. Comp. Neurol. 457:326–344, 2003. © 2003 Wiley‐Liss, Inc.
Emx1 and Emx2 cooperate to regulate cortical size, lamination, neuronal differentiation, development of cortical efferents, and thalamocortical pathfindingBishop, Kathie M.; Garel, Sonia; Nakagawa, Yasushi; Rubenstein, John L.R.; O'Leary, Dennis D.M.
doi: 10.1002/cne.10550pmid: N/A
The homeobox transcription factors Emx1 and Emx2 are expressed in overlapping patterns that include cortical progenitors in the dorsal telencephalic neuroepithelium. We have addressed cooperation of Emx1 and Emx2 in cortical development by comparing phenotypes in Emx1; Emx2 double mutant mice with wild‐type and Emx1 and Emx2 single mutants. Emx double mutant cortex is greatly reduced compared with wild types and Emx single mutants; the hippocampus and dentate gyrus are absent, and growth and lamination of the olfactory bulbs are defective. Cell proliferation and death are relatively normal early in cortical neurogenesis, suggesting that hypoplasia of the double mutant cortex is primarily due to earlier patterning defects. Expression of cortical markers persists in the reduced double mutant neocortex, but the laminar patterns exhibited are less sharp than normal, consistent with deficient cytoarchitecture, probably due in part to reduced numbers of preplate and Reelin‐positive Cajal‐Retzius neurons. Subplate neurons also exhibit abnormal differentiation in double mutants. Cortical efferent axons fail to exit the double mutant cortex, and TCAs pass through the striatum and approach the cortex but do not enter it. This TCA pathfinding defect appears to be non‐cell autonomous and supports the hypothesis that cortical efferents are required scaffolds to guide TCAs into cortex. In double mutants, some TCAs fail to turn into ventral telencephalon and take an aberrant ventral trajectory; this pathfinding defect correlates with an Emx2 expression domain in ventral telencephalon. The more severe phenotypes in Emx double mutants suggest that Emx1 and Emx2 cooperate to regulate multiple features of cortical development. J. Comp. Neurol. 457:345–360, 2003. © 2003 Wiley‐Liss, Inc.
Odor‐evoked activity is spatially distributed in piriform cortexIllig, Kurt R.; Haberly, Lewis B.
doi: 10.1002/cne.10557pmid: 12561076
Much data on the olfactory bulb (OB) indicates that structural characteristics of odorant molecules are encoded as ordered, spatially consolidated sets of active cells. New results with “genetic tracing” (Zou et al. [2001] Nature 414:173–179) suggest that spatial order is also present in projections from the OB to the olfactory cortex. For the piriform cortex (PC), results with this technique indicate that afferents conveying input derived from single olfactory receptors (ORs) are distributed to well‐defined patches in the anterior PC (APC) but that these patches are much larger than in the OB. We have used c‐fos induction to examine how input patterning for single ORs is translated into patterns of odor‐evoked cellular activity in the PC. The laminar distribution of labeled cells and dual‐immunostaining for γ‐aminobutyric acid (GABA)ergic markers indicated that activity was detected largely in pyramidal cells. In odor‐stimulated rats, labeled cells were present throughout the posterior PC (PPC) but were concentrated in prominent rostrocaudal bands in APC. Analysis of responses to different odorants and concentrations revealed that locations and shapes of bands conveyed no apparent information regarding odor quality, rather, they appeared to correspond to subregions of the APC distinguished by cytoarchitecture and connectivity. Small‐scale variations in labeling density were observed within APC bands and throughout the PPC that could reflect the presence of a complex topographical order, but discrete patches at consistent locations as observed by genetic tracing were absent. This finding suggests that as a result of afferent overlap and intracortical processing, odor‐quality information is represented by spatially distributed sets of cells. A distributed organization may be optimal for discriminating biologically relevant odorants that activate large numbers of ORs. J. Comp. Neurol. 457:361–373, 2003. © 2003 Wiley‐Liss, Inc.
Pontine sources of norepinephrine in the cat cochlear nucleusThompson, Ann M.
doi: 10.1002/cne.10540pmid: 12561077
In the current study, the distribution of noradrenergic neurons in the pontine tegmentum that project to the cochlear nucleus was determined with retrograde tract tracing combined with neurotransmitter immunohistochemistry in the cat. Double‐labeled neurons were observed in all noradrenergic cell groups, in both the dorsolateral and the ventrolateral tegmentum. Half of the double‐labeled cells were located in the locus coeruleus complex. Most of these were situated in its ventral division. Most other double‐labeled cells were located in peribrachial regions, especially lateral to the brachium conjunctivum. Relatively few double‐labeled cells were observed in both the A4 and the A5 cell groups, 2% and 0.4%, respectively, of the total. Except for neurons in A5, which projected only contralaterally, the projections were bilateral, with an ipsilateral preponderance. The results indicate that neurons located in the ipsilateral dorsolateral tegmentum, namely, in the locus coeruleus complex and the peribrachial region, are the primary source of pontine noradrenergic afferents to the cochlear nucleus of the cat. J. Comp. Neurol. 457:374–383, 2003. © 2003 Wiley‐Liss, Inc.
Steroid‐triggered programmed cell death of a motoneuron is autophagic and involves structural changes in mitochondriaKinch, Ginger; Hoffman, Kurt L.; Rodrigues, Elizabeth M.; Zee, Michele C.; Weeks, Janis C.
doi: 10.1002/cne.10563pmid: 12561078
Neuronal death occurs during normal development and disease and can be regulated by steroid hormones. In the hawkmoth, Manduca sexta, individual accessory planta retractor (APR) motoneurons undergo a segment‐specific pattern of programmed cell death (PCD) at pupation that is triggered directly and cell autonomously by the steroid hormone 20‐hydroxyecdysone (20E). APRs from abdominal segment six [APR(6)s] die by 48 hours after pupal ecdysis (PE; entry into the pupal stage), whereas APR(4)s survive until adulthood. Cell culture experiments showed previously that 20E acts directly on APRs to trigger PCD, with intrinsic segmental identity determining which APRs die. The APR(6) death pathway includes caspase activation and loss of mitochondrial function. We used transmission electron microscopy to investigate the ultrastructure of APR somata before and during PCD. APR(4)s showed normal ultrastructure at all stages examined, as did APR(6)s until approximately stage PE. During APR(6) death, there was massive accumulation of autophagic bodies and vacuoles, mitochondria became ultracondensed and aggregated into compact clusters, and ribosomes aggregated in large blocks. Nuclear ultrastructure remained normal, without chromatin condensation, until the nuclear envelope fragmented late in the death process. Light microscopic immunocytochemistry showed that dying APR(6)s were TUNEL‐positive, which is diagnostic of fragmented DNA. These observations indicate that the steroid‐induced, caspase‐dependent, cell‐autonomous PCD of APR(6)s is autophagic, not apoptotic, and support an early role for mitochondrial alterations during PCD. This system permits the study of neuronal death in response to its bona fide developmental signal, the rise in a steroid hormone. J. Comp. Neurol. 457:384–403, 2003. © 2003 Wiley‐Liss, Inc.
Visualization of S100B‐positive neurons and glia in the central nervous system of EGFP transgenic miceVives, Virginie; Alonso, Gérard; Solal, Anne Cohen; Joubert, Dominique; Legraverend, Catherine
doi: 10.1002/cne.10552pmid: 12561079
S100B, the EF‐hand Ca++‐binding protein with gliotrophic and neurotrophic properties implicated in the pathogenesis of Alzheimer's disease, is coined as a glial marker, despite its documented presence in rodent brain neurons. We have generated a transgenic mouse whose EGFP reporter, controlled by the −1669/+3106 sequence of the murine S100B gene, allows the direct microscopic observation of most S100B‐expressing cells in the central nervous system (CNS). From embryonic day 13 onward, EGFP expression was targeted to selected neuroepithelial, glial, and neuronal cells, indicating that cell‐specific expression of S100B is regulated at the transcriptional level during development. In adult mice, the highest level of EGFP expression was found in ependymocytes; astrocytes; and spinal, medullar, pontine, and deep cerebellar S100B neurons. Our results, thus, agree with earlier reports suggesting that S100B is not a CNS glial‐specific marker. In addition, we detected EGFP and S100B in forebrain neurons previously thought not to express S100B in the mouse, including neurons of primary motor and somatosensory neocortical areas, the ventral pallidum and prerubral field. Another interesting finding was the selected EGFP targeting to neonatal S100B oligodendrocytes and adult NG2 progenitors as opposed to mature S100B oligodendrocytes. This finding suggests that, except for oligodendrocytes at the last stage of myelin maturation, the −1669/+3106 sequence of the S100B gene is a useful reagent for driving expression of transgenes in most S100B‐expressing cells of mouse brain. J. Comp. Neurol. 457:404–419, 2003. © 2003 Wiley‐Liss, Inc.
Differential morphology of pyramidal tract‐type and intratelencephalically projecting‐type corticostriatal neurons and their intrastriatal terminals in ratsReiner, Anton; Jiao, Yun; Del Mar, Nobel; Laverghetta, Antonio Vincent; Lei, Wan Long
doi: 10.1002/cne.10541pmid: 12561080
Two types of corticostriatal projection neurons have been identified: 1) one whose intrastriatal arborization arises as a collateral of a projection to the ipsilateral brainstem via the pyramidal tract (PT‐type); and 2) one that projects intratelencephalically to the cortex and striatum, in many cases bilaterally, but not extratelencephalically (IT‐type). To assess possible functional differences between these two neuron types, we characterized their laminar location in the cortex, their perikaryal size, and the morphology of their intrastriatal terminals. IT‐type neurons were retrogradely labeled by tetramethylrhodamine‐dextran amine (RDA)3k injection into the contralateral striatum, whereas their intrastriatal terminals were labeled anterogradely by biotinylated dextran amine (BDA)10k injection into the contralateral motor or primary somatosensory cortex. To label PT‐type neurons and their ipsilateral intrastriatal terminals retrogradely, BDA3k was injected into the pontine pyramidal tract. We found that IT‐type neuronal perikarya are medium‐sized (12–13 μm) and located in layer III and upper layer V, whereas PT‐type perikarya are larger (18–19 μm) and most commonly located in lower layer V. At the electron microscopic level, the intrastriatal terminals of both corticostriatal neuron types made asymmetric synaptic contact with spine heads and less frequently with dendrites. IT‐type axospinous terminals were characteristically small (0.4–0.5 μm) and regular in shape, whereas PT‐type terminals were typically large (0.8–0.9 μm) and often irregular in shape. Perforated postsynaptic densities were common for PT‐type terminals, but not IT‐type. The clear differences between these two corticostriatal neuron types in perikaryal size and laminar location in the cortex, and in the size and shape of their intrastriatal terminals, suggest that they may differ in the nature of their influence on the striatum. J. Comp. Neurol. 457:420–440, 2003. © 2003 Wiley‐Liss, Inc.