The transcription factor Nr4a2 was recently revealed as a very early developmental marker of the claustrum (CL) proper in the mouse. The earliest claustral primordium was identified superficially, dorsal to the olfactory cortex, and was subsequently covered by the Nr4a2-negative cells of the insular cortex. Some tangentially migrating claustral derivatives (subplate cells and some endopiriform elements) also expressed this marker. The present study employs the same genetic marker to explore the presence of a comparable pallial division in chicken in which, in principle, the same pallial sectors exist as in mammals. We were indeed able to delineate an early-developing Nr4a2-positive mantle domain at the expected topologic position within the developing chicken lateral pallium. In the chicken as well as in the turtle (from data in the literature), the earliest postmitotic lateropallial cells likewise express Nr4a2 and occupy a corticoid superficial stratum of the mesopallium, which is clearly comparable in spatial and chronological profile to the mouse CL. Other cells produced in this pallial sector include various tangentially migrating Nr4a2-labeled derivatives as well as Nr4a2-negative and Nr4a2-positive local deeper subpopulations that partially interdigitate, forming mesopallial core and shell populations. We hold that the deep avian and reptilian mesopallial formation developing under the superficial corticoid CL homolog represents a field homolog of the insula, although additional studies are required to underpin this hypothesis.

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Models aiming to explain causally the evolutionary or ontogenetic emergence of the pallial isocortex and its regional/areal heterogeneity in mammals use simple or complex assumptions about the pallial structure present in basal mammals and nonmammals. The question arises: how complex is the pattern that needs to be accounted for in causal models? This topic is also paramount for comparative purposes, since some topological relationships may be explained as being ancestral, rather than newly emerged. The mouse pallium is apt to be reexamined in this context, due to the breadth of available molecular markers and correlative experimental patterning results. We center the present essay on a recapitulative glance at the classic theory of concentric mammalian allo‐, meso‐, and neocortex domains. In its simplest terms, this theory postulates a central neocortical island (6 layers) separated by a surrounding mesocortical ring (4–5 layers) from a peripheral allocortical ring (3 layers). These territories show additional partition into regional or areal subdivisions. There are also borderline amygdalar, claustral, and septal areas of the pallium, nuclear in structure. There has been little effort so far to contemplate the full concentric ring model in current “cortex patterning” models. In this essay, we recapitulate the ring idea in mammals (mouse) and consider a potential causal patterning scenario using topologic models. Finally, we briefly explore how far this theory may apply to pallium models proposed recently for sauropsids.

The raphe nuclei represent the origin of central serotonergic projections. The literature distinguishes seven nuclei grouped into rostral and caudal clusters relative to the pons. The boundaries of these nuclei have not been defined precisely enough, particularly with regard to developmental units, notably hindbrain rhombomeres. We hold that a developmental point of view considering rhombomeres may explain observed differences in connectivity and function. There are twelve rhombomeres characterized by particular genetic profiles, and each develops between one and four distinct serotonergic populations. We have studied the distribution of the conventional seven raphe nuclei among these twelve units. To this aim, we correlated 5-HT-immunoreacted neurons with rhombomeric boundary landmarks in sagittal mouse brain sections at different developmental stages. Furthermore, we performed a partial genoarchitectonic analysis of the developing raphe nuclei, mapping all known serotonergic differentiation markers, and compared these results, jointly with others found in the literature, with our map of serotonin-containing populations, in order to examine regional variations in correspondence. Examples of regionally selective gene patterns were identified. As a result, we produced a rhombomeric classification of some 45 serotonergic populations, and suggested a corresponding modified terminology. Only a minor rostral part of the dorsal raphe nucleus lies in the midbrain. Some serotonergic neurons were found in rhombomere 4, contrary to the conventional assumption that it lacks such neurons. We expect that our reclassification of raphe nuclei may be useful for causal analysis of their differential molecular specification, as well as for studies of differential connectivity and function.

Assessment of individual susceptibility to altitude illnesses and more particularly to acute mountain sickness (AMS) by means of tests performed in normobaric hypoxia (NH) or in hypobaric hypoxia (HH) is still debated. Eighteen subjects were submitted to HH and NH tests (PIO2=120 hPa, 30 min) before an expedition. Maximal and mean acute mountain sickness scores (AMSmax and mean) were determined using the self-report Lake Louise questionnaire scored daily. Cardio-ventilatory (f, V(T), PetO2 and PetCO2, HR and finger pulse oxymetry SpO2) were measured at times 5 and 30 min of the tests. Arterial (PaO2, PaCO2, pH, SaO2) and capillary haemoglobin (Hb) measurements were performed at times 30 min. Hypoxic ventilatory (HVR) and cardiac (HCR) responses, peripheral O2 blood content (CpO2) were calculated. A significant time effect is found for DeltaSpO2 (P = 0.04). Lower PaCO2 (P = 0.005), SaO2 (P = 0.07) and higher pH (P = 0.02) are observed in HH compared to NH. AMSmax varied from 3 to12 and AMSmean between 0.6 and 3.5. In NH at 30 min, AMSmax is related to PetO2 (R = 0.61, P = 0.03), CpO2 (R = -0.53, P = 0.02) and in HH to CpO2 (R = -0.57, P = 0.01). In NH, AMSmean is related to Deltaf (R = 0.46, P = 0.05), HCR (R = 0.49, P = 0.04), CpO2 (R = -0.51, P = 0.03) and, in HH at 30 min, to V(T) (R = 0.69, P = 0.01) and a tendency for CpO2 (R = -0.43, P = 0.07). We conclude that HH and NH tests are physiologically different and they must last 30 min. CpO2 is an important variable to predict AMS. For practical considerations, NH test is proposed to quantify AMS individual susceptibility using the formulas: AMSmax = 9.47 + 0.104PetO2(hPa)-0.68CpO2 (%), (R = 0.77, P = 0.001); and AMSmean = 3.91 + 0.059Deltaf + 0.438HCR-0.135CpO2 (R = 0.71, P = 0.017).

Background: Cytokine mRNA quantification is widely used to investigate cytokine profiles, particularly in small samples. Real-time polymerase chain reaction is currently the most reliable method of quantifying low-level transcripts such as cytokine and cytokine receptor mRNAs. This accurate technique allows the quantification of a larger pattern of cytokines than quantification at the protein level, which is limited to a smaller number of proteins.

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