What and how do maggots smell?

The olfactory response of maggots (the larvae of cyclorrhaphous flies) and its neuroanatomical basis have been a subject for scientific investigation since the 17th century, preoccupying both fundamental and applied scientists. Despite its apparently arcane nature, the subject raises a series of major neurobiological problems, in particular, the relationship between the number of odours that can be detected and the apparently simple systems of detection and processing available to larvae. Molecular biological techniques in both neuroanatomy and cell biology have made it possible to begin to resolve some of these problems, if data from a wide range of studies are integrated. Four sectors of research on a large number of species are reviewed: the behaviour involved in the olfactory response, the wide range of odours that can be detected, the neuroanatomical basis of olfaction in cyclorrhaphous larvae and the number of receptors involved in detecting these odours. Finally, a neuroanatomical model of olfactory processing is presented, together with perspectives for future research, emphasising the importance of studying the ecology of the species under investigation.     

Lamina specific postnatal development of PKCγ interneurons within the rat medullary dorsal horn

Protein kinase C gamma (PKCγ) interneurons, located in the superficial spinal (SDH) and medullary dorsal horns (MDH), have been shown to play a critical role in cutaneous mechanical hypersensitivity. However, a thorough characterization of their development in the MDH is lacking. Here, it is shown that the number of PKCγ‐ir interneurons changes from postnatal day 3 (P3) to P60 (adult) and such developmental changes differ according to laminae. PKCγ‐ir interneurons are already present at P3‐5 in laminae I, IIo, and III. In lamina III, they then decrease from P11–P15 to P60. Interestingly, PKCγ‐ir interneurons appear only at P6 in lamina IIi, and they conversely increase to reach adult levels at P11–15. Analysis of neurogenesis using bromodeoxyuridine (BrdU) does not detect any PKCγ‐BrdU double‐labeling in lamina IIi. Quantification of the neuronal marker, NeuN, reveals a sharp neuronal decline (∼50%) within all superficial MDH laminae during early development (P3–15), suggesting that developmental changes in PKCγ‐ir interneurons are independent from those of other neurons. Finally, neonatal capsaicin treatment, which produces a permanent loss of most unmyelinated afferent fibers, has no effect on the development of PKCγ‐ir interneurons. Together, the results show that: (i) the expression of PKCγ‐ir interneurons in MDH is developmentally regulated with a critical period at P11‐P15, (ii) PKCγ‐ir interneurons are developmentally heterogeneous, (iii) lamina IIi PKCγ‐ir interneurons appear less vulnerable to cell death, and (iv) postnatal maturation of PKCγ‐ir interneurons is due to neither neurogenesis, nor neuronal migration, and is independent of C‐fiber development. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 77: 102–119, 2017     

New Aspects of Progesterone Interactions with the Actin Cytoskeleton and Neurosteroidogenesis in the Cerebellum and the Neuronal Growth Cone

The impact of progesterone on neuronal tissues in the central (CNS) and peripheral (PNS) nervous system is of significant scientific and therapeutic interest. Glial and neuronal cells of vertebrates express steroidogenic enzymes, and are able to synthesize progesterone de novo from cholesterol. Progesterone is described to have neuroprotective, neuroreparative, anti-degenerative, and anti-apoptotic effects in the CNS and the PNS. Thus, the first clinical studies promise new therapeutic options using progesterone in the treatment of patients with traumatic brain injury. Additionally, experimental data from different animal models suggest further positive effects of progesterone on neurological diseases such as cerebral ischemia, peripheral nerve injury and amyothropic lateral sclerosis. In regard to this future clinical use of progesterone, we discuss in this review the underlying physiological principles of progesterone effects in neuronal tissues. Mechanisms leading to morphological reorganizations of neurons in the CNS and PNS affected by progesterone are addressed, with special focus on the actin cytoskeleton. Furthermore, new aspects of a progesterone-dependent regulation of neurosteroidogenesis mediated by the recently described progesterone binding protein PGRMC1 in the nervous system are discussed.     

Mitochondrial control of sleep

The function of sleep remains one of biology's biggest mysteries. A solution to this problem is likely to come from a better understanding of sleep homeostasis, and in particular of the cellular and molecular processes that sense sleep need and settle sleep debt. Here, we highlight recent work in the fruit fly showing that changes in the mitochondrial redox state of sleep-promoting neurons lie at the heart of a homeostatic sleep-regulatory mechanism. Since the function of homeostatically controlled behaviours is often linked to the regulated variable itself, these findings corroborate with the hypothesis that sleep serves a metabolic function.     

State transitions in the statistically stable place cell population correspond to rate of perceptual change

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Olfaction in Lamprey Pallium Revisited—Dual Projections of Mitral and Tufted Cells

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