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Cannabis use is associated with increased risk of later psychotic disorder but whether it affects incidence of the disorder remains unclear. We aimed to identify patterns of cannabis use with the strongest effect on odds of psychotic disorder across Europe and explore whether differences in such patterns contribute to variations in the incidence rates of psychotic disorder.

Introducción: Las alucinaciones auditivas (AH) son uno de los síntomas más prevalentes de la esquizofrenia. Pueden causar varias alteraciones cerebrales, especialmente cambios en los volúmenes del hipocampo y la amígdala, regiones relacionadas con la transmisión y el procesamiento de señales auditivas y recuerdos emocionales.

The expression of early developmental markers such as doublecortin (DCX) and the polysialylated-neural cell adhesion molecule (PSA-NCAM) has been used to identify immature neurons within canonical neurogenic niches. Additionally, DCX/PSA-NCAM+ immature neurons reside in cortical layer II of the paleocortex and in the paleo- and entorhinal cortex of mice and rats, respectively. These cells are also found in the neocortex of guinea pigs, rabbits, some afrotherian mammals, cats, dogs, non-human primates, and humans. The population of cortical DCX/PSA-NCAM+ immature neurons is generated prenatally as conclusively demonstrated in mice, rats, and guinea pigs. Thus, the majority of these cells do not appear to be the product of adult proliferative events. The immature neurons in cortical layer II are most abundant in the cortices of young individuals, while very few DCX/PSA-NCAM + cortical neurons can be detected in aged mammals. Maturation of DCX/PSA-NCAM+ cells into glutamatergic and GABAergic neurons has been proposed as an explanation for the age-dependent reduction in their population over time. In this review, we compile the recent information regarding the age-related decrease in the number of cortical DCX/PSA-NCAM+ neurons. We compare the distribution and fates of DCX/PSA-NCAM + neurons among mammalian species and speculate their impact on cognitive function. To respond to the diversity of adult neurogenesis research produced over the last number of decades, we close this review by discussing the use and precision of the term “adult non-canonical neurogenesis.”

Emerging evidence indicates that attention deficits, which are frequently observed as core symptoms of neuropsychiatric disorders, may be elicited by early life stress. However, the mechanisms mediating these stress effects remain unknown. The prefrontal cortex (PFC) has been implicated in the regulation of attention, including dysfunctions in GABAergic transmission, and it is highly sensitive to stress. Here, we investigated the involvement of neuroligin-2 (NLGN-2), a synaptic cell adhesion molecule involved in the stabilization and maturation of GABAergic synapses, in the PFC in the link between stress and attention deficits. First, we established that exposure of rats to stress during the peripubertal period impairs attention in the five-choice serial reaction time task and results in reductions in the GABA-synthesizing enzyme glutamic acid decarboxylase in different PFC subregions (ie, prelimbic (PL), infralimbic, and medial and ventral orbitofrontal (OFC) cortex) and in NLGN-2 in the PL cortex. In peripubertally stressed animals, NLGN-2 expression in the PL and OFC cortex correlated with attention measurements. Subsequently, we found that adeno-associated virus-induced rescue of NLGN-2 in the PFC reverses the stress-induced attention deficits regarding omitted trials. Therefore, our findings highlight peripuberty as a period that is highly vulnerable to stress, leading to the development of attention deficits and a dysfunction in the PFC GABAergic system and NLGN-2 expression. Furthermore, NLGN-2 is underscored as a promising target to treat stress-induced cognitive alterations, and in particular attentional deficits as manifested by augmented omissions in a continuous performance task.

The lizard medial cortex, a region homologous to the mammalian dentate gyrus, shows postnatal neurogenesis and the surprising ability to replace its neurons after being lesioned specifically with the neurotoxin 3‐acetylpyridine. As the polysialylated form of the neural cell adhesion molecule (PSA‐NCAM) is expressed during neuronal migration and differentiation, we have studied its distribution in adult lizards and also during the lesion‐regeneration process. In the medial cortex of control animals, many labeled fusiform somata, presumably corresponding to migratory neuroblasts, appeared in the inner plexiform layer. There were also scattered immunoreactive granule neurons in the cell layer. Double immunocytochemistry with 5′‐bromodeoxyuridine revealed that some of the PSA‐NCAM–expressing cells in the inner plexiform and cell layers were generated recently. PSA‐NCAM immunoreactivity was also present in the dorsomedial, dorsal, and lateral cortices, as well as in the dorsal ventricular ridge, the nucleus accumbens, and the nucleus sphericus. Twelve hours after the injection of 3‐acetylpyridine, some medial cortex granule neurons appeared degenerated, although some of them still expressed PSA‐NCAM. One to 2 days after the injection, most granule neurons appeared degenerated and no PSA‐NCAM immunoreactivity was detected in the medial cortex cell layer. Four to 7 days after treatment, abundant labeled fusiform cells populated the inner plexiform layer and some immunoreactive somata were seen in the cell layer. Fifteen to 30 days after the neurotoxin injection, the number of PSA‐NCAM expressing granule neurons augmented considerably and the level was still above control levels in lizards that survived 42 days. Our results show for the first time the expression of PSA‐NCAM in a reptile brain, where it appears to participate in the migration and differentiation of granule neurons during adult neurogenesis and regeneration. J. Comp. Neurol. 453:145–156, 2002. © 2002 Wiley‐Liss, Inc.

Zinc is one of the most abundant oligoelements in the living cell. It appears tightly bound to metallothioneins, loosely bound to some metalloproteins and nucleic acids, or even as free ion. Small amounts of zinc ions (in the nanomolar range) regulate a plentitude of enzymatic proteins, receptors, and transcription factors; thus, cells need accurate homeostasis of zinc ions. Some neurons have developed mechanisms to accumulate zinc in specific membrane compartments (“vesicular zinc”) which can be revealed using histochemical techniques. This article is a short report on the different direct–indirect experimental approaches for zinc and heavy metal detection in neurons. Substances giving a bright color or emitting fluorescence when in contact with divalent metal ions are currently used to detect them inside cells; their use leads to the so called “direct” methods. The fixation and precipitation of metal ions as insoluble salt precipitates, their maintenance along the histological process, and their demonstration after autometallographic development are essential steps for other methods, the so‐called “indirect methods” (Timm and Danscher Neo‐Timm methods). Microsc. Res. Tech. 56:318–331, 2002. © 2002 Wiley‐Liss, Inc.

The rat collapsin response‐mediated protein 4 (rCRMP‐4) is a member of a family of proteins that are involved in axonal growth. It is found transiently in postmitotic neurons, such as those that are generated in the adult hippocampus. The authors used immunocytochemistry to investigate whether areas of the rat central nervous system (CNS) that retain postnatal neurogenesis express this protein. They found pronounced rCRMP‐4 immunoreactivity in recently generated cells in the dentate granular layer, the subventricular zone, the olfactory bulbs, and the rostral migratory stream, four areas in which the production or migration of neurons occurs in adulthood. However, rCRMP‐4 immunoreactivity also is expressed in many other regions of the rat brain in which there is no record of adult neurogenesis or neuronal migration, e.g., in the olfactory glomeruli and in neurons of the cerebral cortex. In the hypothalamus, intensely rCRMP‐4‐labeled neurons populated the supraoptic, paraventricular, and periventricular nuclei as well as the median eminence and the arcuate nucleus. Immunoreactivity for rCRMP‐4 also was present in certain neurons of the interpeduncular nucleus, median raphe, superior colliculus, and scattered granule cerebellar neurons. Many of these regions are known to display axonal outgrowth and/or synaptic rearrangement in adulthood and to coexpress the polysialylated form of the neural cell adhesion molecule. Thus, the results of this study suggest that rCRMP‐4 expression in the CNS is associated with cells that are migrating or are undergoing axonal growth. Nevertheless, small, rCRMP‐4‐immunoreactive cells were seen throughout the brain. These cells did not express neuronal, astroglial, or microglial markers, although some of them also were immunoreactive for rip antibody, suggesting an oligodendroglial lineage. J. Comp. Neurol. 424:628–639, 2000. © 2000 Wiley‐Liss, Inc.

In adult cornu ammonis hippocampi, erythropoietin (EPO) expression drives the differentiation of new neurons, independent of DNA synthesis, and increases dendritic spine density. This substantial brain hardware upgrade is part of a regulatory circle: during motor-cognitive challenge, neurons experience “functional” hypoxia, triggering neuronal EPO production, which in turn promotes improved performance.Here, we show an unexpected involvement of resident microglia. During EPO upregulation and stimulated neurodifferentiation, either by functional or inspiratory hypoxia, microglia numbers decrease. Treating mice with recombinant human (rh)EPO or exposure to hypoxia recapitulates these changes and reveals the involvement of neuronally expressed IL-34 and microglial CSF1R. Surprisingly, EPO affects microglia in phases, initially by inducing apoptosis, later by reducing proliferation, and overall dampens microglia activity and metabolism, as verified by selective genetic targeting of either the microglial or pyramidal neuronal EPO receptor. We suggest that during accelerating neuronal differentiation, EPO acts as regulator of the CSF1R-dependent microglia.