Time for space at the table: an African American - Native American analyst-in-training's first-hand reflections. A call for the IAAP to publicly denounce (but not erase) the White supremacist writings of C.G. Jung.

This article provides an African American-Native American analyst-in-training's first-hand reflections on Jung's firm depiction of Blacks of African descent and America's First Nations People (the Red man) as inferior, through a theory of primitivity that unveils Jung's belief in and support of White supremacy. With no intended disrespect or neglect intended toward America's First Nations, this article focuses primarily on Jung's apparent disdain for Blacks (the Negro). Utilizing writings from Frederick Douglass, W.E.B. Du Bois and Na'im Akbar, this article highlights ways in which Jung's biases align with the White supremacist perspective of the Negro as a problem, detrimental to social order. The paper concludes with an Appendix which outlines a call to the International Association for Analytical Psychology (IAAP) to take corrective action and to publicly denounce those facets of Jung's writings that diverge from the core of his theory and that promote toxic attitudes of bigotry, perhaps discouraging many people of colour from enrolling in analytic training.

Cet article fournit les réflexions personnelles d'un analyste en formation et d'origine afro-américaine et amérindienne sur les représentations inflexibles de Jung concernant les non-blancs d'origine Africaine et les Peuples des Premières Nations d'Amérique (l'homme Rouge) comme inférieurs, au travers d'une théorie de ce qui est primitif, théorie qui dévoile la croyance et le soutien de Jung en la suprématie blanche. Sans vouloir manquer de respect ou d'intérêt envers les Premières Nations d'Amérique, cet article se concentre principalement sur le mépris manifeste de Jung pour les Noirs (le Nègre). Utilisant les écrits de Frederick Douglass, W.E.B. Du Bois et Na'im Akbar, cet article souligne les façons dont la partialité de Jung concorde avec la perspective de la suprématie de la race blanche qui considère le Nègre en tant que problème, préjudiciable à l'ordre social. L'article se termine par une Annexe qui présente une demande à l'AIPA de se positionner et de dénoncer publiquement ces facettes des écrits de Jung qui divergent du cœur de sa théorie et qui nourrissent des attitudes toxiques de sectarisme, décourageant peut-être un nombre important de personnes non-blanches à s'inscrire dans une formation analytique.

Este artículo ofrece reflexiones de primera-mano de un analista en formación Africano-Americano y Nativo-Americano sobre la descripción de Jung, de las personas de descendencia Africana y de los Pueblos Originarios Americanos (el hombre rojo), como inferior, a partir de una teoría sobre el primitivismo que encubre su creencia y apoyo a la supremacía del blanco. Sin ninguna falta de respeto o atención intencionada hacia los Pueblos Originarios de América, el presente artículo se focaliza principalmente en la aparente desconsideración hacia los Negros. Utilizando escritos de Frederic Douglass, W.E.B. Du Bois y Na'im Akbar, el artículo da cuenta de los modos en los cuales los prejuicios de Jung se alinean con la perspectiva de la supremacía del Blanco que considera al Negro como un problema perjudicial al orden social. El trabajo concluye con un Apéndice que esboza un llamado a la IAAP a tomar una acción correctiva y a denunciar públicamente estos aspectos de los escritos de Jung, que se apartan del centro de su teoría y promueve actitudes tóxicas de intolerancia, quizás desalentando a muchas personas no-blancas, a inscribirse en una formación analítica.

Expression of a retinoic acid receptor (RAR)-like protein in the embryonic and adult nervous system of a protostome species.

The vitamin A metabolite, retinoic acid, is an important molecule in nervous system development and regeneration in vertebrates. Retinoic acid signaling in vertebrates is mediated by two classes of nuclear receptors, the retinoid X receptors (RXRs) and the retinoic acid receptors (RARs). Recently, evidence has emerged to suggest that many effects of retinoic acid are conserved between vertebrate and invertebrate nervous systems, even though the RARs were previously thought to be a vertebrate innovation and to not exist in non-chordates. We have cloned a full-length putative RAR from the CNS of the mollusc Lymnaea stagnalis (LymRAR). Immunoreactivity for the RAR protein was found in axons of adult neurons in the central nervous system and in growth cones of regenerating neurons in vitro. A vertebrate RAR antagonist blocked growth cone turning induced by exogenous all-trans retinoic acid, possibly suggesting a role for this receptor in axon guidance. We also provide immunostaining evidence for the presence of RAR protein in the developing, embryonic CNS, where it is also found in axonal processes. Using qPCR, we determined that LymRAR mRNA is detectable in the early veliger stage embryo and that mRNA levels increase significantly during embryonic development. Putative disruption of retinoid signaling in Lymnaea embryos using vertebrate RAR antagonists resulted in abnormal eye and shell development and in some instances completely halted development, resembling the effects of all-trans retinoic acid. This study provides evidence for RAR functioning in a protostome species.

A potentially novel nicotinic receptor in Aplysia neuroendocrine cells.

Nicotinic receptors form a diverse group of ligand-gated ionotropic receptors with roles in both synaptic transmission and the control of excitability. In the bag cell neurons of Aplysia, acetylcholine activates an ionotropic receptor, which passes inward current to produce a long-lasting afterdischarge and hormone release, leading to reproduction. While testing the agonist profile of the cholinergic response, we observed a second current that appeared to be gated only by nicotine and not acetylcholine. The peak nicotine-evoked current was markedly smaller in magnitude than the acetylcholine-induced current, cooperative (Hill value of 2.7), had an EC50 near 500 µM, readily recovered from desensitization, showed Ca(2+) permeability, and was blocked by mecamylamine, dihydro-ß-erythroidine, or strychnine, but not by α-conotoxin ImI, methyllycaconitine, or hexamethonium. Aplysia transcriptome analysis followed by PCR yielded 20 full-length potential nicotinic receptor subunits. Sixteen of these were predicted to be cation selective, and real-time PCR suggested that 15 of the 16 subunits were expressed to varying degrees in the bag cell neurons. The acetylcholine-induced current, but not the nicotine current, was reduced by double-strand RNA treatment targeted to both subunits ApAChR-C and -E. Conversely, the nicotine-evoked current, but not the acetylcholine current, was lessened by targeting both subunits ApAChR-H and -P. To the best of our knowledge, this is the first report suggesting that a nicotinic receptor is not gated by acetylcholine. Separate receptors may serve as a means to differentially trigger plasticity or safeguard propagation by assuring that only acetylcholine, the endogenous agonist, initiates large enough responses to trigger reproduction.

Decreased response to acetylcholine during aging of aplysia neuron R15.

How aging affects the communication between neurons is poorly understood. To address this question, we have studied the electrophysiological properties of identified neuron R15 of the marine mollusk Aplysia californica. R15 is a bursting neuron in the abdominal ganglia of the central nervous system and is implicated in reproduction, water balance, and heart function. Exposure to acetylcholine (ACh) causes an increase in R15 burst firing. Whole-cell recordings of R15 in the intact ganglia dissected from mature and old Aplysia showed specific changes in burst firing and properties of action potentials induced by ACh. We found that while there were no significant changes in resting membrane potential and latency in response to ACh, the burst number and burst duration is altered during aging. The action potential waveform analysis showed that unlike mature neurons, the duration of depolarization and the repolarization amplitude and duration did not change in old neurons in response to ACh. Furthermore, single neuron quantitative analysis of acetylcholine receptors (AChRs) suggested alteration of expression of specific AChRs in R15 neurons during aging. These results suggest a defect in cholinergic transmission during aging of the R15 neuron.

Developmental expression of a molluscan RXR and evidence for its novel, nongenomic role in growth cone guidance.

It is well known that the vitamin A metabolite, retinoic acid, plays an important role in vertebrate development and regeneration. We have previously shown that the effects of RA in mediating neurite outgrowth, are conserved between vertebrates and invertebrates (Dmetrichuk et al., 2005, 2006) and that RA can induce growth cone turning in regenerating molluscan neurons (Farrar et al., 2009). In this study, we have cloned a retinoid receptor from the mollusc Lymnaea stagnalis (LymRXR) that shares about 80% amino acid identity with the vertebrate RXRalpha. We demonstrate using Western blot analysis that the LymRXR is present in the developing Lymnaea embryo and that treatment of embryos with the putative RXR ligand, 9-cis RA, or a RXR pan-agonist, PA024, significantly disrupts embryogenesis. We also demonstrate cytoplasmic localization of LymRXR in adult central neurons, with a strong localization in the neuritic (or axonal) domains. Using regenerating cultured motor neurons, we show that LymRXR is also present in the growth cones and that application of a RXR pan-agonist produces growth cone turning in isolated neurites (in the absence of the cell body and nucleus). These data support a role for RXR in growth cone guidance and are the first studies to suggest a nongenomic action for RXR in the nervous system.

eIF2B and oligodendrocyte survival: where nature and nurture meet in bipolar disorder and schizophrenia?

Bipolar disorder and schizophrenia share common chromosomal susceptibility loci and many risk-promoting genes. Oligodendrocyte cell loss and hypomyelination are common to both diseases. A number of environmental risk factors including famine, viral infection, and prenatal or childhood stress may also predispose to schizophrenia or bipolar disorder. In cells, related stressors (starvation, viruses, cytokines, oxidative, and endoplasmic reticulum stress) activate a series of eIF2-alpha kinases, which arrest protein synthesis via the eventual inhibition, by phosphorylated eIF2-alpha, of the translation initiation factor eIF2B. Growth factors increase protein synthesis via eIF2B activation and counterbalance this system. The control of protein synthesis by eIF2-alpha kinases is also engaged by long-term potentiation and repressed by long-term depression, mediated by N-methyl-D-aspartate (NMDA) and metabotropic glutamate receptors. Many genes reportedly associated with both schizophrenia and bipolar disorder code for proteins within or associated with this network. These include NMDA (GRIN1, GRIN2A, GRIN2B) and metabotropic (GRM3, GRM4) glutamate receptors, growth factors (BDNF, NRG1), and many of their downstream signaling components or accomplices (AKT1, DAO, DAOA, DISC1, DTNBP1, DPYSL2, IMPA2, NCAM1, NOS1, NOS1AP, PIK3C3, PIP5K2A, PDLIM5, RGS4, YWHAH). They also include multiple gene products related to the control of the stress-responsive eIF2-alpha kinases (IL1B, IL1RN, MTHFR, TNF, ND4, NDUFV2, XBP1). Oligodendrocytes are particularly sensitive to defects in the eIF2B complex, mutations in which are responsible for vanishing white matter disease. The convergence of natural and genetic risk factors on this area in bipolar disorder and schizophrenia may help to explain the apparent vulnerability of this cell type in these conditions. This convergence may also help to reconcile certain arguments related to the importance of nature and nurture in the etiology of these psychiatric disorders. Both may affect common stress-related signaling pathways that dictate oligodendrocyte viability and synaptic plasticity.

Regulation by carbon and nitrogen sources of a family of cellulases in Aspergillus nidulans.

The total amount of Aspergillus nidulans secreted cellulases is affected by both the carbon and nitrogen source present in the medium, and is regulated directly and/or indirectly by the carbon metabolism regulators, CreA, CreB, and CreC, and the global nitrogen metabolism regulator, AreA. We have characterized two A. nidulans genes that encode exo-cellulases, and one gene that encodes an endo-cellulase which is additional to the previously described endo-cellulase encoding gene, eglA. The putative regulatory regions 5(') of all the genes contain potential binding sites for the global carbon and nitrogen regulatory proteins, CreA and AreA. The sequences 5(') of eglA and eglB also contain potential consensus binding sites for XlnR which is involved in induction in Aspergillus niger, but none of the 5(') sequences contains an exact copy of the AceII DNA binding consensus sequence involved in induction in Trichoderma reesei, and thus it is likely that they may be induced by different pathway specific regulatory proteins.