Homosexuality as an issue in the psychoanalytic treatment of Lubavitch Chassidim

There is sparse literature on the psychoanalytic treatment of Chassidic Jews. The authors of this article, both secular nonobservant psychoanalysts, have spent over a decade working with Lubavitch Chassidim in the New York area. In the Lubavitch community, the sexes are separated at three years of age, leading to same-sex cohorts from then until marriage. As with all ultra-orthodox religious groups, homosexuality is viewed in Biblical terms as an abomination and yet, not surprisingly, it exists within this community. This article deals with the analysis of homosexual issues that appear in the treatment of both male and female Lubavitch Chassidim. We discuss how homosexuality is manifested, how it is viewed, denied, and rationalized, and the functions it serves in a subculture that is inherently homocentric. The need for parameters in classical technique is discussed as a necessity for successful psychoanalytic work with this population.     

Viciousness and the structure of reality

Given the centrality of arguments from vicious infinite regress to our philosophical reasoning, it is little wonder that they should also appear on the catalogue of arguments offered in defense of theses that pertain to the fundamental structure of reality. In particular, the metaphysical foundationalist will argue that, on pain of vicious infinite regress, there must be something fundamental. But why think that infinite regresses of grounds are vicious? I explore existing proposed accounts of viciousness cast in terms of contradictions, dependence, failed reductive theories and parsimony. I argue that no one of these accounts adequately captures the conditions under which an infinite regress—any infinite regress—is vicious as opposed to benign. In their place, I suggest an account of viciousness in terms of explanatory failure. If this account is correct, infinite grounding regresses are not necessarily vicious; and we must be much more careful employing such arguments to the conclusion that there has to be something fundamental.     

Behavioral deficits and subregion-specific suppression of LTP in mice expressing a population of mutant NMDA receptors throughout the hippocampus

The NMDA receptor (NMDAR) subunit GluN1 is an obligatory component of NMDARs without a known functional homolog and is expressed in almost every neuronal cell type. The NMDAR system is a coincidence detector with critical roles in spatial learning and synaptic plasticity. Its coincidence detection property is crucial for the induction of hippocampal long-term potentiation (LTP). We have generated a mutant mouse model expressing a hypomorph of the Grin1^N598R allele, which leads to a minority (about 10%) of coincidence detection-impaired NMDARs. Surprisingly, these animals revealed specific functional changes in the dentate gyrus (DG) of the hippocampal formation. Early LTP was expressed normally in area CA1 in vivo, but was completely suppressed at perforant path-granule cell synapses in the DG. In addition, there was a pronounced reduction in the amplitude of the evoked population spike in the DG. These specific changes were accompanied by behavioral impairments in spatial recognition, spatial learning, reversal learning, and retention. Our data show that minor changes in GluN1-dependent NMDAR physiology can cause dramatic consequences in synaptic signaling in a subregion-specific fashion despite the nonredundant nature of the GluN1 gene and its global expression.According to Hebb''s postulate, neurons require a molecular mechanism to detect synchronous activity in order to change the strength of synaptic connectivity (Hebb 1949). NMDA receptors (NMDARs) are molecular coincidence detectors, and selective NMDAR antagonists block the induction of long-term potentiation (LTP) in both the dentate gyrus (DG) and CA1 regions of the hippocampus (Bliss and Collingridge 1993; Martin et al. 2000). NMDARs have been long known for their role in spatial learning, but more recently have been implicated in other forms of cognitive function and dysfunction (Gruart et al. 2006; Whitlock et al. 2006; Castner and Williams 2007; Kristiansen et al. 2007; Wilson and Linster 2008).Neuronal NMDARs are hetero-tetrameric ligand-gated ion channels typically comprised of two types of subunits. Two copies of the mandatory GluN1 subunit (or NR1 subunit [Collingridge et al. 2009] encoded by Grin1) are associated with two copies from the GluN2 family, GluN2A–D (or NR2A–D). The GluN1 subunit is expressed ubiquitously both spatially and temporally throughout the developing and adult brain. Global knockout mice models of the GluN1 subunit are postnatally lethal within hours after birth (Forrest et al. 1994; Li et al. 1994), and cell-specific GluN1 mice knockouts (Tsien et al. 1996; Nakazawa et al. 2002; McHugh et al. 2007; Niewoehner et al. 2007) have provided insights on how specific synapses and regional neuronal networks are dependent on NMDAR function.The early postnatal lethality of the global GluN1 knockout is in contrast to the null mutants of the four AMPA receptor genes and other major synaptic proteins, such as αCaMKII (Silva et al. 1992a,b; Jia et al. 1996; Zamanillo et al. 1999; Meng et al. 2003). This can be at least partially explained by the absence of any close GluN1 homologs, which could functionally compensate for the absence of the GluN1 subunit. Recombinant expression studies defined the GluN1 subunit as a mandatory component of NMDARs. This constellation provides a specific opportunity to test whether different local neuronal subnetworks are affected differentially by mutant Grin1 alleles associated with subtle alterations of the functional properties of NMDARs.GluN1 subunits with the N598R point mutation (GluN1^R) yield functional NMDARs that are Mg²⁺ insensitive and Ca²⁺ impermeable (Burnashev et al. 1992; Mori et al. 1992). The Grin1^N598R allele that codes for GluN1^R subunits is a gain-of-function mutation that is dominant lethal, even in heterozygous and hemizygous lines (Single et al. 2000; Rudhard et al. 2003). NMDARs with GluN1^R subunits do not act as coincidence detectors and, interestingly, mice expressing exclusively the GluN1^R allele lack whisker-related pattern formation in the neonate brainstem (Rudhard et al. 2003).To investigate the functional importance of GluN1 subunits with the N598R point mutation, we took advantage of the generation of a variant mutant line of mice (GluN1^Rneo/+) expressing a minority (around 10%) of these mutant NMDARs. Even though the majority of the NMDARs are normal, all neurons expressing NMDARs will contain a subset of receptors carrying this mutation.Therefore, this mouse model is an ideal candidate to study the impact of subtle alterations of NMDAR function on different neuronal networks, such as those comprising the hippocampal formation.Studies examining region-specific targeted disruption of GluN1 expression in subregions of the hippocampus have revealed subtle yet important contributions of this NMDAR subunit in synaptic plasticity and spatial learning and memory. CA1-restricted knockout of GluN1 expression in the hippocampus caused impaired spatial learning and memory as well as reduced CA1-LTP (Tsien et al. 1996). In the case of the disruption of GluN1 expression in the DG region of the hippocampus, more subtle behavioral impairments were apparent, including the inability to discriminate between two similar contexts (pattern separation) and deficits in spatial working memory despite normal LTP in the CA1 region (McHugh et al. 2007; Niewoehner et al. 2007).Our GluN1^Rneo/+ mice differ from the region-specific GluN1 mutant mice in that they express the mutant hypomorph at the same level in different subregions of the hippocampus. Interestingly, we found that this allele leads to substantial differences in short- and long-term plasticity between area CA1 and the DG of the hippocampus. The specific impairment in the DG was accompanied by impaired spatial recognition, spatial learning, reversal learning, and retention. Our data establish the possibility of a circuit-specific phenotype caused by a mutant variant of a globally expressed major nonredundant synaptic protein.     

Different working memory capacity in normal young adults for visual and tactile letter recognition task

Thirty-nine young adult participants performing the visual and tactile n-back working memory task were compared. In the visual task, letters were presented on a computer screen and in the tactile task, plastic letters embedded on a board were explored tactually. The amount of incorrect responses increased with increasing memory load in both tasks, but was significantly lower in the visual task. Subgrouping the participants with extreme performances into "skilled" and "poor" performers showed that the best performance was found among "skilled" visual performers, and the worst one among "poor" tactile performers. There was more interindividual variation among tactile than visual performance. We conclude that tactile working memory capacity, measured here by letter recognition and letter memory, is generally more limited and shows more variability than visual memory in normal sighted participants.     

Effect of display movement on tactile pattern perception

The effect of display movement on the ability of subjects to rec ognize alphabetic shapes tactually was investigated. The display consisted of a computer-controlled 8-by-6 array of small airjet stimulators that could be physically translated in a small circle by means of a mechanical linkage. The experimental parameters were the stimulus duration, the angular velocity of the display, and the amplitude of the rotation. Recognition accuracy increased with stimulus duration between 100 and 400 msec. For a rotation amplitude of 0.8 cm, a maximum in recognition accuracy occurred at a rotation velocity of 400 rpm, or 150 msec. per revolution. The optimum angular velocity appeared to decrease as the amplitude of rotation increased. From these results and certain related neurophysiological evidence, a hypothetical model is suggested which qualitatively can account for the data.