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This study examined the relation between the sense of self-continuity, defined as the ability to perceive oneself as extending temporally backwards into the past and forwards into the future, and the adaptiveness of strategies of coping with job loss. We created a web site that was linked to several Israeli web sites dealing with unemployment in the high-tech sector. Respondents were 211 Israeli men and women, aged 18-58, both employed and unemployed, who answered some biographical questions and completed two questionnaires online: the Coping Strategies Questionnaire (Roger, Jarvis & Najarian, 1993) and a version of the Possible Selves Questionnaire (Markus & Nurius, 1986). The results indicated that individuals who had suffered job loss had a lower sense of self-continuity than those who had not suffered job loss and this did not differ by the field of their previous employment (high-tech or other) or length of unemployment. Those individuals with a higher sense of self-continuity evidenced greater adaptiveness in coping, independently of the number of months they had been unemployed. This study is important in demonstrating that the sense of self-continuity is a resource in coping adaptively at times of crisis, suggesting that enhancing the sense of self-continuity may be a beneficial means of helping individuals cope more effectively with job loss. (Contains 1 figure and 1 table.)

The ζ-inhibitory peptide (ZIP) is considered a candidate inhibitor of the atypical protein kinase Mζ (PKMζ). ZIP has been shown to reverse established LTP and disrupt several forms of long-term memory. However, recent studies have challenged the specificity of ZIP, as it was reported to exert its effect also in PKMζ knock-out mice. These results raise the question of what are the targets of ZIP that may underlie its effect on LTP and memory. Here we report that ZIP as well as its inactive analog, scrambled ZIP, induced a dose-dependent increase in spontaneous activity of neurons in dissociated cultures of rat hippocampus. This was followed by a sustained elevation of intracellular calcium concentration ([Ca2+]i) which could not be blocked by conventional channel blockers. Furthermore, ZIP caused an increase in frequency of mEPSCs followed by an increase in membrane noise in patch-clamped neurons both in culture and in acute brain slices. Finally, at 5-10 μM, ZIP-induced excitotoxic death of the cultured neurons. Together, our results suggest that the potential contribution of cellular toxicity should be taken into account in interpretation of ZIP's effects on neuronal and behavioral plasticity. [ABSTRACT FROM AUTHOR]