Social bonds fulfill the basic human need to belong. Being rejected thwarts this basic need, putting bonds with others at risk. Attachment theory suggests that people satisfy their need to belong through different means. Whereas anxious attachment is associated with craving acceptance and showing vigilance to cues that signal possible rejection, avoidant attachment is associated with discomfort with closeness and using avoidant strategies to regulate one's relationships. Given these different styles by which people satisfy their need to belong (that can operate simultaneously within the same individual), responses to social rejection may differ according to these individual differences in attachment anxiety and avoidance. To test this hypothesis, we used neuroimaging techniques to examine how the degree to which people display each of the two attachment dimensions (anxiety and avoidance) uniquely correlated with their neural activity during a simulated experience of social exclusion. Anxious attachment related to heightened activity in the dorsal anterior cingulate cortex (dACC) and anterior insula, regions previously associated with rejection-related distress. In contrast, avoidant attachment related to less activity in these regions. Findings are discussed in terms of the strategies that individuals with varying attachment styles might use to promote maintenance of social bonds.

Pain, whether caused by physical injury or social rejection, is an inevitable part of life. These two types of pain-physical and social-may rely on some of the same behavioral and neural mechanisms that register pain-related affect. To the extent that these pain processes overlap, acetaminophen, a physical pain suppressant that acts through central (rather than peripheral) neural mechanisms, may also reduce behavioral and neural responses to social rejection. In two experiments, participants took acetaminophen or placebo daily for 3 weeks. Doses of acetaminophen reduced reports of social pain on a daily basis (Experiment 1). We used functional magnetic resonance imaging to measure participants' brain activity (Experiment 2), and found that acetaminophen reduced neural responses to social rejection in brain regions previously associated with distress caused by social pain and the affective component of physical pain (dorsal anterior cingulate cortex, anterior insula). Thus, acetaminophen reduces behavioral and neural responses associated with the pain of social rejection, demonstrating substantial overlap between social and physical pain.

We summarize the empirical work on schadenfreude, or pleasure felt at someone else's misfortune. Although schadenfreude is a socially undesirable emotion, research reveals at least three conditions in which it commonly arises. One condition is when observers gain from the misfortune. We discuss research showing that gains in ingroup outcomes based on the failures of rival outgroups can create schadenfreude, especially for those highly identified with their ingroups. A second condition is when another's misfortune is deserved. We focus on research showing that the misfortunes of hypocrites are perceived as highly deserved and therefore create schadenfreude in observers. A third condition is when a misfortune befalls an envied person. We summarize studies showing that the core ingredients of envy prime the envying person for schadenfreude when the envied person suffers.

No abstract

No abstract

Functional assessment of animals following experimental cerebral ischemia is often difficult due to the passive nature of many neurologic exams. We attempted to increase the objectivity of motor function evaluation by adapting quantifiable behavioral tests and actively testing rats' motor capability following a cerebral ischemic insult. It was hypothesized that active testing would reveal motor deficits which were not readily apparent upon casual observation and that such testing would provide a more sensitive means of experimental neurologic assessment. Wistar rats were exposed to reversible severe forebrain ischemia using the four-vessel occlusion technique. Motor function was evaluated using the total motor score (sum of scores for screen test, balance beam test, and prehensile-traction test) over the 48 hours which followed 20 minutes of cerebral ischemia. To manipulate neurologic outcome, rats were fed or fasted the day prior to ischemia and then pretreated with either 1,3-butanediol or saline. Fasted saline-treated animals demonstrated improved total motor performance compared with fed animals by 48 hours after ischemia. There was no improvement in motor performance by fasted vs. fed rats from among the butanediol-treated animals. Pretreatment with butanediol resulted in significantly better total motor performance among fasted rats 24 hours after ischemia; however, by 48 hours postischemia, no difference was detectable. This is the first demonstration of motor deficits produced by four-vessel occlusion in rats. The motor tests devised appear to be adequately sensitive to detect changes in motor function that are not apparent with passive observation in this model.

No abstract

The dose-response relation between plasma glucose and brain lactate and the relation of these parameters to intracellular pH during severe cerebral ischemia have not been well characterized over a wide range of plasma glucose levels. Experiments to delineate these relations in the gerbil model of global ischemia were performed by using phosphorus-31 nuclear magnetic resonance spectroscopy to measure intracellular pH and a new method to measure brain lactate. Ischemia increased final brain lactate linearly 4 /tmol/g for every 100 mg/dl increase in plasma glucose up to 650 mg/dl (p=0.0001, ^=0.9); beyond 650 mg/dl, saturation of the glucose transport-glycolysis system occurred. Plasma glucose correlated better with ischemic intracellular pH than did brain lactate. However, when brain lactate levels are compared with intracellular pH during ischemia, the relation may be threshold rather than linear. A narrow transition zone, during which ischemic intracellular pH decreased precipitously with increasing brain lactate, was observed between 17 and 22 fimoUg; below 17 fimollg, intracellular pH remained stable at 6.8-6.9, whereas above 22 /imol/g, intracellular pH decreased maximally to about 62. The marked decrease in intracellular pH that occurs when brain lactate surpasses 17 /unol/g suggests that this sudden drop in intracellular pH may account for the "lactate threshold" for increased cerebral ischemic damage. (Stroke 1990^21:936-942) S ince the observation by Myers and Yamaguchi 1 that glucose infusion increased brain injury from cardiac arrest, the ability of hyperglycemia to enhance cerebral ischemic damage after transient ischemia has become well accepted. "5 The increased ischemic brain damage in the presence of hyperglycemia is believed to be related to increased production of lactate and to the accompanying increase in tissue acidosis. Hyperglycemia produces substantial increases in brain lactate during ischemia, Received September 6, 1989; accepted February 22, 1990. glycolytic inhibitor can block hyperglycemia-enhanced damage. 7 Measurement of interstitial pH and calculation of intracellular pH (pHj) during cerebral ischemia indicate that increased acidosis accompanies increased tissue lactate. -10Nevertheless, hyperglycemia studies are often restricted to comparisons of normoglycemic animals with animals that have been made hyperglycemic by one dose of glucose.2 -6 The dose-response relation between blood glucose and brain lactate over a wide range of blood glucose levels has not been well described in a model of severe cerebral ischemia. Furthermore, the relation between brain lactate and brain pHj during severe global ischemia has not been well characterized over an extensive range of hyperglycemia. The understanding of such relations is especially important in light of the recent finding that brain pathology may be enhanced more by lactic acidosis than by other types of acidosis. 11In these experiments, the relation between plasma glucose, brain lactate, and intracellular pH is described over a wide...