The hippocampus and the amygdala are essential components of the neural circuitry mediating stress responses. The hippocampus, which provides negative feedback regulation of the stress response, is particularly vulnerable to degenerative changes caused by chronic stress. Unlike the hippocampus, relatively little is known about how stress affects the amygdala and the nature of its role in the stress response. Hence, we examined the effects of two different models of chronic stress on hippocampal and amygdaloid neuronal morphology in rats. In agreement with previous reports, chronic immobilization stress (CIS) induced dendritic atrophy and debranching in CA3 pyramidal neurons of the hippocampus. In striking contrast, pyramidal and stellate neurons in the basolateral complex of the amygdala exhibited enhanced dendritic arborization in response to the same CIS. Chronic unpredictable stress (CUS), however, had little effect on CA3 pyramidal neurons and induced atrophy only in BLA bipolar neurons. These results indicate that chronic stress can cause contrasting patterns of dendritic remodeling in neurons of the amygdala and hippocampus. Moreover, CIS, but not CUS, reduced open-arm activity in the elevated plus-maze. These findings raise the possibility that certain forms of chronic stress, by affecting specific neuronal elements in the amygdala, may lead to behavioral manifestations of enhanced emotionality. Thus, stress-induced structural plasticity in amygdala neurons may provide a candidate cellular substrate for affective disorders triggered by chronic stress.

The protozoan parasite Toxoplasma gondii blocks the innate aversion of rats for cat urine, instead producing an attraction to the pheromone; this may increase the likelihood of a cat predating a rat. This is thought to reflect adaptive, behavioral manipulation by Toxoplasma in that the parasite, although capable of infecting rats, reproduces sexually only in the gut of the cat. The ''behavioral manipulation'' hypothesis postulates that a parasite will specifically manipulate host behaviors essential for enhancing its own transmission. However, the neural circuits implicated in innate fear, anxiety, and learned fear all overlap considerably, raising the possibility that Toxoplasma may disrupt all of these nonspecifically. We investigated these conflicting predictions. In mice and rats, latent Toxoplasma infection converted the aversion to feline odors into attraction. Such loss of fear is remarkably specific, because infection did not diminish learned fear, anxiety-like behavior, olfaction, or nonaversive learning. These effects are associated with a tendency for parasite cysts to be more abundant in amygdalar structures than those found in other regions of the brain. By closely examining other types of behavioral patterns that were predicted to be altered we show that the behavioral effect of chronic Toxoplasma infection is highly specific. Overall, this study provides a strong argument in support of the behavioral manipulation hypothesis. Proximate mechanisms of such behavioral manipulations remain unknown, although a subtle tropism on part of the parasite remains a potent possibility.behavioral manipulation ͉ fear ͉ parasites ͉ predator T he ''behavioral manipulation'' hypothesis states that a parasite can alter host behavior specifically to increase its own transmission efficiency (1, 2). After an acute infection, the protozoan parasite Toxoplasma gondii latently persists in the brain for the life of an infected host, offering an opportunity to study the behavioral manipulation hypothesis (3). Toxoplasma reproduces sexually in a two-species life cycle (4). The sexual phase of its reproduction occurs in the feline intestine, from which highly stable oocysts are excreted in the feces. Grazing animals, including rodents, can then ingest these oocysts. In these hosts, Toxoplasma forms cysts and persists in the central nervous system. The life cycle is completed when a cat eats an infected animal. Recent reports indicate that the parasite blunts the innate aversion of rats for the urine of cats, converting this aversion to an attraction (5), although it does not interfere with energetically costly behaviors related to mating success and social status (6). These findings agree with the behavioral manipulation hypothesis, which predicts that parasites will alter only behaviors that are beneficial to their transmission while leaving other behaviors intact.Several studies have investigated the innate fear of laboratory rodents toward cat odors (7-11). These studies have delineated a neuroanatomical circuit comprising ...

It has long been hypothesized that morphological and numerical alterations in dendritic spines underlie long-term structural encoding of experiences. Here we investigate the efficacy of aversive experience in the form of acute immobilization stress (AIS) and chronic immobilization stress (CIS) in modulating spine density in the basolateral amygdala (BLA) of male rats. We find that CIS elicits a robust increase in spine density across primary and secondary branches of BLA spiny neurons. We observed this CIS-induced spinogenesis in the BLA 1 d after the termination of CIS. In contrast, AIS fails to affect spine density or dendritic arborization when measured 1 d later. Strikingly, the same AIS causes a gradual increase in spine density 10 d later but without any effect on dendritic arbors. Thus, by modulating the duration of immobilization stress, it is possible to induce the formation of new spines without remodeling dendrites. However, unlike CIS-induced spine formation, the gradual increase in spine density 10 d after a single exposure to AIS is localized on primary dendrites. Finally, this delayed induction of BLA spinogenesis is paralleled by a gradual development of anxiety-like behavior on the elevated plus-maze 10 d after AIS. These findings demonstrate that stressful experiences can lead to the formation of new dendritic spines in the BLA, which is believed to be a locus of storage for fear memories. Our results also suggest that stress may facilitate symptoms of chronic anxiety disorders like post-traumatic stress disorder by enhancing synaptic connectivity in the BLA.anxiety ͉ dendritic remodeling ͉ immobilization ͉ synapse ͉ rats T he search for cellular substrates underlying experience-related plasticity has focused on dendritic spines ever since Ramón y Cajal (1, 2) proposed that the storage of long-term memory involves strengthening of synaptic connections (or even a building of new connections) among central neurons. More recently, the focus has shifted toward understanding the physiological and molecular basis of synaptic plasticity mechanisms, such as long-term potentiation (LTP), and their relationship to spine plasticity and ultimately behavioral memory (3, 4). A majority of these studies have examined the hippocampus. Although the hippocampus is required for the acquisition and temporary storage of declarative memory, studies with human subjects and animal models suggest that more permanent morphological correlates of long-term memory storage are unlikely to reside in the hippocampus (5-7). In this context, the amygdala, for which the neural circuit underlying emotional memory formation is well characterized (8), provides a significant advantage. The basolateral amygdala (BLA) is believed to be a site of storage for memories of fearful or stressful experiences (9-12). Furthermore, recent studies indicate that the synthesis of new proteins in the BLA is involved in the long-term consolidation of emotional memories (13). Thus, the BLA presents an attractive locus to investigate structural encodi...

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