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The hippocampus has a critical role in several fundamental memory operations, including the conditioning of fear to contextual information. We show that the hippocampus is necessary also for unconditioned fear, and that the involved circuitry is at the ventral pole of the hippocampus. Rats with selective hippocampal lesions failed to avoid open arms in an elevated plus-maze and had decreased neuroendocrine stress responses during confinement to a brightly lit chamber. These effects were reproduced by lesions of the ventral half of the hippocampus, but not by damage to the dorsal three-quarters of the hippocampus or the amygdala. Ventral lesions failed to impair contextual fear conditioning or spatial navigation, suggesting that the ventral hippocampus may specifically influence some types of defensive fear-related behavior.defensive ͉ rat ͉ plus-maze ͉ water maze ͉ corticosterone T he experience of anxiety and fear is controlled by a modular neural system including regions in the brainstem, hypothalamus, and deeper parts of the temporal lobe (1-4). The amygdala plays a pivotal role in this system. It controls a broad range of fear reactions, and exhibits neural plasticity that may permit fear responses to be conditioned to new types of experience (refs. 1-5; but see ref. 6). Conditioned fear depends strongly on the basolateral complex of the amygdala (the lateral, basolateral, and basomedial nuclei), whereas the central nucleus and the bed nucleus of the stria terminalis are thought to be the principal output structures, mediating fear-related signals to behavioral, autonomic, and endocrine response systems in the hypothalamus and brainstem (1-5).Conditioning of fear to multimodal stimuli such as context and spatial location also requires the integrity of the hippocampus (7-9). The hippocampus is strongly involved in the encoding of spatial and episodic memories (10-12), and contextual fear conditioning is thought to require many of the associative algorithms responsible for these types of memory (13)(14)(15). Although the hippocampal influence on fear reactions may be a necessary consequence of its mnemonic operations, it is also possible that the hippocampus controls fear and anxiety independently of learning (16). This view is based particularly on the similar effects that anxiolytic drugs and septal-hippocampal lesions have on behavior in aversively motivated tasks. However, except for early studies showing that rats with large nonselective hippocampal lesions exhibit reduced food neophobia (17)(18)(19) and reduced freezing in the presence of a predator (20), direct evidence is absent. We now show (i) that the hippocampus controls defensive fear responses during exposure to a potentially threatening environment, (ii) that the relevant circuitry is located at the ventral pole of the hippocampus, and (iii) that this circuit may be dissociable from the associative circuits involved in contextual fear conditioning. Methods Subjects.A total of 187 male Long Evans rats (250-450 g) were housed individually in tran...

Gingivitis and periodontitis are thought to result from an imbalance between those oral microorganisms which normally colonize tooth surfaces in close contact with the gingival margin, and the nature and efficiency of the host response. The bacteria are the triggering agents, but host defence mechanisms within the gingival/periodontal tissues seem to be responsible for most of the tissue damage and for the outcome and progression of the diseases. It has recently been shown that emotional or psychological load (stress) may influence immune activities directly via nerve messenger substances (neurotransmitters and neuropeptides) and/or indirectly via neuroendocrine (hormone) substances. This review discusses how emotional stressors and nervous and neuroendocrine responses to psychological stressors may modulate the immune response to bacteria, and thus be expected to influence the progression and course of gingivitis and periodontitis.

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