<p> The social self preservation model posits that threats to the social self result in a unique and coordinated psychobiological response that evolved due to its adaptive benefits. Stressors that threaten the social self elicit feelings of shame and other negative self-conscious emotions, as well as increased hypothalamic-pituitary-adrenal (HPA) axis activity. The current study sought to test this model by exposing individuals to an acute stressor, and determining if they exhibit the emotional, physiological, and behavioral components proposed by the self preservation model. In addition, the physiological and emotional reactions of an observing participant were assessed to determine if they too exhibited a physiological and emotional reaction to observing an individual under social stress. Results supported the social self preservation model in that participants undergoing the acute stressor task exhibited significantly greater cortisol response and self-reported personal distress, as compared to observing participants. The social self preservation model was also extended by the current findings in that participant submissive nonverbal behavior, particularly gaze aversion, was related to their physiological response. Observing participants exhibited a significant salivary alpha-amylase (sAA) response, demonstrating the physiological effects of observing an individual experiencing social stress. In addition, observing participants with greater trait empathy levels exhibited significantly greater physiological reactivity as well as self-reported personal distress. These findings suggest that nonverbal behavior may be a mechanism of physiological resonance of stress.</p>

Thompson-Schill et al. (1997, 1998) proposed that the activation in the left inferior frontal gyrus (IFG) during verb generation was due to the selection of information among competing alternatives. The present study took into account both the effects of selection demands and association strength during retrieval using a semantic retrieval task---verb generation and a phonological retrieval task---stem completion. The results from healthy older adults and undergraduate subjects showed that association strength rather than selection demands influenced the retrieval of semantic and phonological information. A semantic STM deficit patient ML, with left IFG damage, showed great difficulty in verb generation especially when the association strength was weak. A phonological STM deficit patient JJ, with damage in temporo-parietal regions, showed much better performance. These results suggested that the left IFG is responsible for semantic retrieval, with the degree of involvement mediated by association strength between cue and target.

Granule-laden astroglia accumulate with normal aging in several brain regions. Chronic treatment with cysteamine (CSH), a drug which depletes somatostatin (SS), produces accelerated astorcytic granule accumulation in rat hippocampus homologous to that observed in the aging brain. Behavioral tests performed following CSH administration have always been done with CSH present in the animals' systems and have shown cognitive deficits and decreases in locomotor activity, both of which have been attributed to the depletion of SS by CSH. Since chronic CSH exposure will also produce neuropathological changes in hippocampal astrocytes, we tested animals' spatial learning/memory and motor functioning at two time points following a chronic CSH treatment: (1) during CSH treatment to assess the effects of the drug itself, and (2) well after cessation of the drug to test the behavioral effects possibly associated with astrocytic neuropathology, not drug. A tendency toward a cognitive impairment was evident when rats were tested in a water maze 1 month following prolonged CSH treatment, but not during CSH exposure. On the other hand, when tested in locomotor activity boxes, only the animals tested during CSH treatment, not post-treatment, displayed a significant decrease in locomotion. Moreover, five weeks following CSH exposure, CSH-treated animals showed a significant increase in both the number of hippocampal astrocytic granules and SS levels; elevated SS concentration in the hippocampus is unlikely responsible for the seemingly detrimental effects of CSH on cognitive behavior since SS is antiamnesic. Taken together, these results suggest that CSH-induced cognitive deficits previously measured when CSH is in the animals' system may be influenced by concurrent locomotor deficits, and that CSH-induced astrocytic pathology may possibly be associated with a trend towards a deficit in cognition which is separate from the locomotor effects caused by the drug.

Tasks testing linguistic and affective prosody were administered to nine right-hemisphere-damaged (RHD), ten left-hemisphere-damaged (LHD), and ten age-matched control (NC) subjects. Two tasks measured subjects' abilities to make same/different judgments about prosodic patterns which had been filtered of the linguistic content, while six tasks required subjects to identify typical linguistic or affective meanings for intonation contours. The six identification tasks varied in the amount of linguistic structure available to subjects during auditory perception; stimuli were either filtered of their phonetic content, presented as nonsense utterances, or provided appropriate semantic information which biased the prosodic target. Unilateral damage to either cerebral hemisphere did not impair subjects' ability to discriminate prosodic patterns, or to recognize the affective mood conveyed through prosody. Contrary to expectation, RHD patients performed comparably in both propositional and affective contexts, and thus did not show evidence of a specific disturbance of emotional prosody. LHD patients, however, were differentially impaired on linguistic tasks rather than emotional tasks when compared to the NC group, even when semantic information biased the target response. The results are discussed with respect to theories of lateralized processing of linguistic and affective prosody.

Self-esteem is defined as: i Previous research has linked self-esteem to many factors (life-satisfaction, health, stress); however its origins, manifestations, and thus neural correlates are largely unexplored. / This thesis includes two independent neuroimaging studies investigating central nervous system variables possibly linked to self-esteem. The first study investigated hippocampal volume variations in relation to parental bonding and self-esteem. A trend was observed between the left hippocampus and retrospective mother care (smaller volumes = lesser care). The second study used fMRI to explore the differential neural correlates of high/low self-esteem when performing a social acceptance or rejection task. Here, differences in neural reward-pathways could be revealed between high and low self-esteem, suggesting an impact of self-esteem on the neural processing of social evaluation. / In conclusion, these studies provide evidence that self-esteem has strong neural correlates. This adds to previous research showing that this is a trait that is determined early in life and is self-perpetuating.

Using longitudinal MRI volumetry we examined the relationship between the degree of cerebral atrophy and cognitive function in Mild Cognitively Impaired (MCI) subjects during the progression to Dementia of the Alzheimer's type (DAT). We used these patterns of atrophy to examine the Dichotomous Groups and Accelerated Aging theories of progression to DAT. We acquired MRI scans on 20 subjects with Mild Cognitive Impairment (MCI), 3 subjects with DAT, and 19 normal elderly controls. Scanning was carried out at two times with an average of 73 months between scans. At follow-up, 10 of the MCI subjects had progressed to dementia (Progressors) while 10 had remained stable (Non-Progressors). We found that the Progressors had a significant increase in medial temporal atrophy between Time 1 and Time 2, while the Non-Progressors remained stable. This data supports the Dichotomous Groups theory. Cognitively we found that delayed verbal recall followed the same pattern of change as medial temporal atrophy, but that language ability did not follow the same pattern of change as lateral temporal atrophy.

Central administration of pmol and low nmol doses of neurotensin (NT), rapidly stimulated hypothalamic-pituitary adrenal (HPA) activity, increasing adrenocorticotropin hormone (ACTH) and corticosterone (B) release for several hours. This suggests potent effects of centrally administered NT and a role for this neuropeptide in HPA regulation. Of several brain areas thought to be involved in mediating NT-induced effects, one site of particular interest is the paraventricular nucleus of the hypothalamus (PVNh). Chronic implants of the NT antagonist, SR 48692 (powdered form), into the PVNh area decreased HPA activity under both basal and stress-induced conditions. These findings suggest an endogenous role for NT in mediating hypophysiotropic HPA signalling. Decreases in immunoreactive (ir) corticotropin-releasing hormone (CRH) expression was also seen following chronic SR 48692 exposure (day 7). This decrease in irCRH levels paralleled the SR 48692-induced inhibition in ACTH and B release, suggesting that CRH is involved in mediating SR 48692-induced effects on HPA activity. / Chronic intracerebroventricular (icv) delivery of NT (1 pmol/h for 14 days) into the rat brain had an opposing effect than that of SR 48692. / Chronic NT treated animals demonstrated increased fear/anxiety-related behavior. Decreased mean locomotor activity was observed in the chronic NT-treated (1 pmol/h for 14 days) animals upon exposure to a novel environment. Thus, a NT-CRH mechanism of action appears to be involved in mediating behavioral responses to stress. In addition to a proposed role for CRH mediating NT-induced HPA regulation, it also appears to be mediating fear/anxiety-related behavior. / Finally, we examined the status of NT receptors in animals with known deficits in HPA function. Aged, 24 month old Long-Evans rats, were identified as either aged, cognitively impaired (AI) or aged, cognitively unimpaired (AU) compared to young adult control rats. The AI animal showed decreased levels of [125I]NT binding sites in areas such as CA3 (42%) and DG (55%) of the hippocampus and the PVNh (72%) compared to the young controls. The fact that this is occurring in the animal known to exhibit HPA hyperactivity lends further support for a NT role in regulating HPA function. (Abstract shortened by UMI.)

The cholinergic system has been shown to play an important role in cognitive function. Previous work has demonstrated that lesions to the cholinergic pathways originating in the basal forebrain, namely the nucleus basalis magnocellularis (NBM), have profound effects on the working memory function. / The present experiments were designed to assess the manner in which nicotine, a nicotinic cholinergic agonist, administration reverses the cognitive deficits resulting from lesions to the NBM. / The first experiment used the radial arm maze to examine working versus reference memory. Next, delays were imposed between the first four radial arm maze choices and the last, in order to examine short-term memory. Finally, pre-pulse inhibition of acoustic startle was assessed to determine the effects of nicotine on sensorimotor gating in NBM lesioned animals. / The results convincingly show that the cognitive and sensory motor gating impairments of MBN lesions are reversed by nicotine administration.

This study evaluated the effect of attention on pain- and auditory-evoked cortical activity in humans using positron emission tomography (PET). Regional cerebral blood flow (rCBF) was measured while subjects detected changes in thermal intensity or auditory frequency. Subjects rated pain on a visual analogue scale. Using statistical brain maps of the pain-related activity, directed searches were conducted in contralateral insular (IC), anterior cingulate (ACC), primary (S1) and secondary (S2) somatosensory cortices---regions consistently found to be activated by painful stimuli. / Pain intensity was rated higher in the thermal than in the auditory task. Likewise, whereas in the thermal task there were significant pain-related rCBF increases in S1 and S2, none of these regions had significant pain-evoked rCBF increases when subjects performed the auditory task. Only rCBF in S1 was significantly correlated with the pain intensity ratings generated during the thermal and auditory tasks. These results suggest that changes in S1 cortical activity may be involved in attentional modulation of pain.

The behavior of transgenic mice with impaired type II glucocorticoid receptor function was examined in a nonspatial learning task, the forced swim test, as well as in a spatial memory task, the water maze. Antidepressants have been shown to alter behavioral performance in these paradigms, as well as HPA axis activity in these animals. Transgenic and B6C 3F1 mice were therefore chronically or acutely injected with desipramine (10 mg/kg) or fluoxetine (10 mg/kg) for the forced swim test. Both drugs were chronically administered for the water maze. Transgenic mice exhibited impairments in the forced swim test that could be secondary to a cognitive deficit or to disrupted affective processes. Chronic and acute desipramine exacerbated these deficits, whereas chronic and acute fluoxetine ameliorated the performance. Drug resistant impairments in the water maze could be attributable to hippocampal aberrations resulting from glucocorticoid neurotoxicity.