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This study attempts to identify the mechanism of the so-called afternoon nap zone. More specifically, it investigates a recent proposal that the afternoon nap zone represents the point in time after morning awakening when process-S has increased to a sufficiently high level to facilitate sleep onset, while at the same time an SCN-controlled circadian arousal process has not yet risen high enough to reverse this increased sleepiness. Eight normal male subjects aged 20--30 years, were monitored on two separate occasions under low ambient light (150 lux). Night sleep hours were maintained at 23:00--06:00h. PSG monitoring included EEG (C3-A2, O2-A1), right EOG-M1, left EOG-M2, submental EMG and core body temperature recorded continuously by a combination of the Oxford Medilog 9000 8-channel ambulatory recorder and the Minilogger temperature monitoring system. Following a baseline 24-hour day, bright light stimulation (10,000 lux) was given on two consecutive days either in the evening (20:00--22:00h) or morning (06:00--08:00h) in counter-balanced fashion with a 30 day washout periods between. Other than during a period of bright light stimulation, the level of daytime arousal was assessed every 60 min by quantified EEG spectral power followed by a 10 min duration simple reaction time test. In the baseline condition both the performance and Q-EEG variables confirmed the presence of a transitory afternoon nap zone as indexed by the timing of poorest performance and of greatest spectral power in a number of Q-EEG measures. Evening bright light treatment phase delayed these nap zone measures. Conversely, morning bright light phase advanced these measures. The finding that the timing of poorest performance and of the Q-EEG determined nap zone can be phase delayed by evening light and phase advanced by morning light supports the hypothesis tested, as well as supporting the existence of an SCN-dependent circadian arousal system in humans similar to that described by Edgar et al. (1993) in sub-human primates.

The focused sense of self that is central to our experience of consciousness could not exist without human brain's ability to process large amounts of information outside of conscious awareness. The Mismatch Negativity (MMN) is thought to index one such pre-conscious mechanism, a complex novelty detector that compares incoming sounds to rules that it has extracted from the recent acoustic past. Processes that do not require conscious awareness are considered to be "automatic". The automaticity of the MMN, however, has predominantly been studied using very simple stimuli. The present dissertation studied the issue of automaticity using a two-tone alternating pattern (e.g., ABABABAB...) as the "standard" stimuli. MMN-eliciting deviants were rule-violating tone repetitions (e.g., ABABAA&barbelow;AB...). Three studies took complementary approaches to the problem of automaticity. Study 1 tested the automaticity of the detection of rule violations by varying the presumed attentional demands of a visual task, while the auditory pattern was ignored. The MMN was unaffected by visual task difficulty, but it may be impossible for awake, alert subjects to ever fully ignore incoming sounds. Study 2, therefore, studied the MMN during natural sleep, the period of time when the observer is least conscious of the external environment. An MMN was elicited in both the waking state and REM sleep. Interpreted in isolation, these studies might be taken as evidence that the MMN is strongly automatic. Some attention effects, however, have been reported. One proposed mechanism for these attention effects is that attention increases the strength of the memory for the frequently-presented, standard stimuli. Study 3 examined whether the MMN varies with the strength of the memory for the standard by manipulating the number of memory-reinforcing repetitions of the standard that occurred between successive deviants. The results of Study 3 suggest that the amplitude of the MMN is unrelated to the strength of the memory for the standard. Altogether, the results of these studies suggest that even complex, rule-based MMN elicitation is an automatic process, and that studies demonstrating evidence to the contrary should be examined for the influence of other confounding factors.

This dissertation aimed to more fully characterize the involvement of bombesin-like peptides (neuromedin-B [NMB] and gastrin-releasing peptide [GRP]) and corticotropin-releasing hormone (CRH) in fear and anxiety-related processes. To this end, ventricularly injected GRP and antagonists of the NMB receptor decreased fear and/or anxiety across several animal models of behavior. Whereas NMB appeared to be involved in both fear and anxiety-related processes, GRP affected fear-related processes. In order to determine where in the brain these effects might be primarily localized, several neurochemical alterations were assessed in brain areas known to be involved in fear. Endogenous alterations in peptide levels were seen both within the medial prefrontal cortex (mPFC) and amygdala in response to recall of a fear-inducing shock. To explore this finding further, GRP or its receptor antagonist were microinjected into specific nuclei in the aforementioned areas and it was found that GRP consistently reduced fear at these loci, while the receptor antagonist exhibited both agonistic (reduced freezing) effects as well as antagonistic effects (increased freezing). Further, the observed reductions in freezing appeared to be specific to contextual components of conditioned fear, with the exception of drug administration to the infralimbic (IL) cortex within the mPFC, where we saw reduced freezing to a conditioned tone as well. To determine the endogenous release of GRP and CRH in response to conditioned fear, we collected dialysates from the IL of the mPFC and basolateral amygdala (BLA) in response to a previously conditioned tone. GRP and CRH were elevated 24h after fear conditioning at the BLA, an effect that appears to be related to animal's levels of fear. This was not observed at the IL. Finally, we explored whether the mPFC and amygdala communicated with each other via GRP and/or CRH through a GRP-specific pathway(s). We found that there appears to be a functional pathway between the IL cortex and BLA that is specific to GRP but not to CRH, upon manipulation of IL GRP levels. These studies have further characterized the role of BLPs and CRH in conditioned fear, particularly at the level of the mPFC and BLA and have provided a unique and rich foundation for the physiological role of these peptides and future studies to be developed.

The objective of this research was to determine whether access to mother-peer (MP) reared rhesus monkeys (Macaca mulatta) affected the behavior and physiology of juvenile and adolescent surrogate-peer (SP) and peer-only reared (PR) monkeys. Monkeys were housed in a mixed-rearing group (MP, SP, and PR together) or two same-rearing groups (one MP group and one SP and PR group). The studies of this dissertation used behavior and physiology to test three prediction models: SP and PR monkeys would be more similar to MP monkeys in the mixed-rearing group compared to the same-rearing group (acculturation model), more different (dissimilation model), or there would be no effect of MP monkeys in the mixed-rearing group (stability model). In experiment one, basic behavioral responses of 14-month old nursery reared monkeys were consistent with the stability model; however, SP monkeys showed a greater magnitude of difference in initiated social behavior than PR monkeys. In experiment two, SP monkeys preferred both SP and MP partners almost equally for all behaviors in the mixed-rearing group (acculturation model), whereas PR monkeys showed little fluctuation in partner preferences, preferring primarily other PR monkeys as partners (stability model). Also, there were more aggressive responses to aggressive interactions in SP monkeys in the mixed-rearing group (dissimilation model), whereas PR monkeys were similar to MP monkeys (stability model). In experiment three, plasma cortisol (CORT) of 14- and 26-month old SP monkeys and of 37- and 49-month old SP monkeys was similar to MP monkeys of the same ages. However, CORT of PR monkeys became more similar to MP monkeys over time in the mixed-rearing group. Variation in CORT among differently reared monkeys was also reduced over time. Mixed-rearing housing resulted in behavioral acculturation of SP monkeys and the physiological acculturation of PR monkeys; however, it is possible that SP monkeys showed physiological acculturation prior to our blood sampling and PR monkeys showed behavioral acculturation after our behavioral sampling. Thus, future studies evaluating monkeys in same- and mixed-rearing groups are necessary in order to examine this timing effect of behavioral and physiological acculturation.

Difficulty managing the stress of conflict in close relationships can lead to relationship distress and internalizing problems, possibly through dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, the neuroendocrine stress response system. Temperament, an individual characteristic, and attachment, a dyadic characteristic, have both been implicated in emotion regulation processes and physiological reactivity, yet there is no clear consensus on how the two relate to each other and to stress response, especially after childhood. The present study investigated the relationship between temperament and attachment, as well as how temperament and attachment together predict HPA reactivity in late adolescent couples. Analyses using multilevel modeling (HLM) found direct and interactive effects of partners' negative emotionality on their attachment security, as well as effects of temperament and attachment on their HPA trajectories. Partner's temperament and attachment moderated effects of own levels of these variables, and attachment security moderated the effects of temperament within individuals, with different predictive patterns emerging for males vs. females. Results are discussed in terms of emotional coregulation processes in romantic attachment and how gender role expectations intersect with social-emotional constructs to predict adjustment.

This dissertation presents a computational multiscale framework for predicting behavioral tendencies related to human addiction. The research encompasses three main contributions. The first contribution presents a formal, heuristic, and exploratory framework to conduct interdisciplinary investigations about the neuropsychological, cognitive, behavioral, and recovery constituents of addiction. The second contribution proposes a computational framework to account for real-life recoveries that are not dependent on pharmaceutical, clinical, and counseling support. This exploration relies upon a combination of current biological beliefs together with unorthodox rehabilitation practices, such as meditation, and proposes a conjecture regarding possible cognitive mechanisms involved in the recovery process. Further elaboration of this investigation leads on to the third contribution, which introduces a computational hypothesis for exploring the allostatic theory of addiction. A person engaging in drug consumption is likely to encounter mood deterioration and eventually to suffer the loss of a reasonable functional state (e.g., experience depression). The allostatic theory describes how the consumption of abusive substances modifies the brain's reward system by means of two mechanisms which aim to viably maintain the functional state of an addict. The first mechanism is initiated in the reward system itself, whereas the second might originate in the endocrine system or elsewhere. The proposed computational hypothesis indicates that the first mechanism can explain the functional stabilization of the addict, whereas the second mechanism is a candidate for a source of possible recovery. The formal arguments presented in this dissertation are illustrated by simulations which delineate archetypal patterns of human behavior toward drug consumption: escalation of use and influence of conventional and alternative rehabilitation treatments. Results obtained from this computational framework encourage an integrative approach to drug rehabilitation therapies which combine conventional therapies with alternative practices to achieve higher rates of consumption cessation and lower rates of relapse.