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Elucidating the process by which an animal can transduce a brief signal into a predictable set of behaviours has important implications for understanding brain function. I explored the transition from quiescence to repetitive activity in the bag cell neurons of Aplysia californica. Using both cultured neurons and intact ganglia, I demonstrated the involvement of cholinergic transmission in this marked change to excitability. The bag cell neurons are a group of 200-400 electrically-coupled neuroendocrine cells that initiate a set of prescribed reproductive behaviours, culminating in deposition of an egg mass. This fixed action pattern, lasting ~1 h, follows a brief (≤10-sec) stimulus from an afferent input to the bag cell neuron cluster, which causes these previously silent neurons to continuously fire for ~30 min. Central to the maintenance of this increased excitability, are the elevation of various second messenger pathways that modulate multiple ion channels. As such, the initiating stimulus for afterdischarge generation was thought to involve metabotropic receptors. However, I report that an acetylcholine-gated ionotropic current triggers the afterdischarge, as well as two, distinct nicotinic responses that participate in excitability: one associated with channel opening and the other through the inhibition of K+ currents. My data suggest that the interplay between inward Ca2+ and cation currents, and outward K+ channels, regulated by intracellular messengers protein kinase C (PKC) and cyclic adenosine monophosphate (cAMP), respectively, set the baseline level of excitability prior to cholinergic activation. I also observed, distinct negative-feedback mechanisms on the acetylcholine ionotropic current. First, an increase in cAMP inhibits the cholinergic current shortly after the start of the afterdischarge, and once the afterdischarge is fully underway, dephosphorylation by a Src family tyrosine kinase further inhibits the channel. In addition, FMRFamide, an afterdischarge suppressor, appears to directly block the cholinergic channel. By exploring both canonical and non-canonical cholinergic roles in the afterdischarge, I have determined that complex signalling pathways can be reduced to a single variable, provided that the necessary precursors are in place. Furthermore, based on post-synaptic receptor composition and regulation, my work indicates the potential for profound diversity in cholinergic pathways. / Thesis (Ph.D, Physiology) -- Queen's University, 2013-06-28 17:51:30.733

Mini-Dissertation submitted in partial compliance with the requirements of the Master's Degree in Technology: Homoeopathy, Durban Institute of Technology, 2005. / A sudden decrease in the use of nicotine containing products, which was used daily for at least several weeks, can cause Nicotine Withdrawal Syndrome (American Psychiatric Association, 1994: 244). The mental symptoms of the withdrawal syndrome includes depressed mood; irritability, frustration, anger, anxiety, difficulty concentrating, restlessness or impatience. The aim of this placebo-controlled double-blind study was to determine the effectiveness of a homoeopathic complex, compared to homoeopathic similimum treatment in the management of tobacco addiction. The complex was based on the selection of those homoeopathic remedies whose symptomology most accurately matched the symptoms associated with smoking cessation. / M

Dissertation submitted in partial compliance with the requirements for the Master's Degree in Technology: Homoeopathy, Technikon Natal, Durban, 1998. / The purpose of this study was to investigate the use of isotherapy together with the homoeopathic simillimum whilst comparing it with isotherapy combined with placebo in helping people to stop smoking, in terms of a daily smoking log, and the participants attitude to their tobacco smoking addiction. Thirty participants completed this double-blind randornised trial which took place in the northern suburbs of Gauteng. Participants responded to advertisements and were selected according to certain criteria: participants were to be over the age of 18 years of age, and were to have smoked 15 or more cigarettes a day for more than a year. Group 1 received isotherapy and homoeopathic simillimum and group 2 isotherapy and placebo. Each participant received 5 treatments over a period of 3 months. Cigarette consumption was recorded daily by each participant and questionnaires were completed in the presence of the researcher at each consultation. The daily smoking logs and the questionnaire scores were totalled and statistically analysed. Comparison with respect to cigarette consumption between the two groups were analysed using the two-sample unpaired t-test. The Mann-Whitney U-tests were used for inter-group comparisons and the Wilcoxon's signed rank tests for intra-group comparisons with respect to the questionnaires. Data was presented in tables and bar graphs. In each case a was set at 0.05. / M

Individuals high in anxiety sensitivity (AS), a cognitive risk factor denoting a fear of anxiety-related sensations (Reiss & McNally, 1985), may be at increased risk of misinterpreting nicotine withdrawal-relevant interoceptive cues as harmful, thus amplifying their risk for panic problems. This study tested the moderating role of AS on the association between nicotine withdrawal and panic-relevant responding to a carbon dioxide-enriched air laboratory challenge. Specifically, it was hypothesized that AS moderates the relation between nicotine withdrawal (group status) and responding to a carbon dioxide-enriched air procedure (controlling for anticipatory anxiety, gender, negative affectivity, number of axis I diagnoses, and average daily smoking rate), as indexed by: (1) level of anxiety focused on bodily sensations and intensity of panic attack symptoms; (2) skin conductance reactivity; and (3) level of behavioral avoidance of a future challenge. To test this hypothesis, 90 daily smokers (35 women; Mage = 28.87, SD = 12.12, Range = 18-60 years) were enrolled and enlisted to attend two study sessions. At the conclusion of the first session, participants were randomly assigned to one of two groups (12-hour nicotine deprivation or smoking ‗as usual‘). At the second scheduled session, participants in both groups underwent a 10% carbon dioxide-enriched air laboratory challenge to assess panic-relevant responding. Contrary to hypothesis, the AS by nicotine withdrawal (group status) interactive effect was not significantly predictive of post-challenge anxiety, panic attack symptoms, skin conductance reactivity, or behavioral avoidance. However, post hoc tests indicated that the AS by nicotine withdrawal (group status) interaction was significantly predictive of peri-challenge anxiety ratings. Furthermore, post hoc tests demonstrated that between-group (significant) differences in withdrawal symptoms diminished after the first assessment of the challenge session. Results are discussed in the context of the theoretical and clinical implications of the current work, limitations of the current study, and future directions for work relevant to this line of inquiry.

The effect of menthol on nicotine metabolism was examined in liver S9 fractions of four different species and in the in vivo mouse model. The purpose of this study was to investigate three parameters: (1) biotransformation of nicotine to cotinine in various species (human, mouse, rat and trout) using in vitro methods; (2) to determine if the addition of menthol with nicotine altered biotransformation of nicotine to cotinine; (3) and to assess similar parameters in an in vivo mouse model. The major findings of this study include: (1) mice appear to metabolize nicotine, over time, in a manner similar to humans; (2) menthol decreased cotinine production, over time, after a single dose in mice; and (3) menthol increased cotinine production, over time, after repeated doses, in mice.

Chong Kin Ngai. / Summary in Chinese. / Thesis (MBA) - Chinese University of Hong Kong. / Bibliography: l. 118-119.

Cognitive function in the brain is controlled by neurotransmitters whose release is tightly controlled. When normal levels are perturbed deficits in function can be observed both in humans and in animal models. The cholinergic system, acting via muscarinic or nicotinic receptors, modulates neurotransmitter release. The aim of this thesis was to investigate the identity of the nicotinic acetylcholine receptor (nAChR) subtypes involved in modulating noradrenaline (NA) release, in rodent frontal cortex (FC) and hippocampus (HC). Comparisons were made both in vitro and in vivo using pharmacological tools. In vitro, acute application of nicotinic agonists evoked release of previously loaded [3H]-NA from prisms of rat FC and HC. There was a 2000-fold more potent response to β2* selective nAChR agonist 5-iodo-A85380 in FC than HC. A greater response to choline in HC than FC, combined with a lack of response to selective α7 ligands supports α3β4* nAChRs as the main mediator of nicotinic stimulated NA release in vitro in HC. A proportion of the release in each region was mediated via a potentially excitatory action of GABA. The profile of responses was unchanged after the acute or chronic administration of nicotine in vivo. In vivo microdialysis experiments were designed to test whether the nAChR subtype differences in vitro were representative of differences in vivo. 5-iodo-A85380 administered by reverse dialysis increased NA levels to a greater extent in FC than HC, supporting differences in the nAChR composition involved in NA regulation between these two regions. Targeted stimulation of these different nAChR subtypes could allow exploitation of this disparity to improve function with novel compounds such as those described in Chapter 2. Overall the studies described in this thesis show that there are differences in the subtype of nAChRs involved in NA release from terminal fields of FC and HC both in vitro and in vivo.

This study examined the number of conditioning trials necessary to produce associative nicotine tolerance and the changes in corticosterone levels during the procedures. Six independent groups of rats (N = 355) were run through tolerance acquisition procedures for 1, 5, or 10 conditioning sessions. Treatment groups were comprised of animals that received nicotine-environment pairings, animals that received nicotine explicitly unpaired with the drug administration environment, and control groups that received either saline throughout or no treatment. Three of the groups were tested for nicotine-induced analgesia using the tail-flick and hot-plate assays, and three groups were blood sampled after either nicotine or saline injection. Pairing of environment with nicotine produced greater tolerance for rats after 5 conditioning sessions in the tail flick and after 10 conditioning sessions in the hot-plate. Corticosterone levels were elevated in all rats given nicotine. Rats that received the nicotine-environment pairing showed a conditioned release of corticosterone in response the environment after both 5 and 10 conditioning sessions.