Factors affecting a woman's decision to leave an abusive relationship : the theory of planned behaviour /

The present study tested the appHcabiUty of Ajzen's (1985) theory of planned behaviour (TPB), an extension of Fishbein and Ajzen's (1975) theory of reasoned action (TRA), for the first time, in the context of abused women's decision to leave their abusive relationships. The TPB, as a means of predicting women's decision to leave their abusive partners' was drawn from Strube's (1988, 1991) proposed decision-making model based on the principle that the decision-making process is a rational, deliberative process, and regardless of outcome, was a result of a logical assessment of the available data. As a means of predicting those behaviours not under volitional control, Ajzen's (1985) TPB incorporated a measure of perceived behavioural control. Data were collected in two phases, ranging from 6 months to 1 year apart. It was hypothesized that, to the extent that an abused woman held positive attitudes, subjective norms conducive to leaving, and perceived control over leaving, she would form an intention to leave and thus, increase the likelihood of actually leaving her partner. Furthermore, it was expected that perceptions of control would predict leaving behaviour over and above attitude and subjective norm. In addition, severity and frequency of abuse were assessed, as were demographic variables. The TPB failed to account significantly for variability in either intentions or leaving behaviour. All of the variance was attributed to those variables associated with the theory of reasoned action, with social influence emerging as the strongest predictor of a woman's intentions. The poor performance of this model is attributed to measurement problems with aspects of attitude and perceived control, as well as a lack of power due to the small sample size. The insufficiency of perceived control to predict behaviour also suggests that, on the surface at least, other factors may be at work in this context. Implications of these results, and recommendations such as, the importance of obtaining representative samples, the inclusion of self-esteem and emotions as predictor variables in this model, a reevaluation of the target behaviovu" as nonvolitional, and longitudinal studies spanning a longer time period for future research within the context of decision-making are discussed.

The role of cyclic nucleotides in modulation of crayfish neuromuscular junctions by a neuropeptide /

DF2, a heptapeptide, is a member of the family of FMRFamide-like peptides and has been shown to increase the amount of transmitter released at neuromuscular junctions of the crayfish, Procambarus clarkit Recent evidence has shown that protein kinase C (PKC), calcium/calmodulin-dependent protein kinase II (CaMKII) and the cAMPdependent protein kinase (PKA) play a role in the neuromodulatory pathway of DF2. The involvement of these kinases led to the prediction that a G-protein-coupled receptor (GPCR) is activated by DF2 due to the role that each kinase plays in traditional GPCR pathways seen in other organisms and in other cells. G-proteins can also act on an enzyme that generates cyclic guanosine monophosphate (cGMP) which mediates its effects through a cGMP-dependent protein kinase (PKG). This thesis addresses the question of whether or not DF2's effects on synaptic transmission in crayfish are mediated by the cyclic nucleotides cAMP and cGMP. The effects of DF2 on synaptic transmission were examined using deep abdominal extensor muscles of the crayfish Procambarus clarkii. An identified motor neuron was stimulated, and excitatory post-synaptic potentials (EPSPs) were recorded in abdominal extensor muscle LI . A number of activators and inhibitors were used to determine whether or not cAMP, PKA, cGMP and PKG mediate the effect of this peptide. Chemicals that are known to activate PKA (Sp-cAMPS) and/or PKG (8-pCPTcGMP) mimic and potentiate DF2's effect by increasing EPSP amplitude. Inhibitors of either PKA (Rp-cAMPS) or PKG (Rp-8-pCPT-cGMPS) block a portion of the increase in EPSP amplitude induced by the peptide. When both kinase inhibitors are applied simultaneously, the entire effect of DF2 on EPSPs is blocked. The PKG inhibitor blocks the effects of a PKG activator but does not alter the effect of a PKA activator on EPSP amplitude. Thus, the PKG inhibitor appears to be relatively specific for PKG. A trend in the data suggests that the PKA inhibitor blocks a portion of the response elicited by the PKG activator. Thus, the PKA inhibitor may be less specific for PKA. Phosphodiesterase inhibitors, which are known to inhibit the breakdown of cAMP (IBMX) and/or cGMP (mdBAMQ), potentiate the effect of the peptide. These results support the hypothesis that cAMP and cGMP, acting through their respective protein kinase enzymes, mediate the ability of DFi to increase transmitter output.