http://nova.newcastle.edu.au/vital/access/services/Feed ${session.getAttribute("locale")} 5 http://nova.newcastle.edu.au/vital/access/manager/Repository/uon:10380 At present, exposure of a rodent to the odour of a predator is one of the most common animal models of post traumatic stress disorder (PTSD). Despite this, the model remains incompletely characterized, particularly in regard to within subject assessment of major PTSD-like behaviours. In an attempt to redress this situation, we have extensively characterized the two broad categories of behaviour that are considered to characterize PTSD, that is sensitized behaviours such as social withdrawal and hypervigilance and conditioned behaviours such as avoidance of trauma linked cues. Specifically, we determined the presence and duration of both conditioned and sensitized behaviours, in the same cohort of animals, after three exposures to predator odour. Conditioned fear was assessed on the basis of inhibition of locomotor activity upon return to context 2, 7, 14, 21, and 28 days after the last odour exposure session. To assess the impact on sensitization behaviours, we monitored acoustic startle responses and social interaction behaviour 4, 9, 16, 23, and 30 days after the last exposure session. In addition to examining the behavioural consequences associated with odour exposure, we also determined the key brain regions that were activated using ΔFosB immunohistochemistry. Our results show that the two groups of behaviours thought to characterize PTSD (conditioned and sensitized) do not travel together in the predator odour model, with clear evidence of enduring changes in conditioned fear but little evidence of changes in social interaction or acoustic startle. With regard to associated patterns of activity in the brain, we observed that odour-exposed animals exhibited significantly higher numbers of FosB-positive nuclei in only the medial prefrontal cortex (mPFC), a finding that can be viewed as being consistent with the observed behavioural changes. 2012-03-13T00:30:07.605Z ]]> http://nova.newcastle.edu.au/vital/access/manager/Repository/uon:7708 The aim of this study was to determine whether 5-HT2A receptors mediate cardiovascular and thermogenic responses to acute psychological stresses. For this purpose, adult male Wistar hooded rats instrumented for telemetric recordings of either electrocardiogram (ECG) (n=12) or arterial pressure (n=12) were subjected, on different days, to four 15-min episodes of social defeat. Prior to stress, animals received s.c. injection of the selective 5-HT2A receptor antagonist SR-46349B (trans-4-((3Z)3-[(2-dimethylaminoethyl)oxyimino]-3-(2-fluorophenyl)propen-1-yl)-phenol, hemifumarate) (at doses of 0.3, 1.0 and 3.0 mg/kg) or vehicle. The drug had no effect on basal heart rate or heart rate variability indexes, arterial pressure, and core body temperature. Social defeat elicited significant and substantial tachycardic (347±7 to 500±7 bpm), pressor (77±4 to 97±4 mm Hg) and hyperthermic (37.0±0.3 to 38.5±0.1 °C) responses. Blockade of 5-HT2A receptors, at all doses of the antagonist, completely prevented stress-induced hyperthermia. In contrast, stress-induced cardiovascular responses were not affected by the blockade (except small reduction of tachycardia by the highest dose of the drug). We conclude that in rats, 5-HT2A receptors mediate stress-induced hyperthermic responses, but are not involved in the genesis of stress-induced rises in heart rate or arterial pressure, and do not participate in cardiovascular control at rest. 2011-05-12T06:30:51.464Z ]]> http://nova.newcastle.edu.au/vital/access/manager/Repository/uon:7695 Individuals vary in the way in which they cope with stressful situations. It has been suggested that ‘active’ coping behaviour, characterised by aggression and territorial control, is more effective in moderating the stress associated with social defeat than ‘passive’ coping behaviour, as characterised by immobility, decreased reactivity, and low aggression. We used the rodent ‘resident/intruder’ paradigm to determine whether individual differences in coping behaviour modulate the acute adrenocortical response to social defeat. During the 10 min conflict episode, behaviours displayed by the intruder were recorded and subsequently scored. Intruders that engaged in large numbers of fights and/or frequently used physical structures to block the resident's approach (a behaviour referred to as ‘guarding’), displayed smaller corticosterone responses to defeat than other intruders. Corticosterone responses to defeat were unrelated to a measure of coping style preferences (defensive burying test) obtained prior to the defeat encounter. We further chose to investigate the neurobiological basis of this observation by comparing the patterns of defeat-induced neuronal activation in the forebrains of intruders that displayed high versus low numbers of defensive behaviours during the defeat episode. The results of this analysis indicated that ‘low fight’ and ‘low guard’ intruders, i.e. those that achieved a fight or a guard score below the 20th percentile, had significantly higher numbers of Fos-positive neurons in forebrain regions such as the medial prefrontal cortex and the amygdala than did control animals exposed to an empty resident's cage. In summary, the present data suggest that ‘active’ coping behaviour is associated with both a smaller adrenocortical response and a lower level of ‘neural activation’ following social defeat. This outcome differs from that of earlier studies, a difference that we suggest is due to the fact that the present study is the first to assess coping on the basis of behaviour actually displayed during the conflict interaction. 2011-05-10T01:50:03.578Z ]]>