Ptsd

specifie models

Putative animal models

Inescapable shock

Single prolonged stress

Predator exposure

Restraint/immobilization

Forced swim

Early-life maternal separation

Produces opioid-mediated analgesia

Brief one-time exposure produces long-term effects.

Produces conditioned fear responses.

Characterized by time-dependent sensitization.

Produces enhanced HPA negative feedback.

Produces a sustained exaggeration of the acoustic startle response.

Produces exaggerated startle.

Produces amgydala sensitization.

Exposed animals can be divided into "well-adapted" and "mal-adapted".

Single episode can produce sustained behavioral inhibition, perhaps reflective of PTSD-like avoidance.

Produces sensitization of LC-noradrenaline neurons.

Produces short-term glucocorticoid receptor upregulation.

High face validity with regard to potential effects of early-life trauma.

Many behavioral effects are short lasting.

Other behavioral and biological abnormalities have not been characterized.

Whether some neurophysiological effects (e.g., NMDA-mediated LTP) are also features of PTSD remains to be examined.

Characterization of other PTSD-like effects is very limited.

Glucocorticoid receptor effects are not sustained. PTSD-like behavioral effects remain largely uncharacterized.

Neuroendocrine effects in adulthood are more characteristic of depression than PTSD.

its components. In fact, it is becoming apparent that multiple, independent physiological pathways may mediate PTSD. In this case, it may be prudent to focus on endophenotypic models, which attend to one specific physiological pathway or neurobiological system relevant to PTSD. Combining information from numerous such models may prove a more efficient strategy.

It is also becoming more and more evident that PTSD is likely a multifactorial disorder whereby pretrauma vulnerability (genetic, developmental, or both) interacts with environmental insults. In view of this, it may also be of considerable use to begin combining genetic models with the single factor models described above. Thus, for instance, testing Lewis or YGR mice in IES, SPS, or predator models may help to elucidate the interactions between genetic and environmental factors in the development of PTSD symptoms. As well, they may help to determine which biological abnormalities are specifically linked to particular behavioral symptoms. It is likely that many more animal models of PTSD will be introduced in the near future. A number of putative models, such as those described in this chapter, will undergo further development as well. In the context of providing useful information, it will be critical to rigorously evaluate these models for their ability to produce specific features of PTSD, which are reflective of pathophysiological anxiety. In addition to this, consistent communication between animal and clinical research may prove highly critical in providing useful cues and insights into which strategies, avenues, or mechanisms offer the most promise.

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T. Sleekier, N.H. Kaiin andJ.M.H.M. Reul (Eds.) Handbook of Stress and the Brain, Vol. 15 ISBN 0-444-51823-1

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