Current Status of Animal Models of Posttraumatic Stress Disorder: Behavioral and Biological Phenotypes, and Future Challenges in Improving Translation.

Methodological Issues: Electrodermal Mechanisms R. Edelberg. Methological Issues in Electrodermal Measurements W. Boucsein. Neural Control of EDA: Neural Control of Electrodermal Activity J.C. Roy, et al. Cortical and HypthalamoLimbic Control of Electrodermal Responses H. Sequeira, J.C. Roy. General Psychophysiology: Electrodermal Habituation Patterns R. Baltissen. Electrodermal Response Lability-Stability A. Cridder. Psychopathology: Electrodermal Indices as Markers for the Development of Schizophrenia P.H. Venables. Electrodermal Activity and Antisocial Behavior D.C. Fowles. Electrodermal Activity and Hemispherical Asymetry: The Laterality of Electrodermal Responses J. Gruzelier. Brain Asymmetry and Autonomic Conditioning K. Hugdahl, B.H. Johnsen. 13 additional articles. Index.

Progress in electrodermal research

Hughlings (1869) was among the first authors to report cortical influences upon the autonomic nervous system. Following Jackson’s studies, cardiovascular changes were elicited by stimulation of the frontal cortex (Danilewsky, 1875; Bochefontaine, 1876). At the beginning of this century, some authors (Bechterew, 1905; Karplus and Kreidl, 1909) also obtained an increase of sweating in the foot-pads of the cat, evoked by stimulating the sensorimotor cortex. During the next decades, other reports approached the role of cortical areas in the regulation of autonomic responses (see reviews of Kaada, 1951; Delgado, 1960; Hoff et al., 1963).

Cortical and Hypothalamo-Limbic Control of Electrodermal Responses

Understanding the neurobiological basis of post-traumatic stress disorder (PTSD) is fundamental to accurately diagnose this neuropathology and offer appropriate treatment options to patients. The lack of pharmacological effects, too often observed with the most currently used drugs, the selective se

Animal models of post-traumatic stress disorder and novel treatment targets

Lycopene ameliorates PTSD-like behaviors in mice and rebalances the neuroinflammatory response and oxidative stress in the brain.

Paroxetine treatment, following behavioral suppression of PTSD-like symptoms in mice, prevents relapse by activating the infralimbic cortex.

High-frequency stimulation of the infralimbic cortex, following behavioral suppression of PTSD-like symptoms, prevents symptom relapse in mice.

Susceptibility and Resilience to PTSD-Like Symptoms in Mice Are Associated with Opposite Dendritic Changes in the Prelimbic and Infralimbic Cortices Following Trauma.

Cortical and pyramidal stimulation elicit nonlateralized skin potential responses in the cat

Pre- and post-trauma drug use can interfere with recovery from post-traumatic stress disorder (PTSD). However, the biological underpinnings of this interference are poorly understood. Here we examined the effect of pre-fear conditioning cocaine self-administration on PTSD-like symptoms in male rats, and defined impairment of fear extinction as difficulty to recover from PTSD. We also examined cell density changes in brain regions suspected of being involved in resistance to PTSD recovery. Before footshock stress testing, rats were trained to self-administer cocaine during 20 consecutive days, after which they were exposed to footshocks, while other rats continued to self-administer cocaine until the end of the experiment. Upon assessment of three PTSD-like symptoms (fear during situational reminders, anxiety-like behavior, and impairment of recognition memory) and fear extinction learning and memory, changes in cell density were measured in the medial prefrontal cortex, hippocampus, and amygdala. Results show that pre-footshock cocaine exposure did not affect fear during situational reminders. Fear conditioning did not lead to an increase in cocaine consumption. However, in footshock stressed rats, cocaine induced a reduction of anxiety-like behavior, an aggravation of recognition memory decline, and an impairment of extinction memory. These behavioral alterations were associated with increased cell density in the hippocampal CA1, CA2, and CA3 regions and basolateral amygdala, but not in the medial prefrontal cortex. Our findings suggest that enhancement of cell density in the hippocampus and amygdala may be changes associated with drug use, interfering with PTSD recovery.

Repeated cocaine exposure prior to fear conditioning induces persistency of PTSD-like symptoms and enhancement of hippocampal and amygdala cell density in male rats

Saadia Ba-M'hamed

Papers

Paroxetine treatment, following behavioral suppression of PTSD-like symptoms in mice, prevents relapse by activating the infralimbic cortex.

High-frequency stimulation of the infralimbic cortex, following behavioral suppression of PTSD-like symptoms, prevents symptom relapse in mice.

Susceptibility and Resilience to PTSD-Like Symptoms in Mice Are Associated with Opposite Dendritic Changes in the Prelimbic and Infralimbic Cortices Following Trauma.

Cortical and pyramidal stimulation elicit nonlateralized skin potential responses in the cat

Repeated cocaine exposure prior to fear conditioning induces persistency of PTSD-like symptoms and enhancement of hippocampal and amygdala cell density in male rats