Phasic vs sustained fear in rats and humans: role of the extended amygdala in fear vs anxiety.

Brain plasticity refers to the brainis ability to change structure and function Experience is a major stimulant of brain plasticity in animal species as diverse as insects and humans It is now clear that experience produces multiple, dissociable changes in the brain including increases in dendritic length, increases (or decreases) in spine density, synapse formation, increased glial activity, and altered metabolic activity These anatomical changes are correlated with behavioral differences between subjects with and without the changes Experience-dependent changes in neurons are affected by various factors including aging, gonadal hormones, trophic factors, stress, and brain pathology We discuss the important role that changes in dendritic arborization play in brain plasticity and behavior, and we consider these changes in the context of changing intrinsic circuitry of the cortex in processes such as learning

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Brain plasticity and behavior

Role of the bed nucleus of the stria terminalis versus the amygdala in fear, stress, and anxiety

The effects of predator odors in mammalian prey species: A review of field and laboratory studies

DISCLAIMER The use of company or product name(s) is for identification only and does not imply endorsement by the Agency for Toxic Substances and Disease Registry. A toxicological Profile for PCBs, Draft for Public Comment, was released in December 1998. This edition supercedes any previously released draft or final profile. Toxicological profiles are revised and republished as necessary, but no less than once every three years. The toxicological profiles are developed in response to the Superfund Amendments and Reauthorization Act (SARA) of 1986 (Public law 99-499) which amended the Comprehensive Environmental Response, Compensation, and Liability Act of 1980 (CERCLA or Superfund). This public law directed ATSDR to prepared toxicological profiles for hazardous substances most commonly found at facilities on the CERCLA National Priorities List and that pose the most significant potential threat to human health, as determined by ATSDR and the EPA. The availability of the revised priority list of 275 hazardous substances was announced in the Administrator of ATSDR to prepare a toxicological profile for each substance on the list. Toxicological Profiles are a unique compilation of toxicological information on a given hazardous substance. Each profile reflects a comprehensive and extensive evaluation, summary, and interpretation of available toxicologic and epidemiologic information on a substance. Health care providers treating patients potentially exposed to hazardous substances will find the following information helpful for fast answers to often-asked questions. Chapter 1: Public Health Statement: The Public Health Statement can be a useful tool for educating patients about possible exposure to a hazardous substance. It explains a substance's relevant toxicologic properties in a nontechnical, question-and-answer format, and it includes a review of the general health effects observed following exposure. Chapter 3: Health Effects: Specific health effects of a given hazardous compound are reported by type of health effect (death, systemic, immunologic, reproductive), by route of exposure, and by length of exposure (acute, intermediate, and chronic). In addition, both human and animal studies are reported in this section. NOTE: Not all health effects reported in this section are necessarily observed in the clinical setting. Please refer to the Public Health Statement to identify general health effects observed following exposure. The following additional material can be ordered through the ATSDR Information Center: Case Studies in Environmental Medicine: Taking an Exposure History—The importance of taking an exposure history and how to conduct one are described, and an example of a thorough exposure history is provided. Other …

Toxicological profile for polychlorinated biphenyls (PCBs)

Presentation of trimethylthiazoline (TMT, a component of fox feces) to laboratory rats elicits freezing, a prominent behavioral sign of anxiety or fear. The present study investigated the neural basis of this unlearned response. Muscimol, a GABA A receptor agonist, was injected (4.4 nmol/0.5 μl) into the bed nucleus of the stria terminalis (BNST) as well as into the amygdala, two brain areas known to be involved in anxiety and fear. Temporary inactivation of the BNST but not of the amygdala significantly blocked TMT-induced freezing. This effect was not caused by an enhancement of motor activity after BNST inactivation. In addition, these results confirm previous studies showing that freezing is possible despite amygdala inactivation. These results, and other findings in the literature, suggest that the BNST is critically involved in unlearned fear, whereas the amygdala is more involved in the acquisition and expression of learned fear.

https://www.jneurosci.org/content/jneuro/23/1/23.full.pdf

Temporary inactivation of the bed nucleus of the stria terminalis but not of the amygdala blocks freezing induced by trimethylthiazoline, a component of fox feces.

Cat odor elicits a profound defensive reaction in rats that is reduced by benzodiazepine drugs. The neural correlates of this phenomenon were investigated here using Fos immunohistochemistry. Rats received either midazolam (0.75 mg/kg, s.c.) or vehicle and were exposed to pieces of a collar that had been worn by a domestic cat or an unworn (dummy) collar. Cat odor caused midazolam-sensitive defensive behavioral responses, including avoidance of collar contact, inhibition of grooming, and prolonged rearing. Cat odor exposure induced Fos expression in the posterior accessory olfactory bulb (glomerular, mitral, and granule cell layers), with granule cell layer activation attenuated by midazolam. High basal Fos expression, and some cat odor-associated Fos expression, was evident in the main olfactory bulb (glomerular cell layer), and midazolam exerted a strong inhibitory effect in this region. Midazolam inhibited Fos expression in key limbic regions involved in pheromone transduction (medial amygdala and bed nucleus of the stria terminalis) and defensive behavior (prelimbic cortex, lateral septum, lateral and medial preoptic areas, and dorsal premammillary nucleus). However, midazolam failed to affect cat odor-related Fos expression in a range of key defense-related sites, including the ventromedial hypothalamic nucleus, paraventricular nucleus of the hypothalamus, periaqueductal gray, and cuneiform nucleus. These results indicate that midazolam exerts a region-specific effect on the neural substrates activated by predator odor, with effects in the lateral septum and dorsal premammillary nucleus likely to be of major importance. These findings also suggest the intriguing hypothesis that cat odor is processed by rats as a "pheromone-like" stimulus.

https://www.jneurosci.org/content/jneuro/24/17/4134.full.pdf

Raimund Apfelbach

Papers

The effects of predator odors in mammalian prey species: A review of field and laboratory studies

Temporary inactivation of the bed nucleus of the stria terminalis but not of the amygdala blocks freezing induced by trimethylthiazoline, a component of fox feces.

Neural correlates of cat odor-induced anxiety in rats: region-specific effects of the benzodiazepine midazolam.

TMT-induced autonomic and behavioral changes and the neural basis of its processing

Cat odor, but not trimethylthiazoline (fox odor), activates accessory olfactory and defense-related brain regions in rats.