Novelty and fear conditioning induced gene expression in high and low states of anxiety.

Emotional states influence how stimuli are interpreted. High anxiety states in humans lead to more negative, threatening interpretations of novel information, typically accompanied by activation of the amygdala. We developed a handling protocol that induces long-lasting high and low anxiety-like states in rats to explore the role of state anxiety on brain activation during exposure to a novel environment and fear conditioning.

Chronic corticosterone administration does not potentiate unconditioned freezing to the predator odor, trimethylthiazoline.

Chronic high levels of corticosterone (CORT) are known to facilitate learning and memory of aversive events. Whether this effect of chronic CORT also generalizes to unconditioned or unlearned fear behavior is not known. The present study investigated whether high levels of chronic CORT enhance unconditioned fear to a predator odor, trimethylthiazoline (TMT), an innate fear stimulus to rodents.

Not all rat strains are equal: differential unconditioned fear responses to the synthetic fox odor 2,4,5-trimethylthiazoline in three outbred rat strains.

Predator odors induce unconditioned fear in rats; however, the synthetic predator odor 2,4,5-trimethylthiazoline (TMT) either elicits robust fear behavior (e.g., freezing) or no fear responses at all.

Animal studies of amygdala function in fear and uncertainty: relevance to human research.

This article reviews research in both animals and humans on the considerable progress made in elucidating a brain circuitry of fear, particularly the importance of the amygdala in fear conditioning. While there is considerable agreement about the participation of the amygdala in fear in both animals and humans, there are several issues about the function of the amygdala raised by the human research that have not been addressed by or may be answered by animal research. Three of these are addressed in this article: (1) is the amygdala involved in or necessary for both fear learning and unconditioned fear? (2) Does the amygdala code for intensity of fear? (3) Is the amygdala preferentially involved in fear, or is it also activated when there are no overt fear or aversive stimuli, but where the situation can be described as uncertain? We present evidence indicating that the rodent amygdala is involved in some types of fear (conditioned fear), but not all types (unconditioned fear), and may therefore have significance for a differential neurobiology of certain anxiety disorders in humans.

Glucocorticoid receptor antagonism in the basolateral amygdala and ventral hippocampus interferes with long-term memory of contextual fear.

The binding of glucocorticoids to the type II or glucocorticoid receptor (GR) is known to play a role in memory consolidation and long-term memory. The present series of studies investigated the locus for GR effects on learning and memory of contextual fear conditioning. The GR antagonist RU 38486 was administered peripherally (10, 20, or 30 mg/kg/ml), as well as centrally into the lateral ventricle (75 or 150 ng/2 microL), basolateral amygdala (BLA; 0.

An egr-1 (zif268) antisense oligodeoxynucleotide infused into the amygdala disrupts fear conditioning.

Studies of gene expression following fear conditioning have demonstrated that the inducible transcription factor, egr-1, is increased in the lateral nucleus of the amygdala shortly following fear conditioning. These studies suggest that egr-1 and its protein product Egr-1 in the amygdala are important for learning and memory of fear. To directly test this hypothesis, an egr-1 antisense oligodeoxynucleotide (antisense-ODN) was injected bilaterally into the amygdala prior to contextual fear conditioning.