Differential modulation of hippocampal plasticity in a non-noxious conflict model for anxiety.

Abstract

Modulation of synaptic strength may underlie stress-induced changes in cognitive ability. Long-term memory formation underpinning fear and anxiety behaviors, such as those seen in post-traumatic stress and phobic disorders, is thought to be dependent on amygdalo-hippocampal interactions. In most models, however, painful stimuli are used to induced stress and anxiety. Here, the effects of a novel conflict model, developed to generate a more naturalistic model of anxiety, utilizing two non-noxious stressors (predator (cat) odor and light), on hippocampus plasticity were determined. Exposure to the external stimuli elicited typical, stimulus-specific, anxiety-related behaviors. Dual presentation of the stressors evoked an increase in the variability of behaviors, suggesting that the animals were experiencing conflicting drives. Induction of long-term potentiation (LTP) within the CA1 region of the hippocampus was reduced following exposure to light stress, independent of presence, or absence, of odor. However, after a single presentation, LTP was reduced following either odor presentation or dual presentation of the stressors. Furthermore, LTP in ex vivo tissue obtained from conflict-exposed animals showed differential hemispheric responses, suggesting that long-term contextual-related components of anxiety behavior are dependent on modification of hippocampal circuitry.