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Abstract: The amygdala has a well-established role in stress, anxiety, and aversive learning, and anxiolytic and anxiogenic agents are thought to exert their behavioral actions via the amygdala. However, despite extensive behavioral data, the effects of noradrenergic anxiogenic drugs on neuronal activity within the amygdala have not been examined. The present experiments examined how administration of the anxiogenic drug yohimbine affects spontaneous and evoked neuronal activity in the basolateral amygdala (BLA) of rats. Yohimbine produced both excitatory and inhibitory effects on neurons of the BLA, with an increase in spontaneous activity being the predominant response in the lateral and basomedial nuclei of the BLA. Furthermore, yohimbine tended to facilitate neuronal responses evoked by electrical stimulation of the entorhinal cortex, with this facilitation seen more often in lateral and basomedial nuclei of the BLA. These data are the first to examine the effects of the anxiogenic agent yohimbine on BLA neuronal activity, and suggest that neurons in specific subnuclei of the amygdala exhibit unique responses to administration of such pharmacological agents. [Copyright &y& Elsevier]

Abstract: The encoding of reward-predictive stimuli by neurons in the nucleus accumbens (NAcc) depends on integrated synaptic activity from the basolateral amygdala (BLA) and medial prefrontal cortex (mPFC) afferent inputs. In a previous study, we found that single electrical stimulation pulses applied to the BLA facilitate mPFC-evoked spiking in NAcc neurons in a timing-dependent manner, presumably by a fast glutamatergic mechanism. In the present study, the ability of repetitive BLA activation to modulate synaptic inputs to NAcc neurons through dopamine- or N-methyl-d-aspartate (NMDA)-dependent mechanisms is characterized. NAcc neurons receiving excitatory input from both mPFC and BLA were recorded in urethane-anesthetized rats. Train stimulation of the BLA depressed mPFC-evoked spiking in these neurons. This was not attributable to mechanisms involving NMDA or dopamine D1, D2, D3 or D5 receptors, since blockade of these receptors did not affect the BLA-mediated depression. BLA-mediated depression was only evident when the BLA stimulation evoked spikes in the recorded neuron; thus, depolarization of the recorded neuron may be critical for this effect. The ability of the BLA to suppress mPFC-to-NAcc signaling may be a mechanism by which normal or pathologically heightened emotional states disrupt goal-directed behavior in favor of emotionally-driven responses. [Copyright &y& Elsevier]