| An important category of learning involves the use of predictive cues to avoid danger. An example is provided by discriminative avoidance learning (DAL), wherein rabbits learn to avoid foot-shock by stepping in an activity wheel in response to a shock predictive tone (CS+, positive conditional stimulus) and by ignoring a non-predictive tone (CS-, negative conditional stimulus). Previous studies have indicated that neurons in the amygdala initiate discriminative training-induced neuronal activity (dTIA, more activity in response to the CS+ than to the CS-) in the medial geniculate nucleus (MGm), and in the anterior and posterior cingulate cortex (A24 and A29). Inactivation of amygdalar neurons by micro-infusion of muscimol at the onset of training blocked the dTIA in these areas. The MGm did not develop dTIA during later training when amygdalar neurons were not inactivated, whereas A24 and A29 did develop dTIA. This suggested that dTIA development in the MGm requires at least two factors: neuronal input from the amygdala, and a novel training experience. Experiment I supported this hypothesis, showing that 120 trials of pre-inactivation training, which reduced the novelty of the training experience, rescued dTIA in the MGm during post-inactivation training. Additionally, pre-inactivation training promoted dTIA expression in A24 during amygdalar inactivation. Thus, pre-inactivation training rendered A24 neurons independent of amygdalar influence. Pre-inactivation training did not rescue dTIA in the MGm and A29 during amygdalar inactivation, indicating a continuing amygdalar influence in these areas.; Neurons in A29 and the lateral nucleus of the amygdala (LA) characteristically develop maximal dTIA in late stages of DAL. Experiment II tested the hypothesis that LA nucleus is responsible for the late dTIA in A29. As hypothesized, LA nuclear excitotoxic lesions decreased dTIA in A29. Moreover, A29 theta-like neuronal activity was weaker in these subjects. Not in accord with the hypothesis, LA nuclear lesions impaired the early developing dTIA in A24. Thus, the LA nucleus may contribute to dTIA induction in A24, or the lesion may have damaged regions outside of the LA nucleus. Taken together these studies add significantly to understanding amygdalar modulation of neurons in extra-amygdalar regions of the neural circuitry for DAL. |
