Distinct circuits in rat central amygdala for defensive behaviors evoked by socially signaled imminent versus remote danger.

Animals display a rich repertoire of defensive responses adequate to the threat proximity. In social species, these reactions can be additionally influenced by the behavior of fearful conspecifics. However, the majority of neuroscientific studies on socially triggered defensive responses focuses on one type of behavior, freezing. To study a broader range of socially triggered reactions and underlying mechanisms, we directly compared two experimental paradigms, mimicking occurrence of the imminent versus remote threat. Observation of a partner currently experiencing aversive stimulation evokes passive defensive responses in the observer rats. Similar interaction with a partner that has just undergone the aversive stimulation prompts animals to increase active exploration. Although the observers display behaviors similar to those of the aversively stimulated demonstrators, their reactions are not synchronized in time, suggesting that observers' responses are caused by the change in their affective state rather than mimicry. Using opsins targeted to behaviorally activated neurons, we tagged central amygdala (CeA) cells implicated in observers' responses to either imminent or remote threat and reactivated them during the exploration of a novel environment. The manipulation revealed that the two populations of CeA cells promote passive or active defensive responses, respectively. Further experiments confirmed that the two populations of cells at least partially differ in expression of molecular markers (protein kinase C-δ [PKC-δ] and corticotropin-releasing factor [CRF]) and connectivity patterns (receiving input from the basolateral amygdala or from the anterior insula). The results are consistent with the literature on single subjects' fear conditioning, suggesting that similar neuronal circuits control defensive responses in social and non-social contexts.

Increased excitability of cortical neurons induced by associative learning: an ex vivo study.

In adult mice, classical conditioning in which whisker stimulation is paired with an electric shock to the tail results in a decrease in the frequency of head movements, induces expansion of the cortical representation of stimulated vibrissae and enhances inhibitory synaptic interactions within the 'trained' barrels. We investigated whether such a simple associative learning paradigm also induced changes in neuronal excitability. Using whole-cell recordings from ex vivo slices of the barrel cortex we found that layer IV excitatory cells located in the cortical representation of the 'trained' row of vibrissae had a higher frequency of spikes recorded at threshold potential than neurons from the 'untrained' row and than cells from control animals. Additionally, excitatory cells within the 'trained' barrels were characterized by increased gain of the input-output function, lower amplitudes of fast after-hyperpolarization and decreased effect of blocking of BK channels by iberiotoxin. These findings provide new insight into the possible mechanism for enhanced intrinsic excitability of layer IV excitatory neurons. In contrast, the fast spiking inhibitory cells recorded in the same barrels did not change their intrinsic excitability after the conditioning procedure. The increased excitability of excitatory neurons within the 'trained' barrels may represent the counterpart of homeostatic plasticity, which parallels enhanced synaptic inhibition described previously. Together, the two mechanisms would contribute to increase the input selectivity within the conditioned cortical network.

High affinity carnitine transporters from OCTN family in neural cells.

Neurons are known to accumulate L-carnitine--a compound necessary for transfer of acyl moieties through biological membranes, apart from very low beta-oxidation of fatty acids in adult brain. Present study demonstrates expression of octn2 and octn3 genes coding high affinity carnitine transporters, as well as presence of both proteins in neurons obtained from suckling and adult rats, and also in mouse transformed neural cells. Measurements of carnitine transport show activity of both transporters in neural cells, pointing to their importance in physiological processes other than beta-oxidation.