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Basolateral amygdala regulation of adult hippocampal neurogenesis and fear-related activation of newborn neurons.

Kirby ED, Friedman AR, Covarrubias D, Ying C, Sun WG, Goosens KA, Sapolsky RM, Kaufer D - Mol. Psychiatry (2011)

Bottom Line: We show that BLA lesions suppress adult neurogenesis, while lesions of the central nucleus of the amygdala do not.Similarly, we show that reducing BLA activity through viral vector-mediated overexpression of an outwardly rectifying potassium channel suppresses neurogenesis.These results demonstrate that BLA activity regulates adult hippocampal neurogenesis and the fear context-specific activation of newborn neurons.

View Article: PubMed Central - PubMed

Affiliation: Helen Wills Neuroscience Institute, University of California-Berkeley, Berkeley, CA 94720, USA.

ABSTRACT
Impaired regulation of emotional memory is a feature of several affective disorders, including depression, anxiety and post-traumatic stress disorder. Such regulation occurs, in part, by interactions between the hippocampus and the basolateral amygdala (BLA). Recent studies have indicated that within the adult hippocampus, newborn neurons may contribute to support emotional memory, and that regulation of hippocampal neurogenesis is implicated in depressive disorders. How emotional information affects newborn neurons in adults is not clear. Given the role of the BLA in hippocampus-dependent emotional memory, we investigated whether hippocampal neurogenesis was sensitive to emotional stimuli from the BLA. We show that BLA lesions suppress adult neurogenesis, while lesions of the central nucleus of the amygdala do not. Similarly, we show that reducing BLA activity through viral vector-mediated overexpression of an outwardly rectifying potassium channel suppresses neurogenesis. We also show that BLA lesions prevent selective activation of immature newborn neurons in response to a fear-conditioning task. These results demonstrate that BLA activity regulates adult hippocampal neurogenesis and the fear context-specific activation of newborn neurons. Together, these findings denote functional implications for proliferation and recruitment of new neurons into emotional memory circuits.

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Related in: MedlinePlus

Excitotoxic lesionsMinimum (grey) and maximum (black) extent of excitotoxic BLA (a) and CeA (b) lesions.
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Figure 1: Excitotoxic lesionsMinimum (grey) and maximum (black) extent of excitotoxic BLA (a) and CeA (b) lesions.

Mentions: One series of sections was mounted and counterstained with cresyl violet for lesion assessment. If a lesion did not cover at least 75% of the area of interest without affecting surrounding areas, that rat was removed from analysis (Figure 1). For virus expression, if GFP expression was not found in the BLA or if expression was focused outside the BLA, the rat was removed from analysis.


Basolateral amygdala regulation of adult hippocampal neurogenesis and fear-related activation of newborn neurons.

Kirby ED, Friedman AR, Covarrubias D, Ying C, Sun WG, Goosens KA, Sapolsky RM, Kaufer D - Mol. Psychiatry (2011)

Excitotoxic lesionsMinimum (grey) and maximum (black) extent of excitotoxic BLA (a) and CeA (b) lesions.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4310700&req=5

Figure 1: Excitotoxic lesionsMinimum (grey) and maximum (black) extent of excitotoxic BLA (a) and CeA (b) lesions.
Mentions: One series of sections was mounted and counterstained with cresyl violet for lesion assessment. If a lesion did not cover at least 75% of the area of interest without affecting surrounding areas, that rat was removed from analysis (Figure 1). For virus expression, if GFP expression was not found in the BLA or if expression was focused outside the BLA, the rat was removed from analysis.

Bottom Line: We show that BLA lesions suppress adult neurogenesis, while lesions of the central nucleus of the amygdala do not.Similarly, we show that reducing BLA activity through viral vector-mediated overexpression of an outwardly rectifying potassium channel suppresses neurogenesis.These results demonstrate that BLA activity regulates adult hippocampal neurogenesis and the fear context-specific activation of newborn neurons.

View Article: PubMed Central - PubMed

Affiliation: Helen Wills Neuroscience Institute, University of California-Berkeley, Berkeley, CA 94720, USA.

ABSTRACT
Impaired regulation of emotional memory is a feature of several affective disorders, including depression, anxiety and post-traumatic stress disorder. Such regulation occurs, in part, by interactions between the hippocampus and the basolateral amygdala (BLA). Recent studies have indicated that within the adult hippocampus, newborn neurons may contribute to support emotional memory, and that regulation of hippocampal neurogenesis is implicated in depressive disorders. How emotional information affects newborn neurons in adults is not clear. Given the role of the BLA in hippocampus-dependent emotional memory, we investigated whether hippocampal neurogenesis was sensitive to emotional stimuli from the BLA. We show that BLA lesions suppress adult neurogenesis, while lesions of the central nucleus of the amygdala do not. Similarly, we show that reducing BLA activity through viral vector-mediated overexpression of an outwardly rectifying potassium channel suppresses neurogenesis. We also show that BLA lesions prevent selective activation of immature newborn neurons in response to a fear-conditioning task. These results demonstrate that BLA activity regulates adult hippocampal neurogenesis and the fear context-specific activation of newborn neurons. Together, these findings denote functional implications for proliferation and recruitment of new neurons into emotional memory circuits.

Show MeSH
Related in: MedlinePlus