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  • Title: Parvalbumin-containing interneurons in the basolateral amygdala express high levels of the alpha1 subunit of the GABAA receptor.
    Author: McDonald AJ, Mascagni F.
    Journal: J Comp Neurol; 2004 May 17; 473(1):137-46. PubMed ID: 15067724.
    Abstract:
    The basolateral amygdala (ABL) is essential for the amnestic effects of benzodiazepines in aversive learning tasks. Because the alpha1 subunit of the gamma-aminobutyric acid (GABA)(A) receptor is critical for these amnestic actions, knowledge of the neuronal localization of this subunit in the ABL should contribute to an understanding of the candidate neuronal mechanisms involved. To examine this question, we used dual-labeling immunohistochemical techniques to study the localization of the alpha1 subunit in the ABL. Our results suggest that the alpha1 subunit of the GABA(A) receptor is localized primarily in GABAergic interneurons in the ABL at the somal level, although the intense neuropil staining in the lateral nucleus suggests that distal dendrites of pyramidal projection neurons in this nucleus may also contain high levels of the alpha1 subunit. The great majority of alpha1-immunoreactive interneurons also exhibit immunoreactivity for the beta2/3 subunits of the GABA(A) receptor. Parvalbumin-positive (PV+) interneurons are the main interneuronal subpopulation exhibiting alpha1 immunoreactivity, but some calretinin-positive interneurons also express this subunit. These data suggest that certain subpopulations of GABAergic interneurons in the ABL, especially PV+ cells, receive a robust GABAergic innervation. Because the most likely source of this innervation is intrinsic, these results suggest that PV+ interneurons could constitute an important component of interneuronal networks in the ABL. These networks may be critical for the generation of synchronized rhythmic oscillations involved in consolidation of emotional memories. The activation of alpha1-containing GABA(A) receptors in the ABL by benzodiazepines may disrupt rhythmic oscillations critical for memory consolidation.
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