The distribution of calbindin-D28k-immunoreactive cells and fibres in
five human amygdalae was analysed from sections that had been stained
immunohistochemically with a monoclonal antibody raised against calbin
din-D28k. The highest density of calbindin-28k-positive neurons were f
ound in the anterior cortical, medial, posterior cortical and accessor
y basal nuclei, in the parvicellular division of the basal nucleus and
in the amygdalohippocampal area. The lowest densities of immunopositi
ve neurons were found in the paralaminar nucleus, in the periamygdaloi
d cortex (PAC1 and PACo) and in some of the intercalated nuclei. The d
eep nuclei (lateral, basal and accessory basal nuclei) contained a hig
h density of calbindin-D28k-immunoreactive fibres and terminals. The c
ortical nuclei and the central nucleus were characterized by intense n
europil labelling. Morphologically, a large majority of the calbindin-
D28k-immunoreactive neurons were aspiny or sparsely spiny and resemble
d inhibitory local circuit neurons. A small population of lightly-stai
ned, pyramidal-shaped neurons was also observed. In most of the amygda
loid nuclei, calbindin-D28k-immunoreactive fibres travelled close to e
ach other and formed bundles, which suggests that some of the immunost
ained neurons were double-bouquet cells. In the paralaminar nucleus, t
he calbindin-D28k-immunoreactive axons formed tortuous plexus (100-200
micrometers in diameter) that surrounded several unstained somata. Th
is study provides baseline information on the morphology and distribut
ion of calcium-binding protein-containing inhibitory cells and fibres
immunoreactive for calbindin-D28k in the human amygdaloid complex. Thi
s information can be used in future studies on the pathogenesis of dis
eases known to damage the amygdala, such as Alzheimer's disease and te
mporal lobe epilepsy.