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Chronic nicotine exposure during adolescence differentially influences calcium‐binding proteins in rat anterior cingulate cortex
Author(s) -
Liu JenJane,
Mohila Carrie A.,
Gong Yuna,
Govindarajan Nalini,
Onn ShaoPii
Publication year - 2005
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2005.04423.x
Subject(s) - parvalbumin , calretinin , medicine , endocrinology , chemistry , calbindin , calcium binding protein , neuron , gabaergic , nicotine , neuroscience , calcium , receptor , psychology , biology , immunohistochemistry
We have recently shown that chronic amphetamine exposure selectively up‐regulates parvalbumin (PV) calcium‐binding proteins in the anterior cingulate cortex (ACC). In this study, we evaluated the effects of chronic nicotine (NIC) exposure on PV, calbindin D28k (CB) and calretinin (CR) calcium‐binding protein immunostaining in ACC GABAergic interneurons. Chronic NIC exposure for 3 weeks in adolescent rats, either via drinking water (the oral group) or by twice daily subcutaneous injections (the injection group), resulted in the expression of high levels of CR proteins in the ACC but not in the parietal cortex. Larger increases in the density of CR‐immunoreactive (ir) neurons were noted in the NIC‐injected rats at 0‐day withdrawal (45% increase) compared with the oral group (26% increase). The larger increases in CR‐ir neuron density in the NIC‐injected rats were also reflected by prominent CR‐ir processes across cortical layers. The density of PV‐ir neurons was also increased (37%) at 0‐day withdrawal but only in the oral NIC group and no changes in CB‐ir neuron density were observed in either NIC group. Combined dual‐immunofluorescence and confocal microscopy revealed that somatodendritic α4 nicotinic acetylcholine receptors colocalized with cortical neurons stained positively for CR, PV or CB. These results suggest that CR‐ and/or PV‐ir‐containing GABA interneurons may be involved in channeling the effects of NIC in the ACC, which is closely associated with the ventral basal ganglia circuit that is linked to brain reward function.