Chronic nicotine exposure during adolescence differentially influences calcium‐binding proteins in rat anterior cingulate cortex

Abstract

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 alpha4 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.

Cigarette smoking and white matter microstructure

“…A possible mechanism by which smoking could raise FA draws from the following observations: 1) white matter matures through late adolescence faster than in adulthood (Benes 1989; Bartzokis and Lu 2009;); 2) nicotine acting at nAChRs can promote glial activity or proliferation (Garrido et al 2003; Liu et al 2005; Opanashuk et al 2001); and 3) nAChRs exist in subcortical white matter (Ding et al 2004). Oligodendrocyte precursor cells but not the oligodendrocytes and astrocytes into which these precursors differentiate do express nAChRs (Rogers et al 2001; reviewed Bartzokis 2007).…”

Guidelines on nicotine dose selection for in vivo research

“…When nicotine at 200 μg ml −1 (65 μg ml −1 ) is included in the sole source of drinking water supplemented with 2% saccharin for 3 weeks, calcium-binding proteins in GABA neurons of the adolescent accumbens are upregulated (Liu et al 2005). In a twobottle free-choice method, rats will voluntarily consume nicotine at 0.003-0.006% concentrations in water, with gender-independent intake higher in younger than in older rats (Maehler et al 2000).…”

Chronic cigarette smoking and the microstructural integrity of white matter in healthy adults: A diffusion tensor imaging study

“…These effects were attenuated by administration of dihydro-beta-erythroidine, a nicotinic acetylcholine receptor antagonist. In addition, preliminary evidence in humans indicates that chronic smoking (in vivo) and nicotine exposure on cells obtained from humans (in vitro) promotes expression of genes involved in neurogenesis, stimulates nerve growth factor, and upregulates calcium-binding proteins (Garrido, King-Pospisil, Son, Hennig, & Toborek, 2003;Liu, Mohila, Gong, Govindarajan, & Onn, 2005). Similarly, P. G. Shields and colleagues (personal communication) observed significantly greater expression of two genes involved in neurogenesis and neurodevelopment, including sex-determining region Y (SRYbox 14), and glutamate receptor ionotropic, kainate in high compared to low smokers.…”