ArticleExpression of fos protein in various rat brain areas following acute nicotine and diazepam
References (37)
- et al.
Expression of c-fos in regions of the basal limbic forebrain following intracerebroventricular corticotropin-releasing factor in unstressed or stressed male rats
Neuroscience
(1992) - et al.
Peptide injections into the amygdala of conscious rats: Effects on blood pressure, heart rate and plasma catecholamines
Regul. Pept.
(1988) - et al.
Induction of the c-fos proto-oncogene in rat amygdala during unconditioned and conditioned fear
Brain Res.
(1991) - et al.
Fos and Jun: The AP-1 connection
Cell
(1988) - et al.
The use of c-fos as a metabolic marker in neuronal pathway tracing
J. Neurosci. Methods
(1989) - et al.
Autoradiographic localization of [3H]-nicotine binding sites in the rat brain
Neurosci. Lett.
(1985) - et al.
Acute nicotine injections induce c-fos mostly in nondopaminergic neurons of the midrain of the rat
Mol. Brain. Res.
(1993) - et al.
Induction of c-fos immunostaining in the rat brain after the systemic administration of nicotine
Brain Res. Bull.
(1992) - et al.
l-DOPA activates c-fos in the striatum ipsilateral to a 6-hydroxydopamine lesion of the substantia nigra
Eur. J. Pharmacol.
(1989) - et al.
Organization of central cholinergic system
Induction and desensitization of the c-fos mRNA response to nicotine in rat brain
Mol. Cell. Neurosci.
Cholinergic systems in the rat brain: 2. Projections to the interpeduncular nucleus
Brain Res. Bull.
Cholinergic innervation of vasopressin-containing neurons in the supraoptic nucleus of the rat
Intravenous injections of nicotine induce very rapid and discrete reductions of hypothalamic catecholamine levels associated with increases of ACTH, vasopressin and prolactin secretion
Acta Physiol. Scand.
Conditioned fear-induced changes in behavior and in the expression of the immediate early gene c-fos: With and without diazepam pretreatment
J. Neurosci.
Expression of c-fos-like protein as a marker for neuronal activity following noxious stimulation in the rat
J. Comp. Neurol.
Expression of c-fos immunoreactivity in transmitter-characterized neurons after stress
Nicotinic binding in brain—Autoradiographic comparison of [3H]-acetylcholine, [3H]-nicotine and [125I]-a-bungarotoxin
J. Neurosci.
Cited by (59)
Effects of chronic nicotine exposure on Δ<sup>9</sup>-tetrahydrocannabinol-induced locomotor activity and neural activation in male and female adolescent and adult rats
2020, Pharmacology Biochemistry and BehaviorCitation Excerpt :CB1 receptors are widely distributed throughout the brain and thus brain regions of interest in the present study included those which have been found to exhibit increased expression of c-fos in response to acute THC administration, specifically the NAc, dorsal striatum, lateral septum (LS), bed nucleus of the stria terminalis (BNST), hypothalamus, and thalamus (Miyamoto et al., 1996; Erdtmann-Vourliotis et al., 1999; Allen et al., 2003). Acute nicotine administration has been shown to rapidly and transiently induce c-fos expression in limbic and cortical brain regions (Kiba and Jayaraman, 1994; Salminen et al., 1996, 1999; Seppä et al., 2001; Shram et al., 2007), but this effect is attenuated following continuous administration (Salminen et al., 1999). Thus, it was predicted that prior chronic nicotine exposure would increase expression of c-fos in brain regions also associated with cannabinoid signalling and thus potentiate or attenuate acute THC-induced changes in locomotor activity, effects that would be potentially mediated by age and sex in Sprague-Dawley rats.
Involvement of GABA<inf>B</inf> receptors in biochemical alterations induced by anxiety-related responses to nicotine in mice: Genetic and pharmacological approaches
2014, NeuropharmacologyCitation Excerpt :It is known that addictive related behaviors are associated to different molecular adaptations, such as gene regulation, which are observed in specific brain areas (Berke and Hyman, 2000; Nestler, 2001). In line with this, several authors have shown that acute nicotine (Salminen et al., 1996), chronic nicotine (Soderstrom et al., 2007), nicotine self-administration (Pagliusi et al., 1996) and nicotine rewarding effects (Mombereau et al., 2007) induced an increase in Fos-like immunoreactivity in diverse brain regions. As it was expected, in the pharmacological approach of the present study, we found that the anxiolytic dose of nicotine (0.05 mg/kg) increased c-Fos expression in the DRN, but not in the LSN.