Differential effects of response-contingent and response-independent nicotine in rats

Donny, Eric C.; Caggiula, Anthony R.; Rose, Christine; Jacobs, Kimberly S; Mielke, Michelle M.; Sved, Alan F.

doi:10.1016/s0014-2999(00)00532-x

Cited by 56 publications

(55 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Hence, given their current position that the VS is a primary reinforcement, the statement that nicotine self-administration in the above study was dependent on it being response-contingent "in the absence of other reinforcing stimuli" is inexplicable. Just as puzzling is the authors' claim, based on the same study, that nicotine at a dose of 0.03 mg/kg only increases self-administration when contingent on lever press, which is a finding the authors themselves failed to replicate, both in the present study and in a previous one (Donny et al 2000; see discussion in Dar and Frenk 2002).…”

contrasting

confidence: 64%

Reward potentiation or behavioral activation? A comment on Donny et al.

Frenk

Dar

2004

Psychopharmacology

View full text Add to dashboard Cite

contrasting

confidence: 64%

Reward potentiation or behavioral activation? A comment on Donny et al.

Frenk

Dar

2004

Psychopharmacology

View full text Add to dashboard Cite

“…The volitional nature of nicotine exposure may also influence the neurochemical stimuli that provoke AEA production. For example, nicotine SA and YA produce distinct alterations in nAChR expression, DA D 2 receptor binding, and corticosterone levels (Caille et al, 2009;Donny et al, 2000;Metaxas et al, 2010), and each of these systems can influence the production of AEA and related ethanolamides (Centonze et al, 2004;Di et al, 2003Di et al, , 2005Giuffrida et al, 1999;Hill et al, 2010a, b;Stella and Piomelli, 2001). …”

Section: Endocannabinoid Levels Following Nicotine Exposure Mw Buczynmentioning

confidence: 99%

“…For example, the response contingency of drug exposure robustly influences gene expression (Jacobs et al, 2002(Jacobs et al, , 2003(Jacobs et al, , 2005, neural activation (Chang et al, 1994;Peoples and West, 1996;Stuber et al, 2005), and resultant extracellular neurochemistry (Di Ciano et al, 1996;Hemby et al, 1997;Jacobs et al, 2003;Lecca et al, 2007;Orejarena et al, 2009;You et al, 2007). With specific regard to nicotine, differential effects of volitional SA vs forced drug administration have been observed on a 4 b 2 nAChR expression (Metaxas et al, 2010), cortical glutamatergic projection activity and plasticity mechanisms in the ventral tegmental area (VTA) (McFarland et al, 2003;You et al, 2007), and plasma corticosterone levels (Donny et al, 2000). Because nAChR, glutamate (GLU), and glucocorticoid signaling robustly influence eCB production (Di et al, 2003(Di et al, , 2005Hill et al, 2010a, c), self-administered nicotine may produce distinct effects from forced nicotine exposure on brain eCB signaling.…”

Section: Introductionmentioning

confidence: 99%

The Volitional Nature of Nicotine Exposure Alters Anandamide and Oleoylethanolamide Levels in the Ventral Tegmental Area

Buczynski

Polis

Parsons

2012

Neuropsychopharmacol

View full text Add to dashboard Cite

Cannabinoid-1 receptors (CB 1 ) have an important role in nicotine reward and their function is disrupted by chronic nicotine exposure, suggesting nicotine-induced alterations in endocannabinoid (eCB) signaling. However, the effects of nicotine on brain eCB levels have not been rigorously evaluated. Volitional intake of nicotine produces physiological and behavioral effects distinct from forced drug administration, although the mechanisms underlying these effects are not known. This study compared the effects of volitional nicotine self-administration (SA) and forced nicotine exposure (yoked administration (YA)) on levels of eCBs and related neuroactive lipids in the ventral tegmental area (VTA) and other brain regions. Brain lipid levels were indexed both by in vivo microdialysis in the VTA and lipid extractions from brain tissues. Nicotine SA, but not YA, reduced baseline VTA dialysate oleoylethanolamide (OEA) levels relative to nicotine-naïve controls, and increased anandamide (AEA) release during nicotine intake. In contrast, all nicotine exposure paradigms increased VTA dialysate 2-arachidonoyl glycerol (2-AG) levels. Thus, nicotine differentially modulates brain lipid (2-AG, AEA, and OEA) signaling, and these modulations are influenced by the volitional nature of the drug exposure. Corresponding bulk tissue analysis failed to identify these lipid changes. Nicotine exposure had no effect on fatty acid amide hydrolase activity in the VTA, suggesting that changes in AEA and OEA signaling result from alterations in their nicotine-induced biosynthesis. Both CB 1 (by AEA and 2-AG) and non-CB 1 (by OEA) targets can alter the excitability and activity of the dopaminergic neurons in the VTA. Collectively, these findings implicate disrupted lipid signaling in the motivational effects of nicotine.

show abstract

“…These effects depend on the dose, duration, and route of nicotine administration, and on the modality of the stressor. The mode of nicotine delivery (eg forced vs self-administered) is another determinant of its endocrine and neurotransmitter effects (Donny et al, 2000). All these interactions are further complicated by rapid desensitization to the stimulatory effects of nicotine on stress hormone secretion (Sharp and Beyer, 1986).…”

Section: Introductionmentioning

confidence: 99%

Chronic Nicotine Self-Administration Augments Hypothalamic–Pituitary–Adrenal Responses to Mild Acute Stress

Chen

Sharp

2007

Neuropsychopharmacol

View full text Add to dashboard Cite

We investigated the effect of chronic nicotine self-administration (SA) on hypothalamic-pituitary-adrenal (HPA) hormonal responses to acute stressors. Adult male Sprague-Dawley rats were given access to nicotine (0.03 mg/kg) for 23 h per day for 20 days. On day 1 of acquisition of nicotine SA, plasma levels of both adrenocorticotropin and corticosterone were significantly increased 15-30 min after the first dose of nicotine. These hormonal changes were no longer significant on day 3, when adrenocorticotropin levels were o60 pg/ml and corticosterone levels were o110 ng/ml during the hour after the first dose of nicotine. Chronic nicotine SA (20 days) significantly augmented (2-3-fold) both hormonal responses to mild foot shock stress (0.6 mA, 0.5 s per shock, 5 shocks per 5 min), but did not affect hormonal responses to moderate shock (1.2 mA, 0.5 s per shock, 5 shocks per 5 min), lipopolysaccharide or immobilization. Similar data were obtained in Lewis rats. These results provide further support for the concept that chronic nicotine SA is a stressor. In alignment with the effects of other stressors, nicotine activated the HPA axis on the first day of SA, but desensitization occurred with repeated exposure. Furthermore, chronic nicotine SA selectively cross-sensitized the HPA response to a novel stressor. These observations suggest that nicotine may selectively increase the HPA response to stressors in human smokers.

show abstract

Differential effects of response-contingent and response-independent nicotine in rats

Cited by 56 publications

References 43 publications

Reward potentiation or behavioral activation? A comment on Donny et al.

Reward potentiation or behavioral activation? A comment on Donny et al.

The Volitional Nature of Nicotine Exposure Alters Anandamide and Oleoylethanolamide Levels in the Ventral Tegmental Area

Chronic Nicotine Self-Administration Augments Hypothalamic–Pituitary–Adrenal Responses to Mild Acute Stress

Contact Info

Product

Resources

About