Disease relevance of Self Administration

• Toxicity associated with long-term intravenous heroin and cocaine self-administration in the rat [1].
• Intracerebral hemorrhage occurred in a 20-year-old man following self-administration of ephedrine [2].
• Self-administration of C1-inhibitor concentrate in patients with hereditary or acquired angioedema caused by C1-inhibitor deficiency [3].
• In this study, lidocaine hydrochloride was given as a therapeutic abortive agent to patients with cluster headache to elucidate cocaine's mechanism of action in relieving symptoms and to search for a safe, nonaddicting agent for self-administration [4].
• In contrast, doses of haloperidol that suppressed cocaine self-administration induced marked sedation and catalepsy [5].

Psychiatry related information on Self Administration

• An initial discussion of CRF neurobiology is followed by consideration of the role of CRF in drug-induced activation of the hypothalamic-pituitary-adrenocortical (HPA) axis, the behavioral effects of drugs (e.g., locomotor activity, anxiogenic-like responses), drug self-administration, drug withdrawal, and relapse to drug-seeking [6].
• Social dominance in monkeys: dopamine D2 receptors and cocaine self-administration [7].
• An ethanol oral self administration paradigm showed the existence of gender differences in alcohol preference in rats: whereas males and females initiated alcohol drinking at similar rates, females maintained their preference for ethanol over a longer duration [8].
• In a structure that has been shown to be necessary for cocaine self-administration, such a firing pattern is a likely neurophysiological component of the mechanism that transduces declining drug levels into increased drug-related appetitive behavior [9].
• Among these variables, unit dose, schedule of cocaine delivery, availability of alternative nondrug reinforcers, food deprivation, and rearing environment have also been shown to alter pharmacological treatment effects on cocaine self-administration [10].

High impact information on Self Administration

• Here we show that extinction training during withdrawal from chronic cocaine self-administration induces experience-dependent increases in the GluR1 and GluR2/3 subunits of AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate) glutamate receptors in the nucleus accumbens shell, a brain region that is critically involved in cocaine reward [11].
• Using patch-clamp recording, we show that mesencephalic dopaminergic neurons from mice without the beta2 subunit no longer respond to nicotine, and that self-administration of nicotine is attenuated in these mutant mice [12].
• Nicotine is the primary component of tobacco that drives use, and like other addictive drugs, nicotine reinforces self-administration and place preference in animal studies [13].
• Intravenous cocaine self-administration in rats was inhibited by passive transfer of an anti-cocaine monoclonal antibody [14].
• Regional brain activation was assessed by mapping of Fos-related protein expression in rats trained to self-administration of intravenous nicotine and cocaine [15].

Chemical compound and disease context of Self Administration

• Glutamatergic neurotransmission plays a critical role in addictive behaviors, and recent evidence indicates that genetic or pharmacological inactivation of the type 5 metabotropic glutamate receptor (mGluR5) reduces the self-administration of cocaine, nicotine, and alcohol [16].
• CLINICAL IMPLICATIONS: Self-administration of C1-inhibitor concentrate could be a valuable and convenient treatment modality to prevent or treat angioedema attacks in patients with C1-inhibitor deficiency [3].
• The reinforcing effects of MDMA are selectively attenuated by chronic MDMA self-administration, although this behavioral change appears to occur in the absence of any frank neurochemical correlates of toxicity [17].
• Additionally, the dose of 0.8 mg/kg of nicotine not only induced persistent changes in alcohol self-administration but also produced conditioned place aversion and depressed locomotor activity [18].
• Locomotion and conditioned place preference produced by acute intravenous amphetamine: role of dopamine receptors and individual differences in amphetamine self-administration [19].

Biological context of Self Administration

• It is shown here that the potencies of cocaine-like drugs in self-administration studies correlate with their potencies in inhibiting [3H]mazindol binding to the dopamine transporters in the rat striatum, but not with their potencies in binding to a large number of other presynaptic and postsynaptic binding sites [20].
• While individual drugs (i.e., heroin, cocaine, methamphetamine, MDMA) have specific, dose-dependent effects on brain and body temperatures, these effects are strongly modulated by an individual's activity state and environmental conditions, and change dramatically during the development of drug self-administration [21].
• Moreover, rats that are trained in this manner and then made dependent by ethanol-vapor inhalation or liquid diet increase their ethanol self-administration during the withdrawal period [22].
• Up-regulation of brain nicotinic acetylcholine receptors in the rat during long-term self-administration of nicotine: disproportionate increase of the alpha6 subunit [23].
• In light of previous findings that melanocortins antagonize opiate self-administration, analgesic tolerance, and physical dependence, we hypothesize that decreased melanocortin function, via down-regulation of MC4-R expression, may contribute to the development of these opiate-induced behaviors [24].

Anatomical context of Self Administration

• Social stress alters the feedback from prefrontal cortex and thereby may contribute to the dysregulation of dopaminergic activity that is necessary for cocaine self-administration [25].
• Intravenous heroin self-administration is not disrupted by kainic acid lesions of the bed nucleus of the lateral hypothalamus [26].
• These results indicate that cocaine self-administration and subsequent withdrawal induces long-lasting and differential neuroadaptations in basolateral and central amygdala glutamate receptors [27].
• Previous studies have shown that cocaine self-administration induces long-lasting neuroadaptations in glutamate neurons of the ventral tegmental area and nucleus accumbens [27].
• Effects of SCH-23390 infused into the amygdala or adjacent cortex and basal ganglia on cocaine seeking and self-administration in rats [28].

Associations of Self Administration with chemical compounds

• Modulation of cocaine self-administration in the rat through D-3 dopamine receptors [29].
• Self-administration could be attenuated by including equimolar concentrations of the dopaminergic D2-receptor antagonist sulpiride in the microinjection system [30].
• Intravenous self-administration of nomifensine in rats: implications for abuse potential in humans [31].
• The D-3-selective compounds 7-hydroxy-N,N-di-n-propyl-2-aminotetralin (7-OHDPAT) and quinpirole potently decreased cocaine self-administration in the rat at doses that were not by themselves reinforcing [29].
• In addition, these mutant mice showed markedly reduced ethanol self-administration [32].

Gene context of Self Administration

• Further analysis of Homer2 KO mice revealed extensive additional behavioral and neurochemical similarities to cocaine-sensitized animals, including accelerated acquisition of cocaine self-administration and altered regulation of glutamate by metabotropic glutamate receptors and cystine/glutamate exchange [33].
• Because of their opposing actions, it has been suggested that NPY and corticotropin releasing factor (CRF) exert a reciprocal regulation on drug self-administration [34].
• Recent pharmacological and mutant mouse data indicate that NPY activity at its receptors can influence ethanol self-administration, although the direction and strength of this influence are not clear [35].
• CRH receptor antagonists reduce cocaine self-administration and attenuate the reinstatement of extinguished cocaine-seeking behavior, but little is known about the mechanisms involved [36].
• Finally, Dr. Janak presented evidence that increases in the expression of GDNF in the midbrain reduce alcohol self-administration in rats [37].

Analytical, diagnostic and therapeutic context of Self Administration

• The effects of cocaine repeated within a self-administration session and across multiple sessions over a 6 month period were determined by the use of fixed-ratio self-administration and microdialysis procedures [38].
• Neural correlates of high and craving during cocaine self-administration using BOLD fMRI [39].
• It is concluded that the intranasal administration of fenoterol can be considered an alternative way of self-administration by the severely ill asthmatic subject who is unable to inhale the bronchodilator or can be used by the emergency staff on the first contact with the severely ill asthmatic patient in the hospital [40].
• In the current study, the effects of this drug were further examined using an animal model of oral ethanol self-administration in a limited access paradigm [41].
• In tests of cocaine self-administration, rats were trained to lever press for intravenous infusions of 0.25 mg cocaine delivered on either a fixed ratio 5 (FR5) or a progressive ratio schedule [42].

References