The isomers of cocaine and tropacocaine: Effect on 3H-catecholamine uptake by rat brain synaptosomes

Komiskey, H.L.; Miller, Duane D.; LaPidus, Jules B.; Patil, Popat N.

doi:10.1016/0024-3205(77)90110-2

Cited by 46 publications

(14 citation statements)

References 8 publications

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“…This effect also is consistent with a role of NAc dopamine and dopamine D2 receptors in cocaine IVSA (Roberts and Vickers 1984;Woolverton 1986;Robledo et al 1992;Wise et al 1995) and local electrophysiological effects of cocaine (White et al 1993;Uzwiak et al 1997). Although it is known that cocaine decreases dopamine (Komiskey et al 1977;, noradrenaline (Dubocovich et al 1979;Hadfield and Nugent 1980), and serotonin uptake (Taylor and Ho 1978), and increases acetylcholine release (Day et al 1997), our results point to a role for a dopa-minergic D2 mechanism in the rewarding effects of cocaine administered into the NAc. Because replacement of sulpiride by NaCl led to the immediate recovery of intra-NAc cocaine self-administration, it is unlikely that chance level responding would have occurred independently of the D2 antagonist treatment.…”

Section: Anatomical and Pharmacological Specificity Of Intra-nac Cocasupporting

confidence: 73%

Anxiogenic-Like Effects Limit Rewarding Effects of Cocaine in BALB/cByJ Mice

David

Gold

Koob

et al. 2001

Neuropsychopharmacology

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Previous studies have reported intravenous cocaine selfadministration behavior in several strains of mice with the exception of BALB/cByJ, a strain considered a mouse model of high emotional reactivity. The present experiments further investigated acquisition of self-administration in BALB/cByJ mice using a low dose and a habituation session. Following evidence of an initial drug-seeking behavior, we observed a progressive decline of intravenous self-administration. Pretreatment with diazepam (0.5 mg/ kg, IP), reinstated cocaine-maintained responding. To test the hypothesis that injections directly into a rewardrelevant brain region might support consistent cocaineseeking behavior, BALB/cByJ mice implanted in the nucleus accumbens (NAc) or the caudate-putamen nucleus (CPu) were trained to discriminate between the arm enabling a microinjection of cocaine (30 pmol/50 nl or 150 pmol/50 nl) The reinforcing effect of cocaine has long been demonstrated in several species including humans, (Pickens and Thompson 1968;Woods and Schuster 1968;Deneau et al. 1969;Goldberg 1973;Fischman and Schuster 1982). However, in studies using monkeys as well as rats, not all individual subjects exhibit acquisition of self-administration, and data from subjects that fail to acquire selfadministration are usually excluded (Davis and Smith 1987). Consistent with these observations, many humans experiencing psychostimulant drugs do not develop compulsive drug-seeking behavior (Siegel 1984;O'Brien et al. 1986). Recently, an increasing number of studies have investigated the biological basis of the vulnerability to drug abuse in outbred rats. From this work, it is possible to define a vulnerability profile based on a number of behavioral, neurochemical, and endocrinological features (Hooks et al. 1991;Piazza and Le Moal 1996). Importantly, traits associated with a vulnerable phenotype in rats, such as novelty-induced activity, can be compared to psychological dimensions measured in humans, such as novelty-seeking behavior (see Bardo et al. 1996). It is of special interest to note here that novelty- Cocaine Self-Administration in BALB/cByJ Mice 301 seeking and drug-seeking behaviors co-vary in humans as well as laboratory animals (Bardo et al. 1996). These behaviors are also expressed differentially in inbred strains of mice making these mice a potentially important model for further examining the relationship between behavioral traits, their underlying biological basis, and drug-seeking behavior (Crabbe et al. 1994).Of particular interest in this context is the difficulty of demonstrating intravenous cocaine self-administration in BALB/cByJ mice (Deroche et al. 1997;Roberts et al. 1997;Yu et al. 1997), using doses known to maintain self-administration in C57BL/6 or several other strains (Carney et al. 1991;Grahame et al. 1995;Deroche et al. 1997;Rocha et al. 1998). This observation cannot be accounted for by pharmacokinetic differences (Ruth et al. 1988), capacity to learn operant tasks (Cazala 1976;Deroche et al. 1997;Heyser et al. 199...

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Section: Anatomical and Pharmacological Specificity Of Intra-nac Cocasupporting

confidence: 73%

Anxiogenic-Like Effects Limit Rewarding Effects of Cocaine in BALB/cByJ Mice

David

Gold

Koob

et al. 2001

Neuropsychopharmacology

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“…Both D1 and D2 dopamine receptors have been implicated in the ability of prefrontal dopamine to trigger relapse, though the evidence is somewhat stronger for D1 receptors (Ciccocioppo et al 2001;Capriles et al 2003;Sanchez et al 2003;Sun and Rebec 2005). Indeed, administering cocaine directly into the PL-mPFC triggers cocaine relapse (Park et al 2002), presumably due to local inhibition of the dopamine transporter (Komiskey et al 1977).…”

Section: Prefrontal Control Of Extinction Of Conditioned Drug Seekingmentioning

confidence: 99%

Extinction circuits for fear and addiction overlap in prefrontal cortex

Peters

Kalivas²,

Quirk³

2009

Learn. Mem.

661

642

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Extinction is a form of inhibitory learning that suppresses a previously conditioned response. Both fear and drug seeking are conditioned responses that can lead to maladaptive behavior when expressed inappropriately, manifesting as anxiety disorders and addiction, respectively. Recent evidence indicates that the medial prefrontal cortex (mPFC) is critical for the extinction of both fear and drug-seeking behaviors. Moreover, a dorsal-ventral distinction is apparent within the mPFC, such that the prelimbic (PL-mPFC) cortex drives the expression of fear and drug seeking, whereas the infralimbic (IL-mPFC) cortex suppresses these behaviors after extinction. For conditioned fear, the dorsal-ventral dichotomy is accomplished via divergent projections to different subregions of the amygdala, whereas for drug seeking, it is accomplished via divergent projections to the subregions of the nucleus accumbens. Given that the mPFC represents a common node in the extinction circuit for these behaviors, treatments that target this region may help alleviate symptoms of both anxiety and addictive disorders by enhancing extinction memory.

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“…It is approximately 20 times less toxic than cocaine (Woker, 1953a). In rats, benzoylecgonine failed to inhibit the accumulation of [3H]norepinephrine and ['Hldopamine by synaptosomes from the cortex and striatum, respectively (Komiskey et al, 1977). At a concentration of 10V3 M, benzoyleegonine produced approximately 40% inhibition of verat~dine-st~ulat~ 22Na+ uptake in an assay with rat brain membrane homogenate (Matthews and Collins, 1983).…”

Section: Benzoylecgoninementioning

confidence: 95%

“…Benzoyltropine shows both potency and selectivity as an antagonist of 5-hydroxytryptamine on the rabbit heart (Fozard et al, 1979). In rats, benzoyltropine inhibits the [3H]norepinephrine and C3H]-dopamine uptake in the cortex and striatum, respectively (Komiskey et al, 1977).…”

Section: Benzoyltropinementioning

confidence: 99%

“…It shows much less cholinolytic action than benzoyltropine, especially on the postganglionic receptors of the eye (Nador and Scheiber, 1972). In rats, tropacocaine inhibits the [ 3H]norepinephrine and [ 3H]dopamine uptake in the cortex and striatum, respectively (Komiskey et al, 1977). It shows both potency and selectivity as an antagonist of 5hydroxytryptamine on the rabbit heart (Fozard et al, 1979).…”

Section: Tropacocainementioning

confidence: 99%

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