Effect of nitric oxide synthase inhibitor and NMDA receptor antagonist on the development of nicotine sensitization of nucleus accumbens dopamine release: An in vivo microdialysis study

Hong, Soo Kyung; Jung, In Soon; Bang, Seong Ae; Kim, Sang Eun

doi:10.1016/j.neulet.2006.09.052

Cited by 18 publications

(9 citation statements)

References 25 publications

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“…It has been shown that 7‐NI blocks nicotine‐induced conditioned place preference [48], NOS inhibitors attenuate symptoms of nicotine abstinence syndrome and withdrawal [49–51]. NG‐nitro‐L‐arginine (L‐NNA) and l ‐NAME prevents behavioral [52], locomotor [53] and DA overflow induced by nicotine‐sensitization [54]. In line with this, NOS inhibitors have been shown to be able to attenuate the development and expression of the abstinence syndrome for such psychostimulant [25].…”

Section: Discussionmentioning

confidence: 99%

Critical role of Nitric Oxide on Nicotine‐Induced Hyperactivation of Dopaminergic Nigrostriatal System: Electrophysiological and Neurochemical evidence in Rats

Matteo¹,

Pierucci²,

Benigno

et al. 2010

CNS Neuroscience & Therapeutics

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Nicotine, the main psychoactive ingredient in tobacco, stimulates dopamine (DA) function, increasing DA neuronal activity and DA release. DA is involved in both motor control and in the rewarding and reinforcing effects of nicotine; however, the complete understanding of its molecular mechanisms is yet to be attained. Substantial evidence indicates that the reinforcing properties of drugs of abuse, including nicotine, can be affected by the nitric oxide (NO) system, which may act by modulating central dopaminergic function. In this study, using single cell recordings in vivo coupled with microiontophoresis and microdialysis in freely moving animals, the role of NO signaling on the hyperactivation elicited by nicotine of the nigrostriatal system was investigated in rats. Nicotine induced a dose-dependent increase of the firing activity of the substantia nigra pars compacta (SNc) DA neurons and DA and 3,4-dihydroxyphenylacetic acid (DOPAC) release in the striatum. Pharmacological manipulation of the NO system did not produce any change under basal condition in terms of neuronal discharge and DA release. In contrast, pretreatments with two NO synthase (NOS) inhibitors, N-ω-nitro-L-arginine methyl ester (L-NAME) and 7-nitroindazole (7-NI) were both capable of blocking the nicotine-induced increase of SNc DA neuron activity and DA striatal levels. The effects of nicotine in L-NAME and 7-NI-pretreated rats were partially restored when rats were pretreated with the NO donor molsidomine. These results further support the evidence of an important role played by NO on modulation of dopaminergic function and drug addiction, thus revealing new pharmacological possibilities in the treatment of nicotine dependence and other DA dysfunctions.

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Section: Discussionmentioning

confidence: 99%

Critical role of Nitric Oxide on Nicotine‐Induced Hyperactivation of Dopaminergic Nigrostriatal System: Electrophysiological and Neurochemical evidence in Rats

Matteo¹,

Pierucci²,

Benigno

et al. 2010

CNS Neuroscience & Therapeutics

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“…These authors hypothesised that the development of opioid addiction could be associated with neuronal inflammation and degeneration and thus the attenuation of morphine-induced addiction behaviour by memantine may be due to its antiinflammatory and neurotrophic effects rather than through NMDA receptor blockade. Despite these findings, results supporting the role of NMDA receptor in processes associated with drug addiction are reported much more frequently (Wolf et al 1995;Shim et al 2002;Hong et al 2006;Yang et al 2008). Popik et al (2003) in their study tried to compare the effects of memantine in mice on expression of place preferences that were conditioned with morphine administration (10 mg/kg) and furthermore with sexual encounters with females and consumption of regular laboratory food.…”

Section: Discussionmentioning

confidence: 99%

The effect of memantine on behavioural sensitisation to methamphetamine in mice

Landa¹,

Šlais²,

Šulcová³

2012

Vet. Med. - Czech

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After repeated administration the psychostimulant methamphetamine (Met) produces a substantial increase in behavioural responses, which is termed behavioural sensitisation. Many studies have reported that N-methyl-d-aspartate (NMDA) receptors play an important role in the development and expression of behavioural sensitisation. Memantine (Mem) is used particularly for the treatment of Alzheimer's disease and acts as a non-competitive NMDA glutamate receptor antagonist, possessing a variety of psychotropic effects. For example, there are studies indicating that memantine prevents the expression of withdrawal symptoms in mice and causes reversal of opioid dependence. Although not all pharmacological mechanisms of memantine have been clarified yet, it is known that memantine inhibits NMDA receptor inward currents. Thus, the present study was designed to assess whether memantine would influence behavioural sensitisation to the stimulatory effects of methamphetamine on mouse locomotion. Mice were randomly allocated into four groups. They were given vehicle on Day 1of the experiment and after five days without application they were administered seven drug daily doses (i.p.) from Day 7 to Day 13 of the study, as follows: (a) n 1, 2 : 2.5 mg/kg/day of Met; (b) n 3 : combination Met + Mem at the doses of 2.5 mg/kg/day and 5 mg/kg/day, respectively; (c) n 4 : Mem at the dose of 5 mg/kg/day. On Day 14 mice were given the first "challenge treatment" (a) n 1 : Met, (b) n 2 : Met + Mem, (c) n 3 : Met, (d) n 4 : Mem. The second "challenge treatment" was given after a six day wash-out period on Day 21: (a) n 1 : Met, (b) n 2 : Met + Mem, (c) n 3 : Met, (d) n 4 : Mem. Changes in locomotion were measured for a period of 3 min in the Open field on Days 1, 7, 14 and 21 to assess the sensitising phenomenon. Met pre-treatment significantly sensitised to the effects of the challenge doses (n 1 ). Mem given alone did not change the measured behavioural parameters after the acute dose but it significantly decreased locomotion after its repeated administration (n 4 ). Repeated pre-treatment with the Met + Mem combination (n 3 ) did not produce sensitisation after Met challenge doses and similarly, repeated pretreatment with Met did not induce sensitisation after the challenge dose of Met + Mem (n 2 ). Thus, our results suggest that the role of the NMDA receptor antagonist memantine in the development and expression of behavioural sensitisation to Met seems to be an inhibitory one.

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“…Nitric oxide (NO), produced in the nucleus accumbens by a group of GABAergic NO synthase-containing interneurons (1% of the neuron population) [12,20], modulates the excitability of projection neurons in this nucleus [11] and is involved in regulating several of the functions of this structure: sensitization to psychostimulators [8,13], acquisition and execution of conditioned-reflex place preference [27], the execution of conditioned-reflex fear [29] and exploratory behavior [3,5], and the occurrence of phobic responses to novel foods [2]. In particular, our data indicate that the execution of types of behavior such as exploratory activity [3] and conditioned-reflex fear reactions [6,7] Saul'skaya and Terekhova 202 Fig.…”

Section: Discussionmentioning

confidence: 99%

GABA-Nitrergic Interactions in the Nucleus Accumbens during Inhibition of Exploratory Behavior by Danger Signals

Saul’skaya

Terekhova

2015

Neurosci Behav Physi

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The ability to rearrange behavior in response to the appearance of danger signals is a necessary condition for an individual's survival. However, the structural and neurochemical mechanisms underlying acute shifts in behavioral programs in response to the appearance of stimuli with high motivational significance have received insufficient study. The brain structures involved in these processes may include the medial sector of the nucleus accumbens (mNA), in the ventral striatal area, which plays an important role in motivation and reinforcement processes [9,17,20]. It has been suggested that the organization of the neural networks of all parts of the striatum, including the mNA, is based on mechanisms supporting the selection and switching of behavioral programs [10,18,21,23], these being based largely on lateral inhibition via the axon collaterals of the GABAergic projection neurons of this structure (95% of the population) [23]. In the mNA, glutamatergic afferent inputs from the hippocampal formation, amygdala, and prefrontal cortex converge on these neurons in a variety of combinations, carrying information on the novelty, the motivational and emotional significance of incoming signals, and the spatial context, as well as possible variants of behavioral responses (see [14,20]). These same neurons connect the mNA with brain areas involved in mediating the basal forms of feeding and the defensive exploratory behavior activated on receipt of reinforcement [14,15]. It has been suggested that as a result of lateral inhibition, the strongest input signal, reflecting the dominant motivation, and its associated behavioral program are not only sent for execution, but also inhibit the conduction of weaker (i.e., less significant) signals transmitted via parallel channels [23]. This suggestion is supported by the previously demonstrated involvement of the mNA in the inhibition of feeding behavior by danger signals [4,26,30] and our recent studies have shown that competition between the defensive and exploratory behavioral strategies occurs with the involvement of the nitrergic system of the mNA [3]. In particular, we showed that presentation during exploratory behavior of danger signals decreasing exploration activity inhibited the exploratory behavior-induced increase in the extracellular citrulline (a coproduct of NO synthesis) level in the mNA [3].Vital intracerebral microdialysis experiments in Sprague-Dawley rats with high-performance liquid chromatography (HPLC) showed that presentation during exploratory behavior of a tone previously combined with pain stimulation decreased exploratory activity and inhibited the exploratory behavior-induced increase in the extracellular citrulline (a co-product of NO synthesis) level in the medial sector of the nucleus accumbens. Administration of the GABA A receptor antagonist bicuculline (20 μM) into the medial sector of the nucleus accumbens firstly produced partial recovery of the increase in the extracellular citrulline level in this structure induced by exploratory behavior ...

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Effect of nitric oxide synthase inhibitor and NMDA receptor antagonist on the development of nicotine sensitization of nucleus accumbens dopamine release: An in vivo microdialysis study

Cited by 18 publications

References 25 publications

Critical role of Nitric Oxide on Nicotine‐Induced Hyperactivation of Dopaminergic Nigrostriatal System: Electrophysiological and Neurochemical evidence in Rats

Critical role of Nitric Oxide on Nicotine‐Induced Hyperactivation of Dopaminergic Nigrostriatal System: Electrophysiological and Neurochemical evidence in Rats

The effect of memantine on behavioural sensitisation to methamphetamine in mice

GABA-Nitrergic Interactions in the Nucleus Accumbens during Inhibition of Exploratory Behavior by Danger Signals

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