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The behavior of addiction and pattern of firing of the VTA DA neurons are thought to control by glutamatergic synaptic input from prefrontal cortex (PFC). Disturbed functional input from PFC to VTA was shown as decrease the effects of the drug on the addiction process. All abusive drugs, including nicotine, activate mesocorticolimbic system that plays critic roles in nicotine reward and reinforcement development plus engendering glutamatergic synaptic plasticity on the DA secretion neurons in VTA. Nicotine treatment could enhance AMPA/NMDA ratio in VTA DA neurons, which is thought as a common addiction mechanism. In this paper, we investigated whether or not the lack of glutamate transmission from PFC to VTA could make any change in the effects of nicotine.

All drugs of abuse, including nicotine, activate the mesocorticolimbic system, which plays critical roles in nicotine reward and reinforcement development and triggers glutamatergic synaptic plasticity in the dopamine (DA)-secreting neurons in the ventral tegmental area (VTA). The Addictive behavior of addiction and the firing pattern of firing of the VTA DA-secreting neurons in the VTA are thought to be control controlled by glutamatergic synaptic input from the prefrontal cortex  (PFC). Disturbed Interruption of functional input from the PFC to the VTA was has been shown as to decrease the addictive effects of the drugs on the addiction process. All abusive drugs, including nicotine, activate mesocorticolimbic system that plays critic roles in nicotine reward and reinforcement development plus engendering glutamatergic synaptic plasticity on the DA secretion neurons in VTA. The mechanism underlying Nnicotine addiction treatment is thought to involve could enhance an increase in the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/N-methyl-d-aspartate (NMDA) ratio in VTA DA-secreting neurons in the VTA, which is thought as a common addiction mechanism. Therefore, Iin this paperstudy , we investigated whether or not the lack of glutamate transmission from the PFC to the VTA could make any change in can modulate the effects of nicotine.

The behavior of addiction and pattern of firing of the VTA DA neurons are thought to control by glutamatergic synaptic input from prefrontal cortex (PFC). Disturbed functional input from PFC to VTA was shown as decrease the effects of the drug on the addiction process. All abusive drugs, including nicotine, activate mesocorticolimbic system that plays critic roles in nicotine reward and reinforcement development plus engendering glutamatergic synaptic plasticity on the DA secretion neurons in VTA. Nicotine treatment could enhance AMPA/NMDA ratio in VTA DA neurons, which is thought as a common addiction mechanism. In this paper, we investigated whether or not the lack of glutamate transmission from PFC to VTA could make any change in the effects of nicotine.

The Addictive behavior of addiction and the firing pattern of firing of the VTA dopamine (DA)-secreting neurons in the ventral tegmental area (VTA) are thought to be control controlled by glutamatergic synaptic input from the prefrontal cortex (PFC). Disturbed Interruption of functional input from the PFC to the VTA was has been shown as to decrease the addictive effects of the drugs on the addiction process. All abusive drugs of abuse, including nicotine, activate the mesocorticolimbic system, that which plays critic critical roles in nicotine reward and reinforcement development plus and engendering triggers glutamatergic synaptic plasticity on in the DA- secretionsecreting neurons in the VTA. Nicotine intaketreatment  may could enhance increase the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/N-methyl-d-aspartate (NMDA) ratio in VTA DA-secreting neurons in the VTA, and this is commonly consideredwhich is thought as a common the addiction mechanism underlying nicotine addiction . Therefore, Iin this paperstudy, we investigated whether or not the lack of glutamate transmission from the PFC to the VTA could make any change in can modulate the effects of nicotine.

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