Neuroplasticity is influenced by dopamine in various ways. Daily human activities required the brain to use both motor and cognitive functions. Importantly, neural plasticity plays an essential role in motor and cognitive learning. Neuroplasticity is the cortical remapping of the brain. Fundamentally the brain has the ability to alter cortical structures due to its ability to train and relearn skills. Memory formation and learning are ways that dopamine helps in brain development. In neuropsychiatric diseases such as schizophrenia and Parkinson's disease, an individual experiences a barrier in cognitive processes, which is usually followed by dopaminergic dysfunction. The premise of these dopaminergic effects has been found to be involved in long-term depression (LTD) and long-term potentiation (LTP) in neuroplasticity. Scientists have found that, using non-invasive brain stimulation techniques, it is possible to measure the impact of dopamine on plasticity. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essay. These techniques include paired associative stimulation (PAS) and transcranial direct current stimulation (tDCS). Previous research indicates that D1 receptor activation supports LTD and LTP. Dopamine is a neuromodulator in this case due to its ubiquitous function which is inhibitory or excitatory. To confirm this claim, the experimenters induced plasticity using PAS and tDCS in the human motor cortex. Previous studies have been able to generate cortical excitability similar to LTD and LTP for approximately one hour using this technique. Furthermore, brain stimulation is capable of eliciting addiction to the NMDA receptor itself. Brain stimulation in the motor cortex using tDCS promotes nonfocal plasticity. Essentially, excitability is not limited to synaptic subgroups. This technique allows the glutamatergic system to generate polarity-dependent plasticity, which is not limited to a particular subgroup. Similarly, PAS promotes focal plasticity because it is thought to be primarily specific to the somatosensory motor cortex. Cortical excitability is enhanced through the synchronized activation of neurons in the motor cortex. This process occurs through somatosensory afferent neurons. In humans, dopamine has been shown to have an effect on neuroplasticity where it demonstrates a nonlinear dose-dependent effect. The precursor of dopamine is L-dopa. In particular, L-dopa is found to have an effect on plasticity in humans. This drug has been confirmed to have dose-dependent nonlinear effects on neuroplasticity and cognition. This drug appears to have beneficial effects on memory formation and learning. Dopamine agents have been shown to restore PAS-induced plasticity when Parkinson's disease patients are prescribed medications. Because of the nonlinear effect observed in L-dopa, researchers are interested in studying the connection this drug has with plasticity in humans. Furthermore, the current hypothesis that these experimenters are particularly interested in is exploring the importance that D1 receptor activation has in neuroplasticity. For learning processing, the D1 receptor is essential. In an experiment conducted by Fresnoza and colleagues, experimenters were interested in finding the connection between plasticity during D1 receptor activation. Furthermore, they hypothesized that receptor activationD1-like would result in nonlinear effects on plasticity. The researchers performed two experiments using the primary motor cortex as a model. Experimenters conducted experiments for this study. In the first experiment, they blocked the D2 receptors with sulpiride so that the activation was shifted to the D1 receptors. They chose to use sulpiride because it is a selective antagonist for the D2 receptor. This mechanism restores plasticity by blocking D2 receptor activity. In the second experiment, the researchers combined sulpiride with L-dopa to increase D1 receptor activation. The investigators chose this indirect approach because, for humans, no selective D1 receptor agonist is currently available. At each experimental session, subjects were administered a low (25 mg), medium (100 mg), or high (200 mg) dose of L-dopa. L-dopa was combined with a placebo drug or sulpiride for ninety minutes before inducing plasticity. In the first experiment, plasticity was induced using tDCS. An electrode was placed on the designated cortical region in the motor cortex; the return electrode was positioned above the right supraorbital region. After the electrode is placed, a current will be administered to the head. For anodal tDCS the current was administered for 13 minutes and for cathodal tDCS the current was administered for 9 minutes. Notably, current induction allows cortical excitability to persist for an hour after the stimulation ends. In the second experiment, the experimenters used PAS to induce plasticity. An electrical pulse was used to deliver current to the wrist level at the right ulnar nerve. For thirty minutes, 90 pairs of stimuli were conducted to cause a reduction in cortical excitability (PAS10) or an enhancement (PAS25) for approximately one hour after cessation of stimulation. This method is useful because the researchers found that the combination of sulpiride and L-dopa altered the plasticity induced using the tDCS technique. These results show that D1 receptor activation demonstrates a nonlinear dosage dependence on plasticity. furthermore, activation of the D1 receptor is shown to have an effect on memory formation and learning. In humans, for D1-type plasticity to be generated in the motor cortex, a peak amount of D1-type receptor activation would be required. Researchers theorize that the mechanism by which D1 receptor activation occurs is through the GABAergeic and glutamatergic systems. GABAergic and glutamatergic activity have been shown to enhance the activation of D1 receptors. Combining sulpiride with L-Dopa with low-dose administration enhances D1 receptor activation and blocks D2 receptors collectively strengthening GABAergic activity. The researchers in this study were able to effectively distinguish D1 receptor activation that had an effect on plasticity during brain stimulation using PAS and tDCS. this nonlinear effect may be useful for exploring how memory formation and learning are acquired when the D1 receptor is stimulated. Furthermore, this could be used as a possible treatment for people suffering from Parkinson's disease. Activation of D1 receptors through brain stimulation could be effective for improving cognitive functions where there is a reduction in dopamine receptors. Furthermore, this technique targeting the activation of D1 receptors could be useful for the treatment of individuals suffering from schizophrenia. In particular, onelimitation of this study is that the researchers likely activated other dopamine receptors since they used an indirect approach in this experiment. They believe D3 receptors may have been activated in this study. Additionally, sulpiride could be used to block the activation of D3 receptors. In the neocortex, one of the predominant dopamine receptors is the D1 receptor. The researchers demonstrated that in the dorsolateral prefrontal cortex (DLPFC), reorganization of dopamine signaling at D1 receptors may be responsible for the functional changes in working memory found in individuals with schizophrenia. In a study conducted by Abi-Dargham et. Al, the investigators were interested in evaluating the availability of D1 receptors in the DLPFC in individuals with schizophrenia. They paired participants with healthy controls to compare working memory performance and D1 receptor availability. Importantly, the investigators of this study found that increased postsynaptic sensitivity to dopamine release during the execution of the assigned task could be due to the activation of D1 receptors in the DLPFC. This study could also be useful in discovering the impact that the activation of D1 receptors has on plasticity, however further research is still needed. In an experiment conducted by Bergner and colleagues, they were also interested in exploring the ways in which the activation of D1 receptors is involved in neural plasticity. to test this hypothesis, the method used in this experiment is similar to the method used in the experiment performed by Frenezo et. Al. also used the human motor cortex as a model. They used PAS-induced brain plasticity stimulation techniques and tDCS to test the effect of sulpiride combined with L-dopa. When experimenters induced plasticity using PAS in the first experiment, patients were given a drug sulpiride or placebo (PLC). The experimenters found that cortical excitability could be induced and lasted approximately thirty minutes after stimulation without the aid of pharmacological conditions. However, they observed that excitability ceased effects for iPAS under sulpiride. In the second experiment, the experimenters used tDCS-induced plasticity to measure the effects of sulpiride combined with L-dopa. They observed no substantial cortical excitability. Notably, neuroplasticity was unable to be maintained with drug combinations of sulpiride and L-dopa. The results of this study were able to demonstrate that D1 receptor activation has a dose-dependent effect on plasticity. They found that D1 receptor activation had a clear effect on plasticity with L-Dopa alone. The techniques used in this experiment were useful in demonstrating that sulpiride has the ability to block D2 receptors, which involves the activation of D1 receptors, resulting in the absence of iPAS-induced focal inhibitory plasticity. Evidence of seeing nonfocal induced plasticity generated by anodal tDCS would require inhibition of D2 activity. The authors note that in schizophrenia, D2 receptors are overactive, which causes individuals to have intrusive thoughts and be easily distracted and disorganized behavior. This study could be used to help understand dopaminergic dysfunction in this disease. Activation of D1 receptors and blockade of D2 receptors may be essential to stabilize information processing. This could be used as a treatment for patients with schizophrenia. In the central nervous system, dopamine plays.6258-10.2011