Role Of Dopamine Receptors Research Articles

D1-like dopamine receptor dysfunction in the lateral habenula nucleus increased anxiety-like behavior in rat

Lateral habenula (LHb) is important for emotional processing. It is a link node between forebrain and midbrain. LHb is reciprocally connected with ventral tegmental area, acting as a regulatory center for the dopaminergic system. However, the role of dopamine receptors in the LHb in emotional processing is less clear. In the present study, the expression of dopamine D1 and D2 receptors in LHb was testified by western blot. In addition, D1- or D2-like receptor agonist or antagonist was bilaterally administered into the LHb, anxiety-like and depressive-like behaviors were tested 15min later in rats. In addition, the effects of LHb dopamine receptor activation and inactivation on aversive learning and memory were assessed. Our results showed that: (1) activation and inhibition of D1R but not D2R in LHb increased anxiety-like behavior but decreased depressive-like behavior in rats. (2) D1R activation and inactivation in LHb impaired aversive memory acquisition but not consolidation in rats, D1R agonist also impaired aversive memory retrieval in rats. These results might provide new clues about how LHb was involved in emotional processing.

P.1.l.019 - Influence of personality traits on tinnitus severity perception, anxiety and depressive symptoms

Electrical and chemical stimulation of the dorsal periaqueductal gray (dPAG), deep layers of the superior colliculus (dlSC), and inferior colliculus (IC) causes freezing and escape behavior in rodents. Systemic injections of the selective dopamine D2 receptor antagonist sulpiride increased the number of switch-off responses (SORs) to light and auditory evoked potentials in response to loud sounds. Dopamine D2 receptor inhibition in the IC was shown to enhance unconditioned fear. Nevertheless, the role of dopamine receptors in the dlSC and dPAG in the mediation of unconditioned fear has not yet been demonstrated.The purpose of the present study was to characterize the effects of sulpiride injections (4 and 8 μg/0.2 μl) in the dlSC and dPAG in rats that were subjected to unconditioned fear paradigms.Switch-off responses to light and exploratory behavior in the elevated plus maze were used to evaluate unconditioned fear in rats.Intra-dlSC microinjections of sulpiride increased the number of SORs to light. Intra-dlSC and intra-dPAG injections of sulpiride reduced the number of entries into and time spent on the open arms and decreased end-arm exploration and head dipping in the elevated plus maze.These findings suggest that dopamine, through D2 receptors in the dlSC and dPAG, is involved in defense reactions that are organized in the midbrain tectum.

Sex differences and the role of dopamine receptors in the reward-enhancing effects of nicotine and bupropion.

Nicotine and bupropion have been demonstrated to enhance the value of other reinforcers, and this may partially account for nicotine reward and dependence. Evidence suggests that the sexes differ in their sensitivity to the primary and secondary reinforcing effects of nicotine and nicotine-associated stimuli. Whether the sexes also differ in sensitivity to the reward-enhancing effects of nicotine (and bupropion) is yet unclear. The present study evaluated potential sex differences in the enhancement effects of nicotine and bupropion using a reinforcer demand approach. Furthermore, we sought to investigate the role that D1- and D2-type dopamine receptors play in the reward-enhancing effects of nicotine and bupropion. Demand for sensory reinforcement was assessed in male and female rats responding on a progression of fixed ratio schedules. The effects of nicotine and 10 or 20mg/kg bupropion on reinforcer demand were assessed within subjects. Subsequently, the effects of SCH-23390 and eticlopride were assessed on the enhancing effects of nicotine and bupropion on progressive ratio responding. Nicotine and bupropion enhanced demand metrics of reinforcement value in both sexes. Females were more sensitive to the enhancement effects of bupropion assessed by reinforcer demand and progressive ratio performance. D2-like dopamine receptor antagonism by eticlopride attenuated the enhancement effects of bupropion, but not of nicotine. Nicotine and bupropion both enhance reinforcement value in both sexes, though females may be more sensitive to the reward-enhancing effects of bupropion. D2- and possibly D1-type receptors appear to be involved in the reward-enhancing effects of bupropion, but not necessarily nicotine.

Dopamine D1/D5, But not D2/D3, Receptor Dependency of Synaptic Plasticity at Hippocampal Mossy Fiber Synapses that Is Enabled by Patterned Afferent Stimulation, or Spatial Learning.

Although the mossy fiber (MF) synapses of the hippocampal CA3 region display quite distinct properties in terms of the molecular mechanisms that underlie synaptic plasticity, they nonetheless exhibit persistent (>24 h) synaptic plasticity that is akin to that observed at the Schaffer collateral (SCH)-CA1 and perforant path (PP)-dentate gyrus (DG) synapses of freely behaving rats. In addition, they also respond to novel spatial learning with very enduring forms of long-term potentiation (LTP) and long-term depression (LTD). These latter forms of synaptic plasticity are directly related to the learning behavior: novel exploration of generalized changes in space facilitates the expression of LTP at MF-CA3 synapses, whereas exploration of novel configurations of large environmental features facilitates the expression of LTD. In the absence of spatial novelty, synaptic plasticity is not expressed. Motivation is a potent determinant of whether learning about the spatial experience effectively occurs and the neuromodulator dopamine (DA) plays a key role in motivation-based learning. Prior research on the regulation by DA receptors of long-term synaptic plasticity in CA1 and DG synapses in vivo suggests that whereas D2/D3 receptors may modulate a general predisposition toward expressing plasticity, D1/D5 receptors may directly regulate the direction of change in synaptic strength that occurs during learning. Although the CA3 region is believed to play a pivotal role in many forms of learning, the role of dopamine receptors in persistent (>24 h) forms of synaptic plasticity at MF-CA3 synapses is unknown. Here, we report that whereas pharmacological antagonism of D2/D3 receptors had no impact on LTP or LTD, antagonism of D1/D5 receptors significantly impaired LTP and LTD that were induced by solely by means of patterned afferent stimulation, or LTP/LTD that are typically enhanced by the conjunction of afferent stimulation and novel spatial learning. These data indicate an important role for DA acting on D1/D5 receptors in the support of long-lasting and learning-related forms of synaptic plasticity at MF-CA3 synapses and provide further evidence for an important neuromodulatory role for this receptor in experience-dependent synaptic encoding in the hippocampal subfields.

Dropped Head Syndrome after Minor Trauma in a Patient with Levosulpiride-Aggravated Vascular Parkinsonism.

Dropped Head Syndrome after Minor Trauma in a Patient with Levosulpiride-Aggravated Vascular Parkinsonism.

Roles of dopamine receptors in mediating acute modulation of immunological responses in Macrobrachium rosenbergii.

Dopamine (DA) was found to influence the immunological responses and resistance to pathogen infection in invertebrates. To clarify the possible modulation of DA through dopamine receptors (DAR) against acute environmental stress, the levels of DA, glucose and lactate in the haemolymph of Macrobrachium rosenbergii under hypo- and hyperthermal stresses were measured. The changes in immune parameters such as total haemocyte count (THC), differential haemocyte count (DHC), phenoloxidase (PO) activity, respiratory bursts (RBs), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities and phagocytic activity (PA) were evaluated in prawns which received DAR antagonists (SCH23390, SCH, D1 antagonist; domperidone, DOM, D2 antagonist; chlorpromazine, CH, D1+2 antagonist) followed by hypo- (15°C) and hyperthermal (34°C) stresses. In addition, pharmacological analysis of the effect DA modulation was studied in haemocytes incubated with DA and DAR antagonists. The results revealed a significant increase in haemolymph DA accompanied with upregulated levels of glucose and lactate in prawns exposed to both hypo- and hyperthermal stresses in 2h. In addition, a significant decrease in RBs per haemocyte was noted in prawns which received DAR antagonists when they exposed to hyperthermal stress for 30min. In invitro test, antagonism on RBs, SOD and GPx activity of haemocytes were further evidenced through D1, D1, D1+D2 DARs, respectively, in the meantime, no significant difference in PO activity and PA was observed among the treatment groups. These results suggest that the upregulation of DA, glucose and lactate in haemolymph might be the response to acute thermal stress for the demand of energy, and the DAR occupied by its antagonistic action impart no effect on immunological responses except RBs invivo even though the modulation mediated through D1 DAR was further evidenced in RBs, SOD and GPx activities invitro. It is therefore concluded that thermal stress mediate stress responses not only through DAR but also via diverse pathways, and DA might modulate the levels of RBs, SOD and GPx activities mainly through D1 DAR.

Dopamine D2 receptors regulate unconditioned fear in deep layers of the superior colliculus and dorsal periaqueductal gray

RationaleElectrical and chemical stimulation of the dorsal periaqueductal gray (dPAG), deep layers of the superior colliculus (dlSC), and inferior colliculus (IC) causes freezing and escape behavior in rodents. Systemic injections of the selective dopamine D2 receptor antagonist sulpiride increased the number of switch-off responses (SORs) to light and auditory evoked potentials in response to loud sounds. Dopamine D2 receptor inhibition in the IC was shown to enhance unconditioned fear. Nevertheless, the role of dopamine receptors in the dlSC and dPAG in the mediation of unconditioned fear has not yet been demonstrated. ObjectivesThe purpose of the present study was to characterize the effects of sulpiride injections (4 and 8μg/0.2μl) in the dlSC and dPAG in rats that were subjected to unconditioned fear paradigms. MethodsSwitch-off responses to light and exploratory behavior in the elevated plus maze were used to evaluate unconditioned fear in rats. ResultsIntra-dlSC microinjections of sulpiride increased the number of SORs to light. Intra-dlSC and intra-dPAG injections of sulpiride reduced the number of entries into and time spent on the open arms and decreased end-arm exploration and head dipping in the elevated plus maze. ConclusionThese findings suggest that dopamine, through D2 receptors in the dlSC and dPAG, is involved in defense reactions that are organized in the midbrain tectum.

Involvement of D1 and D2 dopamine receptor in the retrieval processes in latent inhibition.

Contemporary theories propose that latent inhibition (LI) is due to a process of interference with the context playing a key role as recovery cue. Physiological studies have demonstrated that LI is a process dependent on striatal dopamine. D2 dopamine receptors have been specifically associated with its expression, while D1 receptor has shown a limited function. However, to evaluate the role of dopamine receptors in LI, it is necessary to analyse their activity during recovery phase, where the mechanisms involved in interference processes are performed. The experiments studied the involvement of the dopaminergic system in the retrieval process of LI. We analysed the effect of the systemic administration of dopaminergic D1 (SCH-23390) and D2 (sulpiride) antagonist during the test phase on LI and on its contextual specificity. Animals were pre-exposed to saccharin solution and conditioned with a LiCl administration in conditioning phase. Dopaminergic antagonist drugs were administered during the test phase. Experiment 2 used the same context in all the phases. Experiment 3 used a new context during conditioning and test phase. The D2 antagonist increased the LI effect and, in turn, diminished the normally suppressant effect of the context shift on LI. The opposite effect was observed under the D1 antagonist administration. This drug disrupted LI and enhanced the effect that the context shift had on this cognitive process. D2 receptor had a relevant role on retrieval processes of pre-exposure learning, while D1 receptor was related with the contextual control of conditioning.

Roles of dopamine receptors and their antagonist thioridazine in hepatoma metastasis.

Tumor metastasis is the most common cause of death and poor prognosis for cancer patients. Therapeutics that prevent tumor metastasis are the key to prolonging the lifespan of cancer patients. Cancer stem cells are believed to be critical in the metastatic process. Recently, drug screening for cancer stem cells reports that antipsychotic drugs displayed potential anticancer activity. Thioridazine, one of the antipsychotic drugs for dopamine receptors (DRs), is shown to induce the differentiation of cancer stem cells in leukemic disease and breast cancer, but it is not known if this drug would affect liver cancer. In this study, expression of DR5 was higher in tumors than in nontumor adjacent tissues, while DR1 was lower in human hepatocellular carcinoma (HCC) than those in the adjacent tissues. Other DRs were very low or undetectable. Treatment of HCC cells with thioridazine displays a dose-dependent response in HCC cell lines SNU449, LM3, and Huh7. Thioridazine treatment reduced cell viability and sphere formation of HCC cell lines through induction of G0/G1 cell cycle arrest and suppression of stemness genes CD133, OCT4, and EpCam. It also inhibited cell migration via suppression of epithelial–mesenchymal transition (EMT)-related genes such as twist2 and E-cadherin. Thioridazine-pretreated LM3 cells decreased the capacity of tumorigenesis in nude mice. Taken together, our data suggest that thioridazine may have the potential role in treatment of HCC.

Regulation of ethanol intake under chronic mild stress: roles of dopamine receptors and transporters.

Studies have shown that exposure to chronic mild stress decreases ethanol intake and preference in dopamine D2 receptor wild-type mice (Drd2+/+), while it increases intake in heterozygous (Drd2+/−) and knockout (Drd2−/−) mice. Dopaminergic neurotransmission in the basal forebrain plays a major role in the reinforcing actions of ethanol as well as in brain responses to stress. In order to identify neurochemical changes associated with the regulation of ethanol intake, we used in vitro receptor autoradiography to measure the levels and distribution of dopamine D1 and D2 receptors and dopamine transporters (DAT). Receptor levels were measured in the basal forebrain of Drd2+/+, Drd2+/−, and Drd2−/− mice belonging to one of four groups: control (C), ethanol intake (E), chronic mild stress exposure (S), and ethanol intake under chronic mild stress (ES). D2 receptor levels were higher in the lateral and medial striatum of Drd2+/+ ES mice, compared with Drd2+/+ E mice. Ethanol intake in Drd2+/+ mice was negatively correlated with striatal D2 receptor levels. D2 receptor levels in Drd2+/− mice were the same among the four treatment groups. DAT levels were lower in Drd2+/− C and Drd2−/− C mice, compared with Drd2+/+ C mice. Among Drd2+/− mice, S and ES groups had higher DAT levels compared with C and E groups in most regions examined. In Drd2−/− mice, ethanol intake was positively correlated with DAT levels in all regions studied. D1 receptor levels were lower in Drd2+/− and Drd2−/− mice, compared with Drd2+/+, in all regions examined and remained unaffected by all treatments. The results suggest that in normal mice, ethanol intake is associated with D2 receptor-mediated neurotransmission, which exerts a protective effect against ethanol overconsumption under stress. In mice with low Drd2 expression, where DRD2 levels are not further modulated, ethanol intake is associated with DAT function which is upregulated under stress leading to ethanol overconsumption.

Dopamine Receptors and Neurodegeneration.

Dopamine (DA) is one of the major neurotransmitters and participates in a number of functions such as motor coordination, emotions, memory, reward mechanism, neuroendocrine regulation etc. DA exerts its effects through five DA receptors that are subdivided in 2 families: D1-like DA receptors (D1 and D5) and the D2-like (D2, D3 and D4). All DA receptors are widely expressed in the central nervous system (CNS) and play an important role in not only in physiological conditions but also pathological scenarios. Abnormalities in the DAergic system and its receptors in the basal ganglia structures are the basis Parkinson's disease (PD), however DA also participates in other neurodegenerative disorders such as Huntington disease (HD) and multiple sclerosis (MS). Under pathological conditions reorganization of DAergic system has been observed and most of the times, those changes occur as a mechanism of compensation, but in some cases contributes to worsening the alterations. Here we review the changes that occur on DA transmission and DA receptors (DARs) at both levels expression and signals transduction pathways as a result of neurotoxicity, inflammation and in neurodegenerative processes. The better understanding of the role of DA receptors in neuropathological conditions is crucial for development of novel therapeutic approaches to treat alterations related to neurodegenerative diseases.

The Role of Dopamine Receptors during Brain Development

The Role of Dopamine Receptors during Brain Development

Role of dopamine receptor in intestinal mucosal barrier change after brain injury in rats

Objective To investigate the effect of dopamine receptor in intestinal mucosal barrier function after brain injury in rats.Methods Twenty-four rats were allocated to control group,brain injury group,dopamine receptor group,and dopamine antagonist group according to the random number table,with 6 rats per group.Feeney' s weight-drop model was introduced to generate rat models of brain injury.Intestinal mucosal specimens were harvested at postoperative 7 days to evaluate intestinal mucosal morphology by HE staining,expressions of dopamine receptor D1 (DRD1) and dopamine receptor D2 (DRD2) by immunohistochemistry,and mRNA and protein expressions of DRD1 and DRD2 by real-time PCR and Western blot.Meantime,urinary samples were collected to measure lactulose to mannitol ratio (L/M) by high performance liquid chromatography (HPLC).Results Intestinal villus integrity was disrupted in brain injury group and dopamine receptor group when compared to control group,but it remained relatively intact in dopamine antagonist group.Ratio of L/M in brain injury group and dopamine receptor group was similar (0.192 ± 0.080 vs 0.183 ± 0.090,P ＞ 0.05),far higher than 0.037 ± 0.008 in control group (P ＜0.01),but it was reversed in dopamine antagonist group (0.071 ± 0.008,P ＜ 0.01).Real-time PCR showed DRD1 and DRD2 mRNAs expressed in brain injury group and dopamine receptor group were similar (0.764 ± 0.074 vs 0.718 ± 0.065,0.439 ± 0.051 vs 0.408 ± 0.090,P ＞ 0.05),far higher than 0.189 ± 0.008 and 0.076 ± 0.011 in control group (P ＜ 0.01),but both lowered in dopamine antagonist group (0.386 ± 0.071,0.270 ± 0.092,P ＜ 0.01).estern blot analysis showed DRD1 and DRD2 proteins in brain injury group and dopamine receptor group were similar,but both were far higher when compared to control group (P ＜ 0.01).Conclusion Impaired intestinal mucosal barrier may be relate to the up-regulated dopamine receptor in intestinal mucosa after brain injury in rats. Key words: Brain injuries ; Receptors, dopamine; Gastrointestinal motility disorders

Dyskinesia in Parkinson's disease: mechanisms and current non-pharmacological interventions.

Dopamine replacement therapy in Parkinson's disease is associated with several unwanted effects, of which dyskinesia is the most disabling. The development of new therapeutic interventions to reduce the impact of dyskinesia in Parkinson's disease is therefore a priority need. This review summarizes the key molecular mechanisms that underlie dyskinesia. The role of dopamine receptors and their associated signaling mechanisms including dopamine-cAMP-regulated neuronal phosphoprotein, extracellular signal-regulated kinase, mammalian target of rapamycin, mitogen and stress-activated kinase-1 and Histone H3 are summarized, along with an evaluation of the role of cannabinoid and nicotinic acetylcholine receptors. The role of synaptic plasticity and animal behavioral results on dyskinesia are also evaluated. The most recent therapeutic advances to treat Parkinson's disease are discussed, with emphasis on the possibilities and limitations of non-pharmacological interventions such as physical activity, deep brain stimulation, transcranial magnetic field stimulation and cell replacement therapy. The review suggests new prospects for the management of Parkinson's disease-associated motor symptoms, especially the development of dyskinesia. This review aims at summarizing the key molecular mechanisms underlying dyskinesia and the most recent therapeutic advances to treat Parkinson's disease with emphasis on non-pharmacological interventions such as physical activity, deep brain stimulation (DBS), transcranial magnetic field stimulation (TMS) and cell replacement therapy. These new interventions are discussed from both the experimental and clinical point of view, describing their current strength and limitations.

Role of Dopamine D2 Receptors in Human Reinforcement Learning

Influential neurocomputational models emphasize dopamine (DA) as an electrophysiological and neurochemical correlate of reinforcement learning. However, evidence of a specific causal role of DA receptors in learning has been less forthcoming, especially in humans. Here we combine, in a between-subjects design, administration of a high dose of the selective DA D2/3-receptor antagonist sulpiride with genetic analysis of the DA D2 receptor in a behavioral study of reinforcement learning in a sample of 78 healthy male volunteers. In contrast to predictions of prevailing models emphasizing DA's pivotal role in learning via prediction errors, we found that sulpiride did not disrupt learning, but rather induced profound impairments in choice performance. The disruption was selective for stimuli indicating reward, whereas loss avoidance performance was unaffected. Effects were driven by volunteers with higher serum levels of the drug, and in those with genetically determined lower density of striatal DA D2 receptors. This is the clearest demonstration to date for a causal modulatory role of the DA D2 receptor in choice performance that might be distinct from learning. Our findings challenge current reward prediction error models of reinforcement learning, and suggest that classical animal models emphasizing a role of postsynaptic DA D2 receptors in motivational aspects of reinforcement learning may apply to humans as well.

Effect of dopamine D1 and D2 receptor antagonism in the lateral hypothalamus on the expression and acquisition of fructose-conditioned flavor preference in rats

The attraction to sugar-rich foods is influenced by conditioned flavor preferences (CFP) produced by the sweet taste of sugar (flavor–flavor learning) and the sugar's post-oral actions (flavor–nutrient) learning. Brain dopamine (DA) circuits are involved in both types of flavor learning, but to different degrees. This study investigated the role of DA receptors in the lateral hypothalamus (LH) on the flavor–flavor learning produced the sweet taste of fructose. In an acquisition study, food-restricted rats received bilateral LH injections of a DA D1 receptor antagonist (SCH23390), a D2 antagonist (RAC, raclopride) or vehicle prior to 1-bottle training sessions with a flavored 8% fructose+0.2% saccharin solution (CS+/F) and a less-preferred flavored 0.2% saccharin solution (CS−). Drug-free 2-bottle tests were then conducted with the CS+ and CS− flavors presented in saccharin. The fructose-CFP did not differ among groups given vehicle (76%), 12nmol SCH (78%), 24nmol (82%) or 24nmol RAC (90%) during training. In an expression study with rats trained drug-free, LH injections of 12 or 24nmol SCH or 12–48nmol RAC prior to 2-bottle tests did not alter CS+ preferences (77–90%) relative to vehicle injection (86%). Only a 48nmol SCH dose suppressed the CS+ preference (61%). The minimal effect of LH DA receptor antagonism upon fructose flavor–flavor conditioning differs with the ability of LH SCH injections to block the acquisition of glucose flavor–nutrient learning.

The role of dopamine receptors in the neurotoxicity of methamphetamine

Methamphetamine is a synthetic drug consumed by millions of users despite its neurotoxic effects in the brain, leading to loss of dopaminergic fibres and cell bodies. Moreover, clinical reports suggest that methamphetamine abusers are predisposed to Parkinson's disease. Therefore, it is important to elucidate the mechanisms involved in methamphetamine-induced neurotoxicity. Dopamine receptors may be a plausible target to prevent this neurotoxicity. Genetic inactivation of dopamine D1 or D2 receptors protects against the loss of dopaminergic fibres in the striatum and loss of dopaminergic neurons in the substantia nigra. Protection by D1 receptor inactivation is due to blockade of hypothermia, reduced dopamine content and turnover and increased stored vesicular dopamine in D1R(-/-) mice. However, the neuroprotective impact of D2 receptor inactivation is partially dependent on an effect on body temperature, as well as on the blockade of dopamine reuptake by decreased dopamine transporter activity, which results in reduced intracytosolic dopamine levels in D2R(-/-) mice.

The Roles of Dopamine Receptor and Adrenoreceptor on the Inhibition of Gastric Emptying and Intestinal Transit by Amphetamine in Male Rats

Amphetamine, a central nervous stimulant, acts on the central nervous system (CNS) by increasing levels of norepinephrine, serotonin and dopamine (DA) in the brain. It stimulates the colonic motility and gastrointestinal (GI) function via the brain-gut connections as well as diminishes appetite to control bodyweight, but the mechanism between amphetamine and GI motility was unclear. We investigated the role of DA receptor and adrenoreceptor in the inhibitory effects of amphetamine on GI motility in male rats. After fasting overnight, the male rats received an intraperitoneal (i.p.) injection of amphetamine (3 mg/ml/kg) 15 min after i.p. injection of different antagonists for dopamine receptors and adrenoreceptors. Gastric emptying and intestinal transit were assessed 15 min after intragastric instillation of a test meal containing radioactive Na₂⁵¹CrO₄ and 10% charcoal. Haloperidol, a DA receptor antagonist, acting exactly as the selective D₂ receptor antagonist, eticlopride, completely prevented amphetamineinduced inhibition of gastric emptying and intestinal transit in male rats. The selective D₁ receptor antagonist, SCH 23390, significantly attenuated the amphetamine-induced inhibition of gastric emptying and intestinal transit in male rats. Both selective and nonselective α adrenoreceptor antagonist, phentolamine, prazosin and yohimbine, did not reverse the inhibitory effects of amphetamine on gastric emptying and intestinal transit. Propanolol, a β adrenoreceptor antagonist, partially attenuated the amphetamine-induced inhibition of gastric emptying but did not significantly attenuate intestinal transit. These results suggest that amphetamine-induced inhibition of gastric emptying and intestinal transit is mediated by an action on dopaminergic mechanism and adrenoreceptor with little involvement. These findings may clarify the influence of central nervous stimulant on GI tract and may provide the appropriate medication in CNS.

Potential Dopamine-1 Receptor Stimulation in Hypertension Management

The role of dopamine receptors in blood pressure regulation is well established. Genetic ablation of both dopamine D1-like receptor subtypes (D1, D5) and D2-like receptor subtypes (D2, D3, D4) results in a hypertensive phenotype in mice. This review focuses on the dopamine D1-like receptor subtypes D1 and D5 (especially D1 receptors), as they play a major role in regulating sodium homeostasis and blood pressure. Studies mostly describing the role of renal dopamine D1-like receptors are included, as the kidneys play a pivotal role in the maintenance of sodium homeostasis and the long-term regulation of blood pressure. We also attempt to describe the interaction between D1-like receptors and other proteins, especially angiotensin II type 1 and type 2 receptors, which are involved in the maintenance of sodium homeostasis and blood pressure. Finally, we discuss a new concept of renal D1 receptor regulation in hypertension that involves oxidative stress mechanisms.

Cannabinoid CB1 and Dopamine D1 Receptors Partnership in the Modulation of Emotional Neural Processing

GENERAL COMMENTARY article Front. Behav. Neurosci., 13 October 2011Sec. Learning and Memory https://doi.org/10.3389/fnbeh.2011.00067