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1.
Chin J Physiol ; 64(5): 218-224, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34708713

RESUMO

Positive feeling or rewarding experience is crucial for individuals to operative their cognitive activities via an outcome evaluation of incentive reinforcement. For a long time, rewarding process or outcome evaluation is assumed greatly influenced by neuronal construct that holds individuals' impulsiveness, a capacity to inhibit unwanted behaviors provoked in a given situation. In the present study, we proposed that the outcome evaluation or rewarding experience can influence the occurrence of impulsiveness too. We hypothesized that animals would be more likely to deliver impulsive action in the place where it was previously associated with reinforcing process, in which central dopamine may play an important role. By employing five-choice serial reaction time task (5-CSRTT), we examined whether one of the five holes where rats made a correct response to get the reward would gain a higher probability to deliver premature or perseverative activities than other holes in the next trial of 5-CSRTT under baseline or longer waiting period condition. The effects of D1 receptor antagonist SCH23390 were also evaluated in the above paradigm. We demonstrated that (i) the influence on motoric impulsive response from previous rewarded experience can be described in a behavioral paradigm such as the 5-CSRTT, (ii) both prematures and perseverations at the hole associated with previous rewarding were about one-fifth of probability, however were statistically not correlated unless the interventions of inter-trial interval = 7 plus SCH23390, and (iii) the hole associated with the positive reinforcement of the 5-CSRTT appears more likely for rats to carry out an intuitive impetus under SCH23390 in a longer waiting condition. Our results may shed some insight toward the role of rewarding process in impulsive behavior.


Assuntos
Comportamento Impulsivo , Recompensa , Animais , Dopamina , Ratos , Tempo de Reação
3.
Behav Brain Res ; 391: 112686, 2020 08 05.
Artigo em Inglês | MEDLINE | ID: mdl-32428628

RESUMO

People may agonize over an intrusive fear-inducing memory even when the traumatic event has passed, which is the principle manifestation of posttraumatic stress disorder (PTSD). However, many traumatized people do not present symptoms of PTSD, implying that certain hidden factors help those individuals to cope with the traumatic stress. Increasing evidence suggests that early life experience may serve as a predisposing factor in the development of PTSD. For example, early life social deprivation disrupts the glucocorticoid system, one of the biological abnormalities of PTSD. By employing isolation rearing (IR) with a subsequent single prolonged stress (SPS) paradigm, we examined the hypothesis that early-life social experience may change the outcome of traumatic stress in both behavioral and neurochemical profiles. Behaviorally, the performance of rats on a Pavlovian fear conditioning test was measured to evaluate their retrieval ability of fear memory extinction. Neurochemically, plasma corticosterone levels and glucocorticoid receptor (GR), FK506-binding proteins 4 and 5 (FKBP4 and FKBP5) and early growth response-1 (Egr-1) expression were measured in GR-abundant brain areas, including the hypothalamus, medial prefrontal cortex, and hippocampus. Our results demonstrated an area-dependent IR effect on the SPS outcomes. IR prevented the SPS-impaired fear extinction retrieval ability and averted the SPS-elevated expression of GR, FKBP4, and Egr-1 in the hippocampus, whereas it did not change the SPS-reduced plasma corticosterone levels and SPS-enhanced GR activity in the mPFC and hypothalamus. The present study provides some new insights to support the hypothesis that early-life experience may play a role in the occurrence of PTSD.


Assuntos
Experiências Adversas da Infância/psicologia , Extinção Psicológica/fisiologia , Transtornos de Estresse Pós-Traumáticos/fisiopatologia , Animais , Encéfalo/metabolismo , Condicionamento Clássico , Corticosterona/sangue , Modelos Animais de Doenças , Medo/fisiologia , Medo/psicologia , Glucocorticoides/análise , Glucocorticoides/metabolismo , Glucocorticoides/farmacologia , Hipocampo/metabolismo , Masculino , Memória/efeitos dos fármacos , Córtex Pré-Frontal/metabolismo , Ratos , Ratos Sprague-Dawley , Receptores de Glucocorticoides/metabolismo , Transtornos de Estresse Pós-Traumáticos/metabolismo , Transtornos de Estresse Pós-Traumáticos/psicologia , Estresse Psicológico/metabolismo
4.
Artigo em Inglês | MEDLINE | ID: mdl-32165120

RESUMO

Individuals may develop fear extinction deficits after life-threatening traumatic events; such deficits indicate posttraumatic stress disorder (PTSD). Because the occurrence of this disorder differs among people who have experienced trauma, hidden underlying factors should be determined. Increasing evidence suggests the involvement of neuronal dysregulation of information processes or cognitive function during development. This neuronal dysregulation is caused by disturbances in dopamine (DA) transmission within the fear circuit, which comprises the medial prefrontal cortex (mPFC), amygdala, and hippocampus. Single prolonged stress (SPS) combined with an isolation rearing (IR) paradigm was used to randomly assign rats to four groups [social rearing-no SPS (SR-NS), SR-SPS, IR-NS, and IR-SPS], and their performance in prepulse inhibition (PPI) and on Pavlovian fear conditioning tests was assessed. Tissue DA levels and the expression of DA receptors (D1R and D2R) in the fear circuit were measured at the end of the experiment. Our results indicated that PPI deficits and fear extinction problems were specific to rats subjected to IR and SPS, respectively. Furthermore, IR-induced PPI deficits were not influenced by SPS, but SPS-induced fear extinction retrieval impairment could be adjusted according to previous IR experiences. Neurochemically, tissue DA levels and D1R expression in the mPFC and amygdala were nonspecifically reduced by IR and SPS, whereas D2R expression in the mPFC and amygdala was higher in IR-SPS than in SR-SPS rats. These findings suggest that early life experiences may influence fear responses in adulthood through a change in DA profiles within the fear circuit.


Assuntos
Dopamina/metabolismo , Extinção Psicológica/fisiologia , Medo/fisiologia , Receptores Dopaminérgicos/metabolismo , Isolamento Social , Transtornos de Estresse Pós-Traumáticos/metabolismo , Animais , Encéfalo/metabolismo , Medo/psicologia , Masculino , Ratos , Ratos Sprague-Dawley , Interação Social , Isolamento Social/psicologia , Transtornos de Estresse Pós-Traumáticos/psicologia , Estresse Psicológico/metabolismo , Estresse Psicológico/psicologia
5.
J Biomed Sci ; 26(1): 26, 2019 Mar 21.
Artigo em Inglês | MEDLINE | ID: mdl-30898126

RESUMO

BACKGROUND: Traumatic experience may lead to various psychological sequelae including the unforgettable trauma-associated memory as seen in posttraumatic stress disorder (PTSD), with a mechanism of impaired fear extinction due to biological imbalance among hypothalamic-pituitary-adrenal (HPA) axis and fear circuit areas such as medial prefrontal cortex (mPFC), hippocampus, and amygdala. Recently the impaired sociability seen in PTSD patients received great attention and the involvement of oxytocin (OXT) mediation is worth being investigated. This study examined whether the trauma-altered prosocial behavior can be modulated by OXT manipulation and its relationship with corticotropin-releasing hormone (CRH) signaling. METHODS: Male rats previously exposed to a single prolonged stress (SPS) were evaluated for their performance in social choice test (SCT) and novel object recognition test (NORT) following the introduction of intranasal oxytocin (OXT) and OXT receptor antagonist atosiban (ASB). OXT receptors (OXTR) and CRH receptors (CRHR1, CRHR2) were quantified in both protein and mRNA levels in medial prefrontal cortex (mPFC), hippocampus, and amygdala. RESULTS: SPS reduced inclination of rats staying at the sociable place with performing less prosocial contacts. OXT can amend the deficit but this effect was blocked by ASB. Expression of OXTR became reduced following SPS in mPFC and amygdala, the latter exhibited higher therapeutic specificity to OXT. Expression of CRHR1 appeared more sensitive than CRHR2 to SPS, higher CRHR1 protein levels were found in mPFC and amygdala. CONCLUSION: Psychological trauma-impaired sociability is highly associated with OXT signaling pathway. Intranasal OXT restored both the SPS-impaired prosocial contacts and the SPS-reduced OXTR expressions in mPFC and amygdala. OXT may have therapeutic potential to treat PTSD patients with impaired social behaviors.


Assuntos
Expressão Gênica/efeitos dos fármacos , Ocitocina/farmacologia , Receptores de Hormônio Liberador da Corticotropina/genética , Receptores de Ocitocina/genética , Comportamento Social , Transtornos de Estresse Pós-Traumáticos/genética , Administração Intranasal , Animais , Antagonistas de Hormônios/farmacologia , Humanos , Masculino , Ocitócicos/administração & dosagem , Ocitócicos/farmacologia , Ocitocina/administração & dosagem , Ratos , Ratos Sprague-Dawley , Receptores de Hormônio Liberador da Corticotropina/metabolismo , Receptores de Ocitocina/metabolismo , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/genética , Transtornos de Estresse Pós-Traumáticos/metabolismo , Vasotocina/análogos & derivados , Vasotocina/farmacologia
6.
Behav Brain Res ; 362: 181-187, 2019 04 19.
Artigo em Inglês | MEDLINE | ID: mdl-30610908

RESUMO

People may suffer from an intruded fear memory when the attributable traumatic events no longer exist. This is of highly clinical relevance to trauma-induced mental disorders, such as posttraumatic stress disorder (PTSD). Mechanism underlying PTSD largely lies in the abnormal process of fear extinction and a functional imbalance within amygdala associated fear circuit areas. Previous evidence suggested central dopamine plays a key role in the regulation of the fear memory process, yet it remains unclear whether the intervention of dopamine modulators would be beneficial for the fear extinction abnormalities. The present study examined the performance of Pavlovian conditioned fear and the changes of dopamine profiles following a subchronic 14-day regimen of aripiprazole (a partial agonist of dopamine D2 receptors to normalize the condition caused by dopamine imbalance) in rats previously experienced a psychologically traumatic procedure of single prolonged stress (SPS). The results demonstrated that aripiprazole at 5.0 mg/kg reversed the SPS-impaired fear memory dysfunction and the SPS-reduced dopamine efflux in the amygdala. The present study suggests a therapeutic potential of subchronic treatment with aripiprazole in managing patients suffered from fear extinction problem.


Assuntos
Aripiprazol/farmacologia , Medo/efeitos dos fármacos , Memória/efeitos dos fármacos , Trauma Psicológico/tratamento farmacológico , Tonsila do Cerebelo/efeitos dos fármacos , Animais , Aripiprazol/administração & dosagem , Condicionamento Clássico/fisiologia , Modelos Animais de Doenças , Extinção Psicológica/fisiologia , Medo/fisiologia , Masculino , Ratos Sprague-Dawley , Transtornos de Estresse Pós-Traumáticos/tratamento farmacológico , Transtornos de Estresse Pós-Traumáticos/fisiopatologia , Estresse Psicológico/tratamento farmacológico
7.
Behav Brain Res ; 359: 861-870, 2019 02 01.
Artigo em Inglês | MEDLINE | ID: mdl-30056129

RESUMO

Individuals with posttraumatic stress disorder (PTSD) are characterized by fear memory problems and hypocortisolemia of which traumatic stress-induced monoaminergic disruption over infralimbic (IL) cortex is considered the key mechanism. Hyperbaric oxygen therapy (HBOT) has recently proven its utility in treating several mental disorders but remains unexplored for PTSD. The present study aimed to examine the effects of 5-day HBO paradigm on traumatic stress (single prolonged stress, SPS, an animal model of PTSD)-induced dysregulation of fear memory/anxiety profiles and related abnormalities in IL monoamines and plasma corticosterone. Rats were randomly assigned to four groups (CON-sham, CON-HBOT, SPS-sham, and SPS-HBOT) and received Pavlovian fear conditioning test or elevated-T maze (ETM). The extracellular and tissue levels of monoamines over the IL cortex and the activity of the hypothalamus-pituitary-adrenal axis (i.e., the plasma corticosterone level and expression of the glucocorticoid receptor (GR) in the IL, hippocampus, amygdala, and hypothalamus) were measured. The results demonstrated that HBOT restored behaviorally the SPS-impaired fear extinction retrieval ability and SPS-induced conditioned anxiety, and neurochemically the SPS-reduced IL monoamines efflux level, and the corticosterone profiles. The present study shows some positive effects of HBOT in both behavioral and neurochemical profiles of PTSD outcomes.


Assuntos
Monoaminas Biogênicas/metabolismo , Medo/psicologia , Oxigenação Hiperbárica/métodos , Transtornos da Memória/etiologia , Transtornos da Memória/terapia , Transtornos de Estresse Pós-Traumáticos/complicações , Animais , Condicionamento Psicológico/efeitos dos fármacos , Corticosterona/sangue , Modelos Animais de Doenças , Reação de Fuga/efeitos dos fármacos , Extinção Psicológica , Locomoção/efeitos dos fármacos , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Microdiálise , Neuroquímica , Ratos , Ratos Sprague-Dawley , Tempo de Reação/efeitos dos fármacos , Fatores de Tempo
8.
Int J Mol Sci ; 19(12)2018 Dec 03.
Artigo em Inglês | MEDLINE | ID: mdl-30513893

RESUMO

Posttraumatic stress disorder (PTSD) is a trauma-induced mental disorder characterized by fear extinction abnormalities, which involve biological dysfunctions among fear circuit areas in the brain. Oxytocin (OXT) is a neuropeptide that regulates sexual reproduction and social interaction and has recently earned specific attention due to its role in adjusting neurobiological and behavioral correlates of PTSD; however, the mechanism by which this is achieved remains unclear. The present study aimed to examine whether the effects of OXT on traumatic stress-induced abnormalities of fear extinction (specifically induced by single prolonged stress (SPS), an animal model of PTSD) are associated with pro-inflammatory cytokines. Seven days after SPS, rats received intranasal OXT 40 min before a cue-dependent Pavlovian fear conditioning-extinction test in which rats' freezing degree was used to reflect the outcome of fear extinction. We also measured mRNA expression of IL-1ß, IFN-γ, and TNF-α in the medial prefrontal cortex (mPFC), hippocampus, and amygdala at the end of the study, together with plasma oxytocin, corticosterone, IL-1ß, IFN-γ, and TNF-α, to reflect the central and peripheral changes of stress-related hormones and cytokines after SPS. Our results suggested that intranasal OXT effectively amends the SPS-impaired behavior of fear extinction retrieval. Moreover, it neurochemically reverses the SPS increase in pro-inflammatory cytokines; thus, IL-1ß and IFN-γ can be further blocked by the OXT antagonist atosiban (ASB) in the hippocampus. Peripheral profiles revealed a similar response pattern to SPS of OXT and corticosterone (CORT), and the SPS-induced increase in plasma levels of IL-1ß and TNF-α could be reduced by OXT. The present study suggests potential therapeutic effects of OXT in both behavioral and neuroinflammatory profiles of PTSD.


Assuntos
Encéfalo/patologia , Medo/efeitos dos fármacos , Inflamação/patologia , Memória/efeitos dos fármacos , Ocitocina/uso terapêutico , Transtornos de Estresse Pós-Traumáticos/tratamento farmacológico , Transtornos de Estresse Pós-Traumáticos/fisiopatologia , Animais , Corticosterona/sangue , Citocinas/metabolismo , Modelos Animais de Doenças , Extinção Psicológica , Mediadores da Inflamação/metabolismo , Masculino , Modelos Biológicos , Ocitocina/sangue , Ocitocina/farmacologia , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Ratos Sprague-Dawley , Transtornos de Estresse Pós-Traumáticos/patologia , Estresse Psicológico/complicações
9.
Psychiatry Investig ; 15(10): 1000-1006, 2018 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-30301302

RESUMO

OBJECTIVE: Post weanling isolation-reared (IR) rats are featured with depressive phenotype, yet its mechanism is not clearly defined particularly in terms of the involvement of central 5-HT1A receptors. The present study aims to examine the effects of 5HT1A activation on forced swim test (FST) in IR rats following 5-HT depletion. METHODS: Social control (SOC) and IR rats received an intracerebraoventricular (ICV) injection of 5-HT depletion agent, 5,7-DHT. 14 days after the surgery, rats were assessed their performance in FST with or without the challenge with a 5-HT1A agonist, 8-OH-DPAT. Rats were then sacrificed for analyzing their 5-HT tissue levels and the expressions of their 5-HA1A receptors in prefrontal cortex (PFC), hippocampus (HPX), and amygdala (AMY). RESULTS: 5,7-DHT decreased the tissue concentration of 5-HT in both IR and SOC rats. IR rats were more immobile and less sensitive to the lesion-induced immobility, however this effect was reversed by acute challenge of 8-OH-DPAT. 5,7-DHT lesion increased the expression of PFC 5-HT1A receptors. CONCLUSION: The integrity of central 5-HT system is developmentally crucial for the 5-HT1A-relevant depression profile in rats of social isolation.

10.
Psychiatry Investig ; 15(2): 193-199, 2018 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-29475221

RESUMO

OBJECTIVE: Central 5-HT1A receptor is involved in the modulation of sensorimotor gating function. However, its precise role is not clearly defined in developmentally social deprived (isolation rearing, IR) rats featured with impaired sensorimotor gating ability. We therefore aimed to examine the effects of 5HT1A activation on acoustic startle response (ASR) and prepulse inhibition (PPI) in IR rats in a condition of compromised presynaptic 5-HT functions. METHODS: Social control (SOC) and IR rats received an intracerebraoventricular (ICV) injection of 5-HT depletor, 5,7-DHT. Seven days later rats entered a protocol of 8-OH-DPAT, a 5-HT1A agonist, in which locomotor activity, ASR and PPI and their tissue levels of 5-HT were measured. RESULTS: Our results found that both IR and 5,7-DHT decreased the tissue concentration of 5-HT. IR-induced hyperactivity and gating impairment were unaffected by 5-HT depletion. 8-OH-DPAT strengthened the ASR in IR but not SOC rats and the drug-reduced PPI could be adjusted by 5,7-DHT pretreatment. 8-OH-DPAT at 100 µg/kg enhanced PPI in 5-HT-depleted SOC rats. However for IR rats, 8-OH-DPAT strengthened PPI in sham rats but downgraded it in depletion condition. CONCLUSION: The integrity of central 5-HT system is important to 5-HT1A-modulated sensorimotor gating in isolation-reared rats.

11.
Eur Neuropsychopharmacol ; 26(9): 1484-1495, 2016 09.
Artigo em Inglês | MEDLINE | ID: mdl-27492886

RESUMO

Central catecholamines regulate fear memory across the medial prefrontal cortex (mPFC), amygdala (AMYG), and hippocampus (HPC). However, inadequate evidence exists to address the relationships among these fear circuit areas in terms of the fear symptoms of posttraumatic stress disorder (PTSD). By examining the behavioral profile in a Pavlovian fear conditioning paradigm together with tissue/efflux levels of dopamine (DA) and norepinephrine (NE) and their reuptake abilities across the fear circuit areas in rats that experienced single prolonged stress (SPS, a rodent model of PTSD), we demonstrated that SPS-impaired extinction retrieval was concomitant with the changes of central DA/NE in a dissociable manner. For tissue levels, diminished DA and increased NE were both observed in the mPFC and AMYG. DA efflux and synaptosomal DA transporter were consistently reduced in the AMYG/vHPC, whereas SPS reduced NE efflux in the infralimbic cortex and synaptosomal NE transporter in the mPFC. Furthermore, a lower expression of synaptosomal VMAT2 was observed in the mPFC, AMYG, and vHPC after SPS. Finally, negative correlations were observed between retrieval freezing and DA in the mPFC/AMYG; nevertheless, the phenomena became invalid after SPS. Our results suggest that central catecholamines are crucially involved in the retrieval of fear extinction in which DA and NE play distinctive roles across the fear circuit areas.


Assuntos
Encéfalo/metabolismo , Dopamina/metabolismo , Extinção Psicológica/fisiologia , Medo/fisiologia , Norepinefrina/metabolismo , Transtornos de Estresse Pós-Traumáticos/metabolismo , Animais , Pressão Sanguínea/fisiologia , Condicionamento Clássico/fisiologia , Corticosterona/sangue , Modelos Animais de Doenças , Espaço Extracelular/metabolismo , Reação de Congelamento Cataléptica/fisiologia , Frequência Cardíaca/fisiologia , Masculino , Atividade Motora/fisiologia , Vias Neurais/metabolismo , Distribuição Aleatória , Ratos Wistar , Transtornos de Estresse Pós-Traumáticos/psicologia , Sinaptossomos/metabolismo
12.
Psychopharmacology (Berl) ; 233(7): 1135-46, 2016 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-26740318

RESUMO

RATIONALE: Posttraumatic stress disorder (PTSD) is a trauma-induced mental disorder characterised by fear extinction dysfunction in which fear circuit monoamines are possibly associated. PTSD often coexists with depressive/anxiety symptoms, and selective serotonin reuptake inhibitors (SSRIs) are recommended to treat PTSD. However, therapeutic mechanisms of SSRIs underlying the PTSD fear symptoms remain unclear. OBJECTIVES: Using a rodent PTSD model, we examined the effects of early SSRI intervention in mood and fear dysfunctions with associated changes of monoamines within the fear circuit areas. METHODS: A 14-day escitalopram (ESC) regimen (5 mg/kg/day) was undertaken in two separate experiments in rats which previously received a protocol of single prolonged stress (SPS). In experiment 1, sucrose preference and elevated T-maze were used to index anhedonia depression and avoidance/escape anxiety profiles. In experiment 2, the percentage of freezing time was measured in a 3-day fear conditioning paradigm. At the end of our study, tissue levels of serotonin (5-HT) in the medial prefrontal cortex, amygdala, hippocampus, and striatum were measured in experiment 1, and the efflux levels of infralimbic (IL) monoamines were measured in experiment 2. RESULTS: In experiment 1, ESC corrected both behavioural (depression/anxiety) and neurochemical (reduced 5-HT tissue levels in amygdala/hippocampus) abnormalities. In experiment 2, ESC was unable to correct the SPS-impaired retrieval of fear extinction. In IL, ESC increased the efflux level of 5-HT but failed to reverse SPS-reduced dopamine (DA) and noradrenaline (NA). CONCLUSIONS: PTSD-induced mood dysfunction is psychopathologically different from PTSD-induced fear disruption in terms of disequilibrium of monoamines within the fear circuit areas.


Assuntos
Ansiedade/tratamento farmacológico , Citalopram/uso terapêutico , Depressão/tratamento farmacológico , Medo/efeitos dos fármacos , Memória/efeitos dos fármacos , Inibidores de Captação de Serotonina/farmacologia , Transtornos de Estresse Pós-Traumáticos/tratamento farmacológico , Animais , Ansiedade/metabolismo , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Citalopram/farmacologia , Depressão/metabolismo , Modelos Animais de Doenças , Ratos , Ratos Wistar , Serotonina/metabolismo , Inibidores de Captação de Serotonina/uso terapêutico , Transtornos de Estresse Pós-Traumáticos/metabolismo
13.
Chin J Physiol ; 58(5): 312-21, 2015 Oct 31.
Artigo em Inglês | MEDLINE | ID: mdl-26387655

RESUMO

Cold stress may produce hemodynamic perturbations but the underlying mechanisms are still not clear. Spectral analysis was used in this study to explore that sympathoadrenal activation could be involved in mechanisms of hemodynamic perturbations to cooling. Conscious rats after treatment with a control vehicle (saline) compared with withdrawal of sympathetic influences by ganglion blocker hexamethonium (HEX) or chemical sympathectomy guanethidine (GUA) were challenged by stressful cooling as acute immersing all four extremities in ice water (4 ± 2°C) for 10 min. Plasma nitric oxide (NO) and the appearance of Dichroitic notch (DN) were measured in comparison between treatment groups throughout the experimental course. Hemodynamic indices were telemetrically monitored, and variability of blood pressure and heart rate (BPV; HRV) were assessed over a range of frequencies: very-low frequency (VLF: 0.02-0.2 Hz), low frequency (LF: 0.2-0.6 Hz), high frequency (HF: 0.6-3 Hz), normalized (n)LF, nHF, ratio LF/HF of HRV (LF/HF(HRV)), and total power (TP: ≤3 Hz). Results showed that the concomitant reciprocal changes of spectral powers existed between frequencies of BPV and HRV to the stressful cooling (i.e. VLF(BPV) versus VLF(HRV), LF(BPV) versus LF(HRV), and nLF(BPV) versus nLF(HRV)) which contribute to the underlying mechanisms of sympathetic efferent influences and myogenic cardiovascular responsiveness. Furthermore, compared with the control vehicle in the stressful cooling, HEX restrained the increase of the pressor, tachycardia and VLF(BPV), except that VLF(HRV) was reduced. GUA abolished pressor, however, restrained the increase of the tachycardia, VLF(BPV) and LF(BPV). In addition, GUA reversed the downward tendency of nLF(BPV) into an upward tendency and attenuated both nLF(HRV) and LF/HF(HRV). DN was virtually undetectable after HEX management but was apparently noticeable after GUA management. Finally, the increase of plasma NO after cooling was diminished after HEX or GUA management. Taken together, these results substantiate that the spectral changes during stressful cooling are highly relevant to the efferent sympathetic rhythmicity and subsequent NO production.


Assuntos
Temperatura Baixa/efeitos adversos , Hemodinâmica , Estresse Fisiológico , Sistema Nervoso Simpático/fisiologia , Glândulas Suprarrenais/fisiologia , Animais , Vias Eferentes/fisiologia , Masculino , Óxido Nítrico/sangue , Distribuição Aleatória , Ratos Sprague-Dawley , Análise Espectral , Telemetria
14.
Artigo em Inglês | MEDLINE | ID: mdl-25151304

RESUMO

Atomoxetine, a noradrenaline reuptake inhibitor (NRI), which is a non-stimulating medicine that is used for the treatment of patients with attention deficit hyperactivity disorder (ADHD), has been found to be effective in reducing behavioral impulsivity in rodents, but its efficacy in a dorsal noradrenergic ascending bundle (DNAB)-lesioned condition has not been examined. The present study aimed to investigate the effects of DNAB lesions on attention and impulsive control in the five-choice serial reaction time task (5-CSRTT) in rats treated with atomoxetine. The drug-induced changes in noradrenaline efflux in the medial prefrontal cortex were also measured. 5-CSRTT-trained rats were included in one of the following groups: N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4)/Atomoxetine, Sham/Atomoxetine, DSP-4/Saline, or Sham/Saline. Acute atomoxetine (0.3 mg/kg) was administered 14 days after the DSP-4 regime. The behavioral testing included manipulations of the inter-trial interval (ITI), stimulation duration and food satiety. In vivo microdialysis of the noradrenaline efflux in the medial prefrontal cortex and the expression of the noradrenaline transporter (NAT) in the DNAB areas were examined. Atomoxetine reduced impulsivity and perseveration in the long-ITI condition with no effects on any other variables. This phenomenon was not influenced by DSP-4 pre-treatment. The DNAB-lesioned rats had lower noradrenaline efflux in the medial prefrontal cortex. DSP-4 caused no change in NAT expression in the DNAB areas. These findings suggested that noradrenaline reuptake may not be exclusively responsible for the atomoxetine effects in adjusting impulsivity. The role of DNAB should also be considered, particularly in conditions requiring greater behavioral inhibition.


Assuntos
Inibidores da Captação Adrenérgica/uso terapêutico , Transtorno do Deficit de Atenção com Hiperatividade/tratamento farmacológico , Lesões Encefálicas/fisiopatologia , Comportamento Impulsivo/efeitos dos fármacos , Norepinefrina/análogos & derivados , Propilaminas/uso terapêutico , Tempo de Reação/efeitos dos fármacos , Adrenérgicos/toxicidade , Inibidores da Captação Adrenérgica/farmacologia , Vias Aferentes/lesões , Vias Aferentes/patologia , Animais , Cloridrato de Atomoxetina , Transtorno do Deficit de Atenção com Hiperatividade/etiologia , Benzilaminas/toxicidade , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Lesões Encefálicas/tratamento farmacológico , Lesões Encefálicas/patologia , Comportamento de Escolha/efeitos dos fármacos , Masculino , Microdiálise , Naltrexona/análogos & derivados , Naltrexona/toxicidade , Norepinefrina/metabolismo , Proteínas da Membrana Plasmática de Transporte de Norepinefrina/metabolismo , Propilaminas/farmacologia , Ratos , Ratos Sprague-Dawley , Zimeldina/farmacologia
15.
Nanoscale Res Lett ; 7(1): 372, 2012 Jul 07.
Artigo em Inglês | MEDLINE | ID: mdl-22768847

RESUMO

One-dimensional pure zinc oxide (ZnO) and Y-doped ZnO nanorod arrays have been successfully fabricated on the silicon substrate for comparison by a simple hydrothermal process at the low temperature of 90°C. The Y-doped nanorods exhibit the same c-axis-oriented wurtzite hexagonal structure as pure ZnO nanorods. Based on the results of photoluminescence, an enhancement of defect-induced green-yellow visible emission is observed for the Y-doped ZnO nanorods. The decrease of E2(H) mode intensity and increase of E1(LO) mode intensity examined by the Raman spectrum also indicate the increase of defects for the Y-doped ZnO nanorods. As compared to pure ZnO nanorods, Y-doped ZnO nanorods show a remarked increase of saturation magnetization. The combination of visible photoluminescence and ferromagnetism measurement results indicates the increase of oxygen defects due to the Y doping which plays a crucial role in the optical and magnetic performances of the ZnO nanorods.

16.
Nanoscale Res Lett ; 7(1): 260, 2012 May 18.
Artigo em Inglês | MEDLINE | ID: mdl-22607485

RESUMO

Aligned ZnO nanowires with different lengths (1 to approximately 4 µm) have been deposited on indium titanium oxide-coated glass substrates by using the solution phase deposition method for application as a work electrode in dye-sensitized solar cells (DSSC). From the results, the increases in length of zinc oxide (ZnO) nanowires can increase adsorption of the N3 dye through ZnO nanowires to improve the short-circuit photocurrent (Jsc) and open-circuit voltage (Voc), respectively. However, the Jsc and Voc values of DSSC with ZnO nanowires length of 4.0 µm (4.8 mA/cm2 and 0.58 V) are smaller than those of DSSC with ZnO nanowires length of 3.0 µm (5.6 mA/cm2 and 0.62 V). It could be due to the increased length of ZnO nanowires also resulted in a decrease in the transmittance of ZnO nanowires thus reducing the incident light intensity on the N3 dye. Optimum power conversion efficiency (η) of 1.49% was obtained in a DSSC with the ZnO nanowires length of 3 µm.

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