Nursing institutions' professors' perception and distant education experience during COVID-19 pandemic lockdown.

BACKGROUND: The nursing profession represents a demanding and challenging profession with a purpose to keep up with the evolving health-care demands of the population. AIMS: The purpose of this study is to assess nursing institutions' professors' previous experience about information and communication technologies (ICTs) and their perception of distant education during the pandemic lockdown. MATERIALS AND METHODS: This present is a cross-sectional study among participants n = 249 recruited from all academic staff (N = 694) of 23 higher institutes of nursing professions and health techniques in Morocco. The Chi-square test for independence (χ2) and adjusted Z scores were used as a data analysis method to assess the association between the professors' education levels and ICT experience. RESULTS: A significant association [χ2 (1, n = 249) = 19.510, P < 0.001] was revealed between professors' education level and taken training related to ICT in education; significant few professors (16; 9.3%) reported that taken training session [χ2 (1, n = 249) = 8.940, P = 0.003] belonged to the bachelor degree group. In matters of perception, a few proportion (10%) reported that using technology effectively belonged to the bachelor and low education background group. CONCLUSIONS: The findings showed that having previous experience in teaching remotely and training related to the ICT was significantly associated with a higher education background. Moreover, professors with higher degrees agreed that distant education could be an alternative to face-to-face course during quarantine.

Factors Affecting Sleep Quality among University Medical and Nursing Students: A Study in Two Countries in the Mediterranean Region.

Poor sleep quality, a global public health concern, poses a significant burden on individuals, particularly health care university students facing intense academic stress. A three-center cross-sectional study was conducted at the Higher Institute of Nursing and Health Sciences in Tetouan (Morocco), Faculty of Medicine in Tangier (Morocco) and Faculty of Nursing in Valencia (Spain). We collected various data using a sociodemographic questionnaire, the Pittsburgh sleep quality questionnaire, the international physical activity questionnaire (IPAQ) and the smartphone addiction questionnaire short-version (SAS-SV). A total of 1210 students were included in our study (mean age 20.4 years, 67.2% female, nursing students (66.2%) and medical students (33.8%), 76.1% students from Morocco and 33.9% from Spain). Analysis revealed a higher prevalence of poor sleep quality among Moroccans students compared to Spanish ones (p < 0.001), that nursing students showed less favorable sleep quality than medical students (p < 0.011) and that living with a chronic disease was linked to less favorable sleep quality (p < 0.001). Lastly, intense or weak physical activity and smartphone addiction were correlated with poor sleep quality (p < 0.001). In the multivariate analysis, an association persisted between poor sleep quality and factors such as the country of study (Odds ratio (OR): 6.25 [95% Confidence Interval (CI): 4.34-9.09]), involvement in nursing studies (OR: 3.50 [95% CI: 2.36-5.27]), and the presence of chronic diseases (OR: 2.70 [95% CI: 1.72-4.16]), (p < 0.01 each). Our findings highlight the multifaceted factors affecting sleep quality in young university students. The implications underscore the imperative of interventions tailored to this demographic group.

Hair cortisol concentration associates with insomnia and stress symptoms in breast cancer survivors.

Stress, depressive symptoms and sleep quality are important and modifiable determinant of health and their association with hair cortisol concentrations (HCC) in breast cancer survivors has not been evaluated. We selected a random sample of 65 participants (mean age 57.9 years old, range 44-75 years) recruited from local patients' associations of breast cancer survivors. Each provided a hair sample at enrollment and basic clinical data and psychological evaluation regarding self-perceived stress (PSS-scale), depressive (GDS scale) and insomnia symptoms (Athens scale). We observed a direct and significant (p = 0.001) association between HCC and stress-levels. Depressive symptoms associated significantly (p < 0.01) with stress levels but not with HCC. There were also a significant and direct correlation between hair cortisol concentration and totals core of insomnia symptoms (p = 0.002), and the subdimension of sleep difficulty symptoms (p = 0.002), and with daytime sleepiness symptoms (p = 0.016). Further investigations into the association between stress and insomnia and changes in HCC in breast cancer survivors are warranted in order to validate this biomarker for diagnosis of psychological alterations and to tailor the effects of interventions aimed to reduced stress and improve sleep quality in these women.

Psychological Alterations in Youths with Type I Diabetes: Associations with Salivary Cortisol Concentration.

Background and Objectives: Type 1 diabetes mellitus (T1DM) is one of the most common chronic diseases in children and adolescents, and is associated with stress and other psychological alterations. This study aims to assess psychological and sleep disorders and health-related quality of life in young people with T1DM and to determine the relationship between these parameters and levels of salivary cortisol, a hormone widely associated with stress and several psychological symptoms. Materials and Methods: In our cross-sectional study performed in 60 Moroccan children and adolescents with T1DM, detailed psychological evaluations were performed to assess symptoms of anxiety, attention-deficit hyperactivity disorder (ADHD), sleep quality and diabetes-specific quality of life (using the RCMAS-2, ADHD rating scale, Pittsburgh scale and the DQoL scale, respectively), and cortisol concentration was measured from saliva samples taken mid-morning. Results: A total of 60 children and adolescents with T1DM were recruited. The mean age was 11.05 ± 0.35 (6-17). The mean salivary cortisol level in ng/mL was 4.7 ± 0.49 (0.7-20.2) and was significantly associated with an anxiety RCMAS2 score for the Worry subdomain and DQoL subdomain "Anxiety". Linear regression analysis showed that salivary cortisol was significantly higher in girls compared to boys (p = 0.004) (beta coefficient: 3.384 CI95%: 1.137-5.630) and with Hb1AC level as a continuous variable (p = 0.0001) (beta coefficient: 1.135 CI95%: 0.509-1.760). The other variables included in the model were not significant (p > 0.05). There was an association between salivary cortisol concentration with anxiety RCMAS2 score for Worry subdomain and QoL sub-domain "Anxiety". Still, a significant (p = 0.018) association emerged for anxiety RCMAS2 score Worry subdomain and QoL anxiety subdomain (p = 0.044). Conclusions: Children and adolescents with T1DM experienced significantly elevated symptoms of anxiety and sleep disturbances, particularly in girls, and frequent symptoms of ADHD, particularly in boys. Salivary cortisol concentration collected in the morning is associated with anxiety burden but not with other psychological alterations. Further studies are needed to clarify the associations between salivary cortisol concentration and anxiety in type 1 diabetes in order to propose the hormone as a biomarker for interventions aimed to reduce anxiety levels in these patients.

Salivary Biomarkers Associated with Psychological Alterations in Patients with Diabetes: A Systematic Review.

The care of individuals with diabetes needs a holistic perspective, taking into account both the physical disease and the mental health problems that may be associated. Different studies show a higher prevalence of depression or anxiety issues in diabetes patients than in the general population, which is why diabetes can be considered one of the chronic diseases in which psychological care is crucial to maintain quality of life. The objective of this review is to examine the published articles that relate the bidirectional associations between objective and subjective measures of anxiety, depressive symptomatology, stress, sleep quality, and salivary biomarkers in patients with diabetes. For this, a search was carried out in the electronic databases PubMed, Cochrane, and SCOPUS using the keywords "diabetes", "saliva", "sleep", "anxiety", "depression", and "stress" for works published up until May 2022 and limited to the English and Spanish languages. The sample comprised 14 articles, 5 of which analysed the associations between depressive symptomatology and salivary biomarkers in people with diabetes. Among the salivary biomarkers most frequently used to evaluate psychological alterations in persons with diabetes are cortisol and melatonin. Thus, significant changes in the levels of these biomarkers were observed in most studies. Four out of five studies reported a statistically significant relationship between increased salivary cortisol in the evening/midnight or the cortisol awakening response and depressive symptoms. In contrast, lower cortisol levels upon waking in the morning were observed when there was no depression or anxiety. Regarding the association between salivary cortisol values and sleep quality in patients with diabetes, lower morning cortisol values related to prolonged nighttime sleep were common in the analysed studies. Low melatonin concentrations showed a negative correlation with sleep quality. As it is an easy-to-apply and non-invasive method, the measurement of salivary biomarkers can be very useful for predicting psychological alterations in patients with diabetes. Further scientific studies are required to determine the sensitivity of these biological substances acting as biomarkers for detecting sleep disorders and psychological alterations.

Hair Cortisol Concentration as a Biomarker of Sleep Quality and Related Disorders.

Cortisol is the end product of the hypothalamic-pituitary-adrenal (HPA) axis, and its production is increased mainly in stressful situations or in chronic disorders accompanied by stress enhancement. Altered cortisol concentrations have been reported in a number of neuropsychiatric diseases and sleep disorders. Cortisol concentrations have been measured using several methods, and in several matrixes, such as blood, saliva, and urine. However, lately, hair cortisol, for several reasons, has emerged as a promising biomarker of long-term retrospective HPA activation. Several experimental approaches for cortisol measurement with the corresponding concentration reference ranges and a summary of findings from scientific literature on this field are presented. There is evidence of a close relationship between HPA functional alteration and the development of neuropsychiatric disorders. Sleep disorders are the most common manifestation in several neuropsychiatric conditions, and have also been associated to cortisol alterations in both adults and children. Many studies indicate that hair cortisol constitutes a valuable tool for further contributing to existing data on salivary, plasma, or urinary cortisol concentrations in patients with sleep disorders.

Circadian Rhythm and Concentration of Melatonin in Breast Cancer Patients.

BACKGROUND: Melatonin is a biomarker of the central circadian clock and its chronobiotic actions entraining circadian rhythms to the light-dark cycle are well known. Reduction in melatonin levels and altered circadian rhythms have been associated with a high risk of breast cancer. Melatonin has also been shown to display anti-proliferative effects on breast cancer growth and proliferation. Evaluation of melatonin circadian rhythm alterations in patients bearing breast cancer may have interesting prognostic and therapeutic applications. OBJECTIVE: To review studies evaluating the circadian rhythm of melatonin in breast cancer patients. The effects of surgery and chemotherapy on melatonin secretion were also reviewed. METHODS: Electronic databases, including PubMed/MEDLINE and Scopus, were searched from their inception to May 2020, using the keywords "Melatonin", "Circadian rhythm" and "Breast cancer". RESULTS: Patients with breast cancer maintain a circadian rhythm of melatonin secretion with relatively high levels during the night and low levels during the day, however, a reduction in nocturnal melatonin peak and decreased amplitude of melatonin circadian rhythms in these patients have also been reported. Melatonin levels can influence estrogen receptor concentrations in hormone-dependent estrogen- positive breast cancer. Chemotherapy alters melatonin levels and breast surgery tends to alter melatonin secretion at first-day post-operation. Melatonin levels correlate with clinical and psychological symptoms of breast cancer, such as sleep quality and depression severity. CONCLUSION: Circadian rhythm and the concentration of melatonin in the blood are altered in patients with breast cancers, and it can modify not only the sleep-wake cycle and, thus, patients' quality of life but due to melatonin's antioxidant effects, the effect of therapies can be modulated. Due to the heterogonous protocols used to assess melatonin and variable environmental factors during sampling, further studies need to control, such variables in order to tailor clinical trials based on melatonin rhythm adjustment and/or supplementation in breast cancer patients.

The African striped mouse Lemniscomys barbarus as a model for aggression. Brain areas activated by agonistic encounters

During agonistic behavior several brain areas became differentially activated depending on the role the subject is taking. Several areas are mostly activated during the offender role and several others are activated if the subject plays a defensive role. The main goal of this work is to study in detail the anatomic areas involved in agonistic behavior using a novel animal model, the striped mouse Lemniscomys barbarus, a North African diurnal rodent well known by its natural high aggressiveness toward conspecifics. After social encounters, neural activation in brain areas related to agonistic behavior was measured by c-fos immunostaining. The encounters were recorded and behaviors related to the encounter were analyzed. We differentiated between the aggressive behavior (offender) and escape behavior (defender or defeated). Our results showed that conspecific confrontation induced general c-fos activation in both offender and defender in all measured areas in comparison with non-confronted control. Differences in neural activity between offender and defender were observed specifically in the lateral, cortical and medial amygdala, suprachiasmatic nucleus and the nucleus incertus, suggesting a potential role of these areas in displaying different kinds of behavior during conspecific confrontation. We found that, while in the lateral, medial and cortical amygdala defenders express significantly more c-fos than offenders, in the nucleus incertus of the brainstem the differential activation is just the opposite, Additionally, defenders display significantly more freezing than offenders. This work provides data showing that Lemniscomys barbarus is a widely useful model to study the anatomic background supporting agonistic behavior

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Assessment of the Nature and Severity of Pain Using SF-MPQ for Cancer Patients at the National Institute of Oncology in Rabat in 2015.

BACKGROUND: Cancer is a worldwide health problem and pain is among the most common and unpleasant effects affecting well-being of cancer patients. Accurate description of pain can help physicians to improve its management. Many English tools have been developed to assess pain. Only a limited number of these are applied in Arab countries. Our aim was to assess the quality, the nature and the severity of pain using the short McGill Pain Questionnaire (SF-MPQ) on cancer patients in the National Institute of Oncology (NIO) in Rabat, Morocco. MATERIALS AND METHODS: The tool used was the SF-MPQ inspired from the Arabic version of the MPQ. The subjects were cancer patients (N=182) attending the NIO, from 24th October 2015 to 8th January 2016, ≥18 years old, experiencing pain and coming to have or to update their pain medication. RESULTS: The rate of participation was 96.3%. Eight patients haddif culties to express their pain using descriptors, but could use the Visual Analogue Scale (VAS) and the body diagram. The most frequent sensory descriptors were 'Throbbing', 'Shooting', 'Hot-Burning'. The most used affective descriptor was 'Tiring-Exhausting'. The mean VAS was 6.6 (2.4). The mean score of all items was 11.9 (7.8). The patients were suffering from severe pain. The internal consistency of the form was acceptable. CONCLUSIONS: The findings indicate that most of the patients attending the pain center of the NIO could use the descriptors of the SF-MPQ to describe their pain. They indicate the usefulness of the SF-MPQ to assess the nature and the severity of pain in cancer patients. This tool should now be tested in other Moroccan and Arabic contexts associated with other tools in clinical trials.

Alterations in adipocytokines and cGMP homeostasis in morbid obesity patients reverse after bariatric surgery.

OBJECTIVE: Obesity-associated nonalcoholic fatty liver disease (NAFLD), covering from simple steatosis to nonalcoholic steatohepatitis (NASH), is a common cause of chronic liver disease. Aberrant production of adipocytokines seems to play a main role in most obesity-associated disorders. Changes in adipocytokines in obesity could be mediated by alterations in cyclic GMP (cGMP) homeostasis. The aims of this work were: (1) to study the role of altered cGMP homeostasis in altered adipocytokines in morbid obesity, (2) to assess whether these alterations are different in simple steatosis or NASH, and (3) to assess whether these changes reverse in obese patients after bariatric surgery. DESIGN AND METHODS: In 47 patients with morbid obesity and 45 control subjects, the levels in blood of adipocytokines, cGMP, nitric oxide (NO) metabolites, and atrial natriuretic peptide (ANP) were studied. Whether weight loss after a bariatric surgery reverses the changes in these parameters was evaluated. RESULTS: NO metabolites and leptin increase (and adiponectin decreases) similarly in patients with steatosis or NASH, suggesting that these changes are due to morbid obesity and not to liver disease. Inflammation and cGMP homeostasis are affected both by morbid obesity and by liver disease. The increases in interleukin 6 (IL-6), interleukin 18 (IL-18), plasma cGMP, ANP, and the decrease in cGMP in lymphocytes are stronger in patients with NASH than with steatosis. All these changes reverse completely after bariatric surgery and weight loss, except IL-18. CONCLUSION: Altered cGMP homeostasis seems to contribute more than inflammation to changes in leptin and adiponectin in morbid obesity.

Patients with minimal hepatic encephalopathy show impaired mismatch negativity correlating with reduced performance in attention tests.

UNLABELLED: Attention deficit is an early event in the cognitive impairment of patients with minimal hepatic encephalopathy (MHE). The underlying mechanisms remain unclear. Mismatch negativity (MMN) is an auditory event-related potential that reflects an attentional trigger. Patients with schizophrenia show impaired attention and cognitive function, which are reflected in altered MMN. We hypothesized that patients with MHE, similarly to those with schizophrenia, should show MMN alterations related with attention deficits. The aims of this work were to assess whether (1) MMN is altered in cirrhotic patients with MHE, compared to those without MHE, (2) MMN changes in parallel with performance in attention tests and/or MHE in a longitudinal study, and (3) MMN predicts performance in attention tests and/or in the Psychometric Hepatic Encephalopathy Score (PHES). We performed MMN analysis as well as attention and coordination tests in 34 control subjects and in 37 patients with liver cirrhosis without MHE and 23 with MHE. Patients with MHE show reduced performance in selective and sustained attention tests and in visuomotor and bimanual coordination tests. The MMN wave area was reduced in patients with MHE, but not in those without MHE. In the longitudinal study, MMN area improved in parallel with performance in attention tests and PHES in 4 patients and worsened in parallel in another 4. Logistic regression analyses showed that MMN area predicts performance in attention tests and in PHES, but not in other tests or critical flicker frequency. Receiver operating characteristic curve analyses showed that MMN area predicts attention deficits in the number connection tests A and B, Stroop tasks, and MHE, with sensitivities of 75%-90% and specificities of 76%-83%. CONCLUSION: MMN area is useful to diagnose attention deficits and MHE in patients with liver cirrhosis.

Chronic hyperammonemia alters the circadian rhythms of corticosteroid hormone levels and of motor activity in rats.

Patients with liver cirrhosis may present hepatic encephalopathy with a wide range of neurological disturbances and alterations in sleep quality and in the sleep-wake circadian rhythm. Hyperammonemia is a main contributor to the neurological alterations in hepatic encephalopathy. We have assessed, in an animal model of chronic hyperammonemia without liver failure, the effects of hyperammonemia per se on the circadian rhythms of motor activity, temperature, and plasma levels of adrenal corticosteroid hormones. Chronic hyperammonemia alters the circadian rhythms of locomotor activity and of cortisol and corticosterone levels in blood. Different types of motor activity are affected differentially. Hyperammonemia significantly alters the rhythm of spontaneous ambulatory activity, reducing strongly ambulatory counts and slightly average velocity during the night (the active phase) but not during the day, resulting in altered circadian rhythms. In contrast, hyperammonemia did not affect wheel running at all, indicating that it affects spontaneous but not voluntary activity. Vertical activity was affected only very slightly, indicating that hyperammonemia does not induce anxiety. Hyperammonemia abolished completely the circadian rhythm of corticosteroid hormones in plasma, completely eliminating the peaks of cortisol and corticosterone present in control rats at the start of the dark period. The data reported show that chronic hyperammonemia, similar to that present in patients with liver cirrhosis, alters the circadian rhythms of corticosteroid hormones and of motor activity. This suggests that hyperammonemia would be a relevant contributor to the alterations in corticosteroid hormones and in circadian rhythms in patients with liver cirrhosis.

Mechanisms of cognitive alterations in hyperammonemia and hepatic encephalopathy: therapeutical implications.

Patients with liver diseases (e.g. cirrhosis) may present hepatic encephalopathy (HE), an alteration in cerebral function which is a consequence of previous failure of liver function. Patients with minimal or clinical HE present different levels of cognitive impairment. Hyperammonemia is considered a main contributor to the neurological alterations in HE. Animal models of chronic HE (e.g. rats with portacaval shunts) or of "pure" hyperammonemia also show impaired cognitive function. The studies summarized here show that the impairment of some types of cognitive function in chronic HE is due to the impaired function of the glutamate-nitric oxide-cGMP pathway in brain. Both hyperammonemia and neuroinflammation contribute to the impairment of the pathway and of cognitive function. Treatment of rats with chronic HE or hyperammonemia with inhibitors of phosphodiesterase 5 restores the function of the glutamate-nitric oxide-cGMP pathway and cGMP levels in brain as well as the ability to learn a Y maze conditional discrimination task. The same beneficial effects may be obtained by treating the rats chronically with an anti-inflammatory, ibuprofen. As the function of this pathway is also altered in brain of patients died in HE, this alteration would also contribute to cognitive impairment in patients with HE. Increasing cGMP by using inhibitors of phosphodiesterase 5 (PDE-5) or anti-inflammatories (under safe conditions) would be therefore a new therapeutic approach to improve learning and memory performance in individuals with minimal or clinical HE.

Glutamatergic and gabaergic neurotransmission and neuronal circuits in hepatic encephalopathy.

Patients with hepatic encephalopathy (HE) may present different neurological alterations including impaired cognitive function and altered motor activity and coordination. HE may lead to coma and death. Many of these neurological alterations are the consequence of altered neurotransmission. Hyperammonemia is a main contributor to the alterations in neurotransmission and in neurological functions in HE. Both glutamatergic and GABAergic neurotransmission are altered in animal models of HE. We review some of these alterations, especially those alterations in glutamatergic neurotransmission responsible for some specific neurological alterations in hyperammonemia and HE: the role 1) of excessive NMDA receptors activation in death induced by acute hyperammonemia; 2) of impaired function of the glutamate-nitric oxide-cGMP pathway, associated to NMDA receptors, in cognitive impairment in chronic HE; 3) of increased extracellular glutamate and activation of metabotropic glutamate receptors in substantia nigra in hypokinesia in chronic HE. The therapeutic implications are discussed. We also review the alterations in the function of the neuronal circuits between basal ganglia-thalamus-cortex modulating motor activity and the role of sequential alterations in glutamatergic and GABAergic neurotransmission in these alterations. HE would be a consequence of altered neuronal communication due to alterations in general neurotransmission involving different neurotransmitter systems in different neurons.

Chronic hyperammonemia reduces the activity of neuronal nitric oxide synthase in cerebellum by altering its localization and increasing its phosphorylation by calcium-calmodulin kinase II.

Impaired function of the glutamate-nitric oxide-cGMP pathway contributes to cognitive impairment in hyperammonemia and hepatic encephalopathy. The mechanisms by which hyperammonemia impairs this pathway remain unclear. Understanding these mechanisms would allow designing clinical treatments for cognitive deficits in hepatic encephalopathy. The aims of this work were: (i) to assess whether chronic hyperammonemia in vivo alters basal activity of neuronal nitric oxide synthase (nNOS) in cerebellum and/or its activation in response to NMDA receptor activation and (ii) to analyse the molecular mechanisms by which hyperammonemia induces these alterations. It is shown that hyperammonemia reduces both basal activity of nNOS and its activation following NMDA receptor activation. Reduced basal activity is because of increased phosphorylation in Ser847 (by 69%) which reduces basal activity of nNOS by about 40%. Increased phosphorylation of nNOS in Ser847 is because of increased activity of calcium-calmodulin-dependent protein kinases (CaMKII) which in turn is because of increased phosphorylation at Thr286. Inhibiting CaMKII with KN-62 normalizes phosphorylation of Ser847 and basal NOS activity in hyperammonemic rats, returning to values similar to controls. Reduced activation of nNOS in response to NMDA receptor activation in hyperammonemia is because of altered subcellular localization of nNOS, with reduced amount in post-synaptic membranes and increased amount in the cytosol.

NMDA receptors in hyperammonemia and hepatic encephalopathy.

The NMDA type of glutamate receptors modulates learning and memory. Excessive activation of NMDA receptors leads to neuronal degeneration and death. Hyperammonemia and liver failure alter the function of NMDA receptors and of some associated signal transduction pathways. The alterations are different in acute and chronic hyperammonemia and liver failure. Acute intoxication with large doses of ammonia (and probably acute liver failure) leads to excessive NMDA receptors activation, which is responsible for ammonia-induced death. In contrast, chronic hyperammonemia induces adaptive responses resulting in impairment of signal transduction associated to NMDA receptors. The function of the glutamate-nitric oxide-cGMP pathway is impaired in brain in vivo in animal models of chronic liver failure or hyperammonemia and in homogenates from brains of patients died in hepatic encephalopathy. The impairment of this pathway leads to reduced cGMP and contributes to impaired cognitive function in hepatic encephalopathy. Learning ability is reduced in animal models of chronic liver failure and hyperammonemia and is restored by pharmacological manipulation of brain cGMP by administering phosphodiesterase inhibitors (zaprinast or sildenafil) or cGMP itself. NMDA receptors are therefore involved both in death induced by acute ammonia toxicity (and likely by acute liver failure) and in cognitive impairment in hepatic encephalopathy.

Altered modulation of motor activity by group I metabotropic glutamate receptors in the nucleus accumbens in hyperammonemic rats.

One of the neurological complications in hepatic encephalopathy is the impairment of motor coordination and function. Clinical signs of basal ganglia, cortico-spinal and cerebellar dysfunction have been commonly detected in these patients. We are studying the molecular bases of the alterations in motor coordination and function in hepatic encephalopathy. Hyperammonemia is considered the main factor responsible for the neurological alterations in patients with hepatic encephalopathy. Activation of metabotropic glutamate receptors (mGluRs) in the nucleus accumbens (NAcc) induces locomotion in rats. Asa first step in our studies on the alterations in motor co-ordination and function in hyperammonemia and hepatic encephalopathy we studied whether the control of motor function by mGluRs in the NAcc is altered in hyperammonemic rats. The locomotor activity induced by injection into the nucleus accumbens (NAcc) of DHPG, an agonist of group I mGluRs was significantly increased in hyperammonemic rats. Injection of DHPG increased extracellular dopamine but not glutamate in the NAcc of control rats. In hyperammonemic rats DHPG-induced increase in dopamine was significantly reduced, and extracellular glutamate increased 6-fold. The content of mGluR 1 but not mGluR 5, is increased in the NAcc of hyperammonemic rats. Blockade of mGluR 1 completely prevented motor and neurochemical effects induced by DHPG. These results show that modulation of both motor function and extracellular concentration of neurotransmitters by mGluRs in the NAcc is altered in hyperammonemia. This may contribute to the alterations in motor function in hepatic encephalopathy.