Mental health services implementation in Colombia-A systematic review.

Colombia's mental health services have a complex history shaped by 60 years of armed conflict, a predominantly clinical approach to mental health, and social factors such as inequities and stigma. The 1990 Caracas declaration proposed a shift towards decentralised community mental health services and interventions based on the recovery approach and emphasis on social determinants of mental health in the Americas. Colombia has adopted these approaches in its legal and practical framework in recent years, but implementation has been uneven. This systematic review aims to contribute to mental health services understanding in Colombia by examining the barriers and facilitators to the implementation of mental health services in Colombia. A search was conducted to explore available peer-reviewed studies on Colombian mental health services across five databases (Medline, PubMed, Scopus, Scielo and BVS) on quantitative and qualitative research papers published in the last ten years and without language restrictions. The Consolidated Framework for Implementation Research (CFIR) was used to structure the analysis and identify barriers and facilitators during the implementation of mental health services. We adapted the CFIR to attend to gender, race and age informed by the Socio-Political Economy of Global Mental Health framework, given the importance of these factors to the Colombian health landscape. Finally, narrative synthesis was used to summarise the data. 1 530 records were identified, and 12 articles met all inclusion criteria and were included in the analysis. 8 papers described substance use disorders services, 11 involved multidisciplinary healthcare professionals, and 7 were implemented at a local scale. The primary barriers to implementation were the lack of coordination, high workloads, and low funding. Facilitators included the use of protocols, and the involvement of communities, stakeholders, users, and external champions. Findings suggest the continued importance of community and recovery approaches and efforts to improve coordination between multi-sector actors involved in the mental health spaces (e.g., public, and private organisations, users and their families).

Think global, act local: using a translocal approach to understand community-based organisations' responses to planetary health crises during COVID-19.

Little is known on how community-based responses to planetary health crises, such as the COVID-19 pandemic, can integrate concerns about livelihoods, equity, health, wellbeing, and the environment. We used a translocal learning approach to co-develop insights on community-based responses to complex health and environmental and economic crises with leaders from five organisations working with communities at the front line of intersecting planetary health challenges in Finland, India, Kenya, Peru, and the USA. Translocal learning supports collective knowledge production across different localities in ways that value local perspectives but transcend national boundaries. There were three main findings from the translocal learning process. First, thanks to their proximity to the communities they served, community-based organisations (CBOs) can quickly identify the ways in which COVID-19 might worsen existing social and health inequities. Second, localised CBO actions are key to supporting communities with unique challenges in the face of systemic planetary health crises. Third, CBOs can develop rights-based, ecologically-minded actions responding to local priorities and mobilising available resources. Our findings show how solutions to planetary health might come from small-scale community initiatives that are well connected within and across contexts. Locally-focused globally-aware actions should be harnessed through greater recognition, funding, and networking opportunities. Globally, planetary health initiatives should be supported by applying the principles of subsidiarity and translocalism.

Calcitriol protects against reductions in striatal serotonin in rats treated with neurotoxic doses of methamphetamine.

The present experiments were designed to examine the ability of calcitriol to protect against methamphetamine (METH)-induced reductions in striatal serotonin (5-HT) release and content. Male Fischer-344 rats were administered vehicle or calcitriol (0.3, 1.0, or 3.0 µg/kg, s.c.) once a day for 8 consecutive days. After the seventh day of treatment the animals were given METH (5 mg/kg, s.c.) or saline 4 times in 1 day at 2 h intervals. Seven days after the METH or saline treatments in vivo microdialysis experiments were conducted to measure potassium and d-amphetamine evoked overflow of 5-HT from the striatum. In animals treated with vehicle and METH there were significant reductions in both potassium and d-amphetamine evoked overflow of 5-HT. The 1.0 and 3.0 µg/kg/day doses of calcitriol provided significant protection against the 5-HT depleting effects of METH. A similar pattern of neuroprotection was found for post-mortem tissue levels of 5-HT. The calcitriol treatments did not prevent hyperthermia during the multiple injections of METH, indicating that the protective effects of calcitriol are not due to prevention of METH-induced increases in body temperature. These results suggest that calcitriol can provide significant protection against the 5-HT depleting effects of neurotoxic doses of METH.

Synthesising the shifting terminology of community health: A critiquing review of agent-based approaches.

The field of community health promotion encompasses a wide range of approaches, including bottom-up approaches that recognise and build on the agency and strengths of communities to define and pursue their health goals. Momentum towards agent-based approaches to community health promotion has grown in recent years, and several related but distinct conceptual and methodological bodies of work have developed largely in isolation from each other. The lack of a cohesive collection of research, practice, and policy has made it difficult to learn from the innovations, best practices, and shortcomings of these approaches, which is exacerbated by the imprecise and inconsistent use of related terms. This article provides a review of three agent-based approaches to promoting community health: asset-based approaches, capacity building, and capabilities approaches, noting the theoretical origins and fundamental concepts, applications and methodologies, and limitations and critiques of each. This article discusses their commonalities and differences in terms of how they conceptualise and approach the promotion of community health, including a critical consideration of their limitations and where they may prove to be counterproductive. This article argues that agent-based approaches to community health must be met with meaningful opportunities to disengage from the structures that constrain their health.

Toward resourcefulness: pathways for community positive health.

Communities are powerful and necessary agents for defining and pursuing their health, but outside organizations often adopt community health promotion approaches that are patronizing and top-down. Conversely, bottom-up approaches that build on and mobilize community health assets are often critiqued for tasking the most vulnerable and marginalized communities to use their own limited resources without real opportunities for change. Taking into consideration these community health promotion shortcomings, this article asks how communities may be most effectively and appropriately supported in pursuing their health. This article reviews how community health is understood, moving from negative to positive conceptualizations; how it is determined, moving from a risk-factor orientation to social determination; and how it is promoted, moving from top-down to bottom-up approaches. Building on these understandings, we offer the concept of 'resourcefulness' as an approach to strengthen positive health for communities, and we discuss how it engages with three interrelated tensions in community health promotion: resources and sustainability, interdependence and autonomy, and community diversity and inclusion. We make practical suggestions for outside organizations to apply resourcefulness as a process-based, place-based, and relational approach to community health promotion, arguing that resourcefulness can forge new pathways to sustainable and self-sustaining community positive health.

Delivering the Promise of Sendai Framework for Disaster Risk Reduction in Fragile and Conflict-Affected Contexts (FCAC): A Case Study of the NGO GOAL's Response to the Syria Conflict.

The Sendai Framework for Disaster Risk Reduction (SFDRR) has helped to reduce global disaster risk, but there has been a lack of progress in disaster risk reduction (DRR) for people living in fragile and conflict affected contexts (FCAC). Given the mounting evidence that DRR cannot be implemented through conventional approaches in FCAC, serious efforts must be made to understand how to meet SFDRR's goals. This paper offers a case study of international non-governmental organization GOAL's programming that responds to the protracted crisis in Syria, with critical discussion on SFDRR and how to adapt humanitarian relief and disaster resilience.

Terra incognita: the contribution of disaster risk reduction in unpacking the sustainability-peace nexus.

The pursuit of sustainable development in the context of global environmental change requires enhanced capability to deal with changing hazard profiles, across scales and geographies. Humans attempt to manage human and natural systems interactions in ways that minimize disaster risks, and the political expression of this ambition is the Sendai Framework for Disaster Risk Reduction 2015-2030 ('Sendai Framework'). These efforts lay the foundation for sustainable development, as since the onset of the Sendai Framework, the policy objective of disaster risk reduction has been explicitly linked to global progress on the Sustainable Development Goals. Separately, peace is a focal point of SDG 16, and widely regarded as foundational to attainment of all SDGs. Meanwhile in academic and policy arenas throughout the 2000s, evidence attests of the amplifying negative impact of climate-related disaster events on increasing violent conflict. What remains underexplored are questions of whether and how effective management of human and natural systems interaction, through disaster risk reduction, can contribute towards conditions of peace through peacebuilding. This paper explores how delivery of the Sendai Framework is necessary for sustainability, and potentially also for peace. In the context of the sustainability-peace nexus, the contribution of disaster risk reduction is terra incognita. This paper aims to deepen understanding of those under-researched tripartite links.

Reduced ability of calcitriol to promote augmented dopamine release in the lesioned striatum of aged rats.

Parkinson's disease (PD) is a progressive and debilitating neurodegenerative disorder that affects over one million people in the United States. Previous studies, carried out in young adult rats, have shown that calcitriol, the active metabolite of vitamin D, can be neuroprotective in 6-hydroxydopamine (6-OHDA) models of PD. However, as PD usually affects older individuals, the ability of calcitriol to promote dopaminergic recovery was examined in lesioned young adult (4 month old), middle-aged (14 month old) and aged (22 month old) rats. Animals were given a single injection of 12 µg 6-OHDA into the right striatum. Four weeks later they were administered vehicle or calcitriol (1.0 µg/kg, s.c.) once a day for eight consecutive days. In vivo microdialysis experiments were carried out three weeks after the calcitriol or vehicle treatments to measure potassium and amphetamine evoked overflow of DA from both the left and right striata. In control animals treated with 6-OHDA and vehicle there were significant reductions in evoked overflow of DA on the lesioned side of the brain compared to the contralateral side. The calcitriol treatments significantly increased evoked overflow of DA from the lesioned striatum in both the young adult and middle-aged rats. However, the calcitriol treatments did not significantly augment DA overflow in the aged rats. Postmortem tissue levels of striatal DA were also increased in the young and middle-aged animals, but not in the aged animals. In the substantia nigra, the calcitriol treatments led to increased levels of DA in all three age groups. Thus, the effects of calcitriol were similar in the young adult and middle-aged animals, but in the aged animals the effects of calcitriol were diminished. These results suggest that calcitriol may help promote recovery of dopaminergic functioning in injured nigrostriatal neurons; however, the effectiveness of calcitriol may be reduced in aging.

Calcitriol promotes augmented dopamine release in the lesioned striatum of 6-hydroxydopamine treated rats.

Current therapies for Parkinson's disease (PD) offer symptomatic relief but do not provide a cure or slow the disease process. Treatments that could halt progression of the disease or help restore function to damaged neurons would be of substantial benefit. Calcitriol, the active metabolite of vitamin D, has been shown to have significant effects on the brain. These effects include upregulating trophic factor levels, and reducing the severity of some central nervous system lesions. While previous studies have shown that calcitriol can be neuroprotective in 6-hydroxydopamine (6-OHDA) rodent models of PD, the present experiments were designed to examine the ability of calcitriol to promote restoration of extracellular dopamine (DA) levels and tissue content of DA in animals previously lesioned with 6-OHDA. Male Fischer-344 rats were given a single injection of 12 µg 6-OHDA into the right striatum. Four weeks later the animals were administered vehicle or calcitriol (0.3 or 1.0 µg/kg, s.c.) once a day for eight consecutive days. Three weeks after the calcitriol treatments in vivo microdialysis experiments were conducted to measure potassium and amphetamine evoked overflow of DA from both the left and right striata. In control animals treated with 6-OHDA and vehicle there were significant reductions in both potassium and amphetamine evoked overflow of DA on the lesioned side of the brain compared to the contralateral side. In animals treated with 6-OHDA followed by calcitriol there was significantly greater potassium and amphetamine evoked overflow of DA from the lesioned striatum compared to that from the control animals. The calcitriol treatments also led to increases in postmortem tissue levels of DA in the striatum and substantia nigra. These results suggest that calcitriol may help promote recovery of dopaminergic functioning in injured nigrostriatal neurons.

Evoked dopamine overflow is augmented in the striatum of calcitriol treated rats.

Calcitriol, the active metabolite of vitamin D, has been shown to have significant effects on the brain. These actions include reducing the severity of some central nervous system lesions, possibly by upregulating trophic factors such as glial cell line-derived neurotrophic factor (GDNF). GDNF has substantial effects on the nigrostriatal dopamine (DA) system of young adult, aged and lesioned animals. Thus, the administration of calcitriol may lead to significant effects on nigrostriatal DA neuron functioning. The present experiments were designed to examine the ability of calcitriol to alter striatal DA release, and striatal and nigral tissue levels of DA. Male Fischer-344 rats were administered vehicle or calcitriol (0.3, 1.0, or 3.0 µg/kg, s.c.) once daily for eight consecutive days. Three weeks later in vivo microdialysis experiments were conducted to measure basal and stimulus evoked overflow of DA from the striatum. Basal levels of extracellular DA were not significantly affected by the calcitriol treatments. However, the 1.0 and 3.0 µg/kg doses of calcitriol led to increases in both potassium and amphetamine evoked overflow of striatal DA. Although post-mortem tissue levels of striatal DA were not altered by the calcitriol injections, nigral tissue levels of DA and its main metabolites were increased by both the 1.0 and 3.0 µg/kg doses of calcitriol. In a separate group of animals GDNF levels were augmented in the striatum and substantia nigra after eight consecutive daily injections of calcitriol. These results suggest that systemically administered calcitriol can upregulate dopaminergic release processes in the striatum and DA levels in the substantia nigra. Increases in the levels of endogenous GDNF following calcitriol treatment may in part be responsible for these changes. The ability of calcitriol to lead to augmented DA release in the striatum suggests that calcitriol may be beneficial in disease processes involving dopaminergic dysfunction.

Neurturin protects against 6-hydroxydopamine-induced reductions in evoked dopamine overflow in rat striatum.

Neurturin (NTN), a member of the glial cell line-derived neurotrophic factor (GDNF) family, has substantial effects on normal and lesioned nigrostriatal dopamine systems. However, its ability to protect against toxin-induced loss of striatal dopamine release has not been previously reported. The goal of the present study was to determine if NTN could protect against 6-hydroxydopamine (6-OHDA)-induced reductions in striatal dopamine overflow and tissue levels of dopamine and to compare the effects of NTN with those of GDNF. Male Fischer-344 rats were given a single injection of vehicle, or 5 microg NTN or GDNF, into the right striatum. The following day the animals were given a single injection of 12 microg 6-OHDA into the striatum at the same site where the trophic factor was injected. Microdialysis experiments conducted three weeks later indicated that the 6-OHDA decreased basal levels of dopamine and metabolites in the lesioned striatum compared to the contralateral striatum, and NTN was able to partially protect against the 6-OHDA-induced reductions. Injection of NTN one day prior to 6-OHDA also led to significant protection against loss of both potassium- and amphetamine-evoked overflow of dopamine. The NTN treatments partially protected against 6-OHDA-induced reductions in striatal tissue levels of dopamine and completely protected against loss of nigral dopamine content. The protective effects of NTN were similar in magnitude to those of GDNF. These results support that within the experimental parameters used in this study, NTN is as effective as GDNF in protecting against the dopamine-depleting effects of intrastriatal 6-OHDA.

Neurturin effects on nigrostriatal dopamine release and content: comparison with GDNF.

Neurturin (NTN) is a member of the glial cell line-derived neurotrophic factor (GDNF) family; and, while GDNF has been shown to increase dopamine (DA) release in normal animals, the ability of NTN to alter DA release has not been previously reported. The purpose of the present study was to determine if NTN could alter striatal DA release, and to compare the effects of NTN to GDNF. Male Fischer-344 rats were given a single injection of vehicle or 5 microg NTN or GDNF into the right substantia nigra. Three weeks later microdialysis experiments were conducted to assess striatal DA release. Basal extracellular levels of striatal DA were not affected by either NTN or GDNF. However, both NTN and GDNF led to increases in amphetamine-evoked overflow of DA from the ipsilateral striatum, and there was a trend for potassium-evoked overflow to be augmented. Postmortem tissue levels of DA were decreased by approximately 20% in the striatum, and increased by approximately 100% in the substantia nigra, on the ipsilateral side of the brain compared to the contralateral side following both NTN and GDNF injection. Thus, NTN, like GDNF, can augment striatal DA release, and the magnitude of the NTN effects are similar to those of GDNF.

Strain difference in the up-regulation of FGF-2 protein following a neurotoxic lesion of the nigrostriatal pathway.

Lesions of the nigrostriatal pathway are known to induce a compensatory up-regulation of various neurotrophic factors. In this study we examined protein content of basic fibroblast growth factor (FGF-2) in tissue samples taken from the ventral midbrain and striatum at two different time points following a neurotoxic lesion of the nigrostriatal pathway in two different rat strains, the outbred Sprague-Dawley (SD) and inbred F344 9 Brown Norway F1 hybrid (F344BNF1). Despite both rat strains having comparable lesions of the nigrostriatal pathway, we observed a difference in the temporal up-regulation of FGF-2 in ventral midbrain samples taken from the side ipsilateral to the lesion. Basic FGF was significantly upregulated in ventral midbrain in SD rats 1 week post-lesion while we did not observe an up-regulation of FGF-2 in the lesioned ventral midbrain of F344BNF1 at this same time point. However, both strains showed a significant up-regulation of FGF-2 in the lesioned ventral midbrain 3 weeks post-lesion. Sprague-Dawley rats also appeared to be more sensitive to the lesion in terms of up-regulating FGF-2 expression. The differences reported here suggest currently unknown genetic differences between these two strains may be important factors for regulating the compensatory release of neurotrophic factors, such as FGF-2, in response to a neurotoxic lesion of the nigrostriatal pathway.

Calcitriol protects against the dopamine- and serotonin-depleting effects of neurotoxic doses of methamphetamine.

Repeated methamphetamine (METH) administration to animals can result in long-lasting decreases in brain dopamine (DA) and serotonin (5-HT) content. Calcitriol, the active metabolite of vitamin D, has potent effects on brain cells, both in vitro and in vivo, including the ability to upregulate trophic factors and protect against various lesions. The present experiments were designed to examine the ability of calcitriol to protect against METH-induced reductions in striatal and nucleus accumbens levels of DA and 5-HT. Male Fischer-344 rats were administered vehicle or calcitriol (1 microg/kg, s.c.) once a day for eight consecutive days. After the seventh day of treatment the animals were given METH (5 mg/kg, s.c.) or saline four times in 1 day at 2-h intervals. Seven days later the striata and accumbens were harvested from the animals for high-performance liquid chromatography (HPLC) analysis of monoamines and metabolites. In animals treated with vehicle and METH, there were significant reductions in DA, 5-HT, and their metabolites in both the striatum and accumbens. In animals treated with calcitriol and METH, the magnitude of the METH-induced reductions in DA, 5-HT, and metabolites was substantially and significantly attenuated. The calcitriol treatments did not reduce the hyperthermia associated with multiple injections of METH, indicating that the neuroprotective effects of calcitriol are not due to the prevention of increases in body temperature. These results suggest that calcitriol can provide significant protection against the DA- and 5-HT-depleting effects of neurotoxic doses of METH.

Protection by GDNF and other trophic factors against the dopamine-depleting effects of neurotoxic doses of methamphetamine.

Repeated methamphetamine (METH) administration to animals can result in long-lasting decreases in striatal dopamine (DA) content. It has previously been shown that glial cell line-derived neurotrophic factor (GDNF) can reduce the DA-depleting effects of neurotoxic doses of METH. However, there are several other trophic factors that are protective against dopaminergic toxins. Thus, the present experiments further investigated the protective effect of GDNF as well as the protective effects of several other trophic factors. Male Fischer-344 rats were given an intracerebral injection of trophic factor (2-10 microg) 1 day before METH (5 mg/kg, s.c., 4 injections at 2-h intervals). Seven days later DA levels in the striatum were measured using high-performance liquid chromatography (HPLC). Initial experiments indicated that only intrastriatal GDNF, and not intranigral GDNF, was protective. Thereafter, all other trophic factors were administered into the striatum. Members of the GDNF family (GDNF, neurturin, and artemin) all provided significant protection against the DA-depleting effects of METH, with GDNF providing the greatest protection. Brain-derived neurotrophic factor, neurotrophin-3, acidic fibroblast growth factor, basic fibroblast growth factor, ciliary neurotrophic factor, transforming growth factor-alpha (TGF-alpha), heregulin beta1 (HRG-beta1), and amphiregulin (AR) provided no significant protection at the doses examined. These results suggest that the GDNF family of trophic factors can provide significant protection against the DA-depleting effects of neurotoxic doses of METH.

Reductions in spontaneous locomotor activity in aged male, but not female, rats in a model of early Parkinson's disease.

The excessive loss of dopamine (DA) neurons that occurs with Parkinson's disease is usually confined to older individuals. While 6-hydroxydopamine (6-OHDA) is often used in animal models of DA neuron degeneration, there have been relatively few studies that have examined the effects of 6-OHDA in older animals. In the present study, we compared the effects of a bilateral, partial lesion with 6-OHDA in young (4 months), middle-aged (14 months), and aged (24 months) Fischer-344 rats of both sexes. Animals were given a single injection of vehicle or 100 mug 6-OHDA into the right lateral ventricle. Four weeks later, spontaneous locomotor activity was monitored. Microdialysis experiments were carried out 1 to 3 days later. The 6-OHDA treatments had no effect on horizontal activity or total distance traveled in young adults. However, with aged rats, there was a decrease in both measures in the vehicle-treated control rats compared to young adult controls, and a further decrease in the lesioned aged male rats. The 6-OHDA treatments led to significant decreases in both potassium- and amphetamine-evoked overflow of DA from the striatum in all groups. Thus, partial bilateral lesions of the nigrostriatal DA system led to decreases in evoked release of DA in the striatum of male and female rats of all three ages, but to changes in spontaneous activity only in the aged males. These results indicate that there are both age and sex differences in the brain's response to 6-OHDA, and imply that compensatory or neuroprotective mechanisms in the young brain and aged female brain are more efficient than in the aged male brain.

HIV-1 protein Tat potentiation of methamphetamine-induced decreases in evoked overflow of dopamine in the striatum of the rat.

HIV-1 infection of the brain can lead to the development of clinical syndromes reminiscent of Parkinson's disease, suggesting that HIV infection may damage nigrostriatal dopamine (DA) neurons. Although the responsible mechanisms have not been well defined, neurotoxic viral proteins, such as Tat, released from infected cells may be involved. Drug abuse is a major risk factor for contracting HIV infection. Methamphetamine (METH), a psychostimulant with high abuse potential, may also be toxic to brain DA neurons. Thus, the combination of METH abuse and HIV infection may lead to substantial alterations in DA neuron functioning. The present experiments examined how Tat, alone and with METH, affects DA release in the striatum. Male rats were given an intrastriatal injection of Tat (25 micro g) or vehicle 24 h before treatment with saline or neurotoxic doses of METH. Seven days later microdialysis studies were carried out to measure potassium- and amphetamine-evoked overflow of DA from the striatum. The Tat treatment alone led to no change in potassium-evoked overflow of DA, a 20% decrease in amphetamine-evoked overflow of DA, and a 16% decrease in striatal DA content. The METH alone led to a 37-42% decrease in striatal DA overflow and content. The combined treatment with Tat and METH led to significantly greater 70-78% decreases in striatal DA overflow and content. These results indicate that Tat enhances METH-induced reductions in striatal DA release and content, possibly in a synergistic manner, and suggest that METH abusers infected with HIV may be at increased risk for basal ganglia dysfunction.