Recent evidence has implicated neurokinin B (NKB) in the complex neuronal network mediating the effects of gonadal steroids on the regulation of gonadotrophin-releasing hormone (GnRH) secretion. Since the neurokinin 3 receptor (NK3R) is thought to mediate the effects of NKB at the cellular level, we determined the distribution of immunoreactive NK3R in the septal region, preoptic area (POA) and hypothalamus of the ewe. NK3R cells and/or fibres were found in areas including the bed nucleus of the stria terminalis, POA, anterior hypothalamic and perifornical areas, dopaminergic A15 region, dorsomedial and lateral hypothalamus, arcuate nucleus (ARC) and the ventral premammillary nucleus. We also used dual-label immunocytochemistry to determine whether a neuroanatomical basis for direct modulation of GnRH neurones by NKB was evident. No GnRH neurones at any rostral-caudal level were observed to contain NK3R immunoreactivity, although GnRH neurones and fibres were in proximity to NK3R-containing fibres. Because NKB fibres formed close contacts with NKB neurones in the ARC, we determined whether these NKB neurones also contained immunoreactive NK3R. In luteal-phase ewes, 64% ± 11 of NKB neurones colocalised NK3R. In summary, NK3R is distributed in areas of the sheep preoptic area and hypothalamus known to be involved in the control of reproductive neuroendocrine function. Colocalization of NK3R in NKB neurones of the ARC suggests a potential mechanism of autoregulation of this subpopulation; however, the lack of NK3R in GnRH neurones suggests that the actions of NKB on GnRH neurosecretory activity in the ewe are mediated indirectly via other neurones and/or neuropeptides.

In this review, we focus on the relationship among Parkinson’s disease (PD), stress and depression. Parkinson’s disease patients have a high risk of developing depression, and it is possible that stress contributes to the development of both pathologies. Stress dysfunction may have a role in the etiology of preclinical non-motor symptoms of PD (such as depression) and, later in the course of the disease, may worsen motor symptoms. However, relatively few studies have examined stress or depression and the injured nigrostriatal system. This review discusses the effects of stress on neurodegeneration and depression, and their association with the symptoms and progression of PD.

low HDL cholesterol was associated with depression, but this association was only significant for participants carrying one or two copies of the s-allele of the 5-HTTLPR gene, which are associated with depression in the context of environmental adversity. 9 One possible, albeit speculative, scenario would be that the brain has to handle increasing cumulative stress over time, which would decrease brain reserve and disrupt homeostatic systems. The ability of these systems to handle stress would be partly determined by susceptibility genes and partly by environmental factors, some of which would facilitate regeneration. One such factor could be HDL cholesterol. This study presented data showing that the 5-year probability of depression in older men increases as the plasma concentration of HDL cholesterol decreases. The link between low HDL cholesterol and depression seems physiologically plausible and the results of our analyses suggest that it might be causal. Sufficiently powered randomized trials are now required to determine whether the prevalence and incidence of depression in later life can be decreased by raising the plasma concentration of HDL cholesterol through diet, exercise or other effective interventions. 10