The course of depressive symptoms during the postmenopause: a review

As the Australian population ages, significantly more women are entering the postmenopausal stage of the climacteric, yet research focusing on the prevalence of depressive symptoms in this stage of ovarian ageing is scarce. This review will examine the information provided by studies that have a cohort with data of adequate duration to explore depressive symptom prevalence in the early and late postmenopause. Longitudinal epidemiological studies of women transitioning through the postmenopause that included measures of mood and/or depressive symptoms were identified through searches of MEDLINE (1980-2014) and PsycINFO (1980-2014) databases. Population based studies with at least two time points of assessment were included. Longitudinal studies of ageing that did not categorise women as postmenopausal were not included, as this was outside the scope of this review. Prevalence estimates of depressive symptoms varied between studies and ranged from 8.5 % to 25.7 % with percentages between 22 and 25 % being most consistently reported. Surgical postmenopause groups reported higher ratings of depressive symptoms at 18-42 % and higher incidence of major depressive disorder in all but one study. The prevalence of Major Depressive Disorder also varied with ranges from <1 % to 42 % reported. Wide ranges in prevalence were reported in the literature. Differences in definitions, inconsistent sample sizes and varying measures make it difficult to compare results across studies. The specific inclusions and exclusions of sub-samples of larger cohorts are at times inconsistent with epidemiological acquisition and, as such, impact upon generalizability of results to a healthy population

Galanin receptors in human basal forebrain differ from receptors in the hypothalamus: Characterization using [\u3csup\u3e125\u3c/sup\u3eI]galanin (porcine) and [\u3csup\u3e125\u3c/sup\u3eI]galantide

Galanin, a 29-amino acid peptide, is uniquely distributed in human basal forebrain and may play a role in cholinergic cell dysfunction in Alzheimer\u27s disease. We report a detailed evaluation of galanin receptors in human basal forebrain (67 ± 12 years) and hypothalamus (67 ± 15 years) with radioligand binding techniques. The binding of [125I]galanin (porcine) (agonist) or [125I]galantide [GAL (1-3)-substance P (5-11)-NH2] (putative antagonist) saturated in 2 hr, and only 15% to 30% of either radioligand was removed in the presence of unlabeled peptide. [125I]Galanin or [125I]galantide binding in basal forebrain revealed similar B(max) values, with [125I]galanin having a higher affinity for the galanin receptor. In contrast, [125I]galanin showed a lower affinity and labeled 42% more receptors than [125I]galantide in the hypothalamus. Differences were noted in competition studies of galanin and galanin chimeric peptides (M15, M35, M40 and C7) between [125I]galanin and [125I]galantide binding and in both regions. M35, M40 and C7 showed high affinity for galanin receptors in the hypothalamus with Hill coefficients close to unity, whereas in the basal forebrain these peptides competed differently. 5\u27-Guanylylimidodiphosphate reduced the specific binding of either radioligand in both regions. Based on the derived data, both radioligands irreversibly bind with high affinity and act as agonists at galanin receptors in human basal forebrain and hypothalamus. Galanin and galanin chimeric peptides compete differently for galanin receptors depending on the radioligand and region tested, suggesting subtype differences

Galanin receptor plasticity within the nucleus basalis in early and late Alzheimer\u27s disease: An in vitro autoradiographic analysis

Hypertrophy of fibers containing galanin (GAL), the inhibitory neurotransmitter of acetylcholine, occur on remaining cholinergic nucleus basalis neurons in late stage Alzheimer\u27s disease (AD). The present investigation evaluated whether changes in the number of GAL receptors (GALR) were detectable within the nucleus basalis in the early or late stage of AD when compared to age-matched controls. Postmortem neuropathological specimens were obtained at autopsy from three groups: late AD, early (possible) AD, and normal (age-matched controls) human subjects. Autoradiography of GALR binding was performed on human brain sections from each of the three groups. Analysis of autoradiographic images show no change in the distribution of ([125])hGAL binding sites in early AD cases throughout the nucleus basalis. In contrast, the number of ([125])hGAL binding sites was increased over the anterior nucleus basalis subfield in late stage AD. A region-of-interest densitometric analysis of the anterior nucleus basalis in the late stage AD cases depict an increase in the number of ([125])hGAL binding sites by approximately two-three-fold when compared to normal (age-matched controls). Quantitative measures of ([125])hGAL binding densities were not significantly different in the anterolateral, intermediate or posterior nucleus basalis subsectors of early or late stage AD when compared to age-matched controls. These observations show that the occurrence of overexpression of GALRs coincide with earlier reports showing galaninergic fibers hyperinnervating surviving cholinergic basal forebrain neurons in late stage AD. Copyright (C) 2000 Elsevier Science Ltd

Characterization and localization of galanin receptors in human entorhinal cortex

The neuropeptide galanin (GAL) has a widespread distribution throughout the human cortex. The entorhinal cortex (ENT) plays a crucial role in the transfer of cortico-cortical information related to memory and displays severe degeneration in Alzheimer\u27s disease (AD). However, very little is known about the pharmacology of the GAL receptor (GALR) in normal human ENT. Therefore, we pharmacologically visualized their distribution and characterized GALRs using in vitro receptor autoradiography and radioligand binding assays. Autoradiograms revealed intense GALR labeling, mainly in the substantia innominata, hypothalamus, the bed nucleus of the stria terminalis and within layers 2 and 4 of the ENT. Kinetic experiments showed that saturation of GALR sites by [125I]GAL (human) (hGAL) occurred within 2 h and that this binding readily reversed in the presence of a GTP analog, but not in the presence of excess unlabeled hGAL. Analysis of [125I]hGAL binding data from saturation experiments gave K(D) values of 98.6±21.6 pM, B(max) values of 52.9±32.4 fmol/mg protein and identified a high and low affinity state of the GALR. The presence of 5\u27-guanylylimidodiphosphate (GppNHp) or NaCl reduced the agonist labeling of hGALR in ENT membranes. Copyright (C) 1998 Elsevier Science B.V

The Role of the Selective Serotonin Reuptake Inhibitor Fluoxetine in Temperature Regulation in Ovariectomized Rat Models

Thermoregulation is an integrated network of neuroendocrine, autonomic and somatosensory responses. Thermoregulatory dysfunction occurs during fluctuations or decline of gonadal hormone levels and results in vasomotor symptoms such as hot flushes and/or night-time sweating. The neurotransmitter serotonin (5-HT), has been reported to play a role in thermoregulation via changes in extracellular 5-HT levels and/or activation of various 5-HT receptors. The purpose of this study was to evaluate the role of the selective 5-HT reuptake inhibitor (SSRI), fluoxetine (FLX), on temperature regulation using ovariectomized (OVX) rodent models of thermoregulation. Single, subcutaneous (s.c.) administration of FLX (3, 10, 30 and 60 mg/kg) dose-dependently reduced core body temperature (CBT). FLX at 3 and 10 mg/kg s.c. showed no statistically significant decrease on tail-skin temperature (TST), whereas at higher doses (30 and 60 mg/kg) a significant decrease in TST was noted in the telemetry model. To mimic chronic SSRI treatment, a 5-HT&lt;sub&gt;1A&lt;/sub&gt; antagonist (WAY-100635; 0.3 mg/kg) was administered 20 min prior to FLX (10 mg/kg). This combination showed no significant improvement on temperature dysfunction compared to FLX alone. Similarly, in a morphine-dependent model of temperature dysfunction FLX, was inactive at 10 mg/kg whereas the 30 and 60 mg/kg s.c. dose abated the naloxone-induced increase in TST by 55 and 81%, respectively. In summary, FLX affected CBT at all doses, but alleviated thermoregulatory dysfunction only at higher doses that are non-selective for the 5-HT system.</jats:p