Risk factors associated with retinal vein occlusion.

AIMS: Retinal vein occlusion (RVO) is the most frequent retinal vascular disease after diabetic retinopathy in which arterial risk factors are much more relevant than venous factors. The objective was to evaluate the role of risk factors in the development of the first episode of RVO. SUBJECTS AND METHODS: One hundred patients with RVO [mean age 56 years, 42% females and mean body mass index (BMI) 27.5 kg/m(2)] were recruited consecutively from the outpatient clinic of a tertiary hospital in Valencia (Spain). All subjects underwent clinical assessment including anthropometric and blood pressure measurements and laboratory test including homocysteine, antiphospholipid antibodies (aPLAs) and thrombophilia studies. In half of the subjects, a carotid ultrasonography was performed. Three control populations matched by age, sex and BMI from different population-based studies were used to compare the levels and prevalence of arterial risk factors. One cohort of young patients with venous thromboembolic disease was used to compare the venous risk factors. RESULTS: Blood pressure levels and the prevalence of hypertension were significantly higher in the RVO population when compared with those for the general populations. There was also a large proportion of undiagnosed hypertension within the RVO group. Moreover, carotid evaluation revealed that a large proportion of patients with RVO had evidence of subclinical organ damage. In addition, homocysteine levels and prevalence of aPLAs were similar to the results obtained in our cohort of venous thromboembolic disease. CONCLUSIONS: The results indicate that hypertension is the key factor in the development of RVO, and that RVO can be the first manifestation of an undiagnosed hypertension. Furthermore, the majority of these patients had evidence of atherosclerotic disease. Among the venous factors, a thrombophilia study does not seem to be useful and only the prevalence of hyperhomocysteinaemia and aPLAs is higher than in the general population.

Spatio-temporal variation in the structure of a chromosomal polymorphism zone in the house mouse.

Several long-term temporal analyses of the structure of Robertsonian (Rb) hybrid zones in the western house mouse, Mus musculus domesticus, have been performed. Nevertheless, the detection of gradual or very rapid variations in a zone may be overlooked when the time elapsed between periods of study is too long. The Barcelona chromosomal polymorphism zone of the house mouse covers about 5000, km(2) around the city of Barcelona and is surrounded by 40 chromosome telocentric populations. Seven different metacentrics and mice with diploid numbers between 27 and 40 chromosomes and several fusions in heterozygous state (from one to seven) have been reported. We compare the present (period 2008-2010) and past (period 1996-2000) structure of this zone before examining its dynamics in more detail. Results indicate that there is not a Rb race in this area, which is consistent with the proposal that this zone was probably originated in situ, under a primary intergradation scenario. The lack of individuals with more than five metacentrics in heterozygous state in the current period suggests that selection acted against such mice. By contrast, this situation did not occur for mice with fewer than five fusions in heterozygous condition. Changes in human activity may affect the dynamics of gene flow between subpopulations, thus altering the chromosomal composition of certain sites. Although these local variations may have modified the clinal trend for certain metacentrics, the general staggered structure of the zone has not varied significantly in a decade.

Past and future of HIV infection. A document based on expert opinion.

HIV infection is now almost 40 years old. In this time, along with the catastrophe and tragedy that it has entailed, it has also represented the capacity of modern society to take on a challenge of this magnitude and to transform an almost uniformly lethal disease into a chronic illness, compatible with a practically normal personal and relationship life. This anniversary seemed an ideal moment to pause and reflect on the future of HIV infection, the challenges that remain to be addressed and the prospects for the immediate future. This reflection has to go beyond merely technical approaches, by specialized professionals, to also address social and ethical aspects. For this reason, the Health Sciences Foundation convened a group of experts in different aspects of this disease to discuss a series of questions that seemed pertinent to all those present. Each question was presented by one of the participants and discussed by the group. The document we offer is the result of this reflection.

Evolutionary modularity of the mouse mandible: dissecting the effect of chromosomal reorganizations and isolation by distance in a Robertsonian system of Mus musculus domesticus.

The mouse mandible consists of several morphogenetic units that are usually grouped into two main modules: the alveolar region and the ascending ramus. The genetic/ontogenetic modularity of the two regions implies that they might evolve independently to some extent. In particular, evolutionary modularity in quantitative traits could arise during chromosomal speciation due to lower gene flow in rearranged chromosomes. With the aim of uncovering the autonomous evolution of the mandible modules, the form variation of each of them was assessed in the house mouse Robertsonian system from Barcelona, in which chromosomal variation and geographical distance may act as isolation factors. The association between these factors and morphological changes was analysed to determine their contribution to the differentiation of each module. Although size changes in the two modules were highly correlated, shape changes were not, and their association with karyotype differences, but not geographical distance, was dependent on the module. The results support the existence of two evolutionary modules and highlight the importance of size in morphological integration of the mandible. They also suggest that geographical distance and chromosomal reorganizations reduce gene flow between karyotypically divergent populations, but although geographical distance represents a global barrier to gene flow, the isolation produced by a set of chromosomal reorganizations only affects particular modules, probably depending on the number and location of loci with effects on a particular morphological region.

Impact of cocaine on adult hippocampal neurogenesis in an animal model of differential propensity to drug abuse.

Hippocampal plasticity (e.g. neurogenesis) likely plays an important role in maintaining addictive behavior and/or relapse. This study assessed whether rats with differential propensity to drug-seeking behavior, bred Low-Responders (bLR) and bred High-Responders (bHR) to novelty, show differential neurogenesis regulation after cocaine exposure. Using specific immunological markers, we labeled distinct populations of adult stem cells in the dentate gyrus at different time-points of the cocaine sensitization process; Ki-67 for newly born cells, NeuroD for cells born partway, and 5-bromo-2'-deoxyuridine for older cells born prior to sensitization. Results show that: (i) bHRs exhibited greater psychomotor response to cocaine than bLRs; (ii) acute cocaine did not alter cell proliferation in bLR/bHR rats; (iii) chronic cocaine decreased cell proliferation in bLRs only, which became amplified through the course of abstinence; (iv) neither chronic cocaine nor cocaine abstinence affected the survival of immature neurons in either phenotype; (v) cocaine abstinence decreased survival of mature neurons in bHRs only, an effect that paralleled the greater psychomotor response to cocaine; and (vi) cocaine treatment did not affect the ratio of neurons to glia in bLR/bHR rats as most cells differentiated into neurons in both lines. Thus, cocaine exerts distinct effects on neurogenesis in bLR vs. bHR rats, with a decrease in the birth of new progenitor cells in bLRs and a suppression of the survival of new neurons in bHRs, which likely leads to an earlier decrease in formation of new connections. This latter effect in bHRs could contribute to their enhanced degree of cocaine-induced psychomotor behavioral sensitization.

Regulation of the extrinsic and intrinsic apoptotic pathways in the prefrontal cortex of short- and long-term human opiate abusers.

Opiate addiction is a chronic medical disorder characterized by drug tolerance and dependence, behavioral sensitization, vulnerability to compulsive relapse, and high mortality. In laboratory animals, the potential effect of opiate drugs to induce cell death by apoptosis is a controversial topic. This postmortem human brain study examined the status of the extrinsic and intrinsic apoptotic pathways in the prefrontal cortex of a large group of well-characterized heroin or methadone abusers. In these subjects (n=36), the immunocontent of apoptosis-1 protein (Fas) death receptor did not differ from that in age-, gender-, and postmortem delay-matched controls. In contrast, Fas-associated protein with death domain (FADD), the mediator of the death signal, was significantly decreased in the same brain samples (all addicts: 30%, n=36; short-term abuse (ST): 31%, n=15; long-term abuse (LT): 29%, n=21). The initiator caspase-8 was not altered, but FLIP(L) (Fas-associated protein with death domain-like interleukin-1beta-converting enzyme-inhibitory protein), a dominant inhibitor of caspase-8, was increased in LT addicts (19%). In the intrinsic pathway, the pro-apoptotic mitochondrial proteins Bax (Bcl-2-associated X protein) and AIF (apoptosis-inducing factor) remained unchanged, but cytochrome c was decreased (all addicts: 25%; ST: 31%; LT: 20%) and anti-apoptotic B-cell leukemia 2 (Bcl-2) increased in LT addicts (24%). The content of executioner caspase-3 and the pattern of cleavage of the nuclear enzyme poly-(ADP-ribose)-polymerase-1 (PARP-1) were similar in opiate addicts and control subjects. Taken together, the data revealed that the extrinsic and intrinsic canonical apoptotic pathways are not abnormally activated in the prefrontal cortex of opiate abusers. Instead, the chronic modulation of some of their components (downregulation of FADD and cytochrome c; upregulation of FLIP(L) and Bcl-2) suggests the induction of non-apoptotic actions by opiate drugs related to phenomena of synaptic plasticity in the brain. These neurochemical adaptations could play a major role in the development of opiate tolerance, sensitization and relapse in human addicts.

[Venous thromboembolism and liver cirrhosis]. / Enfermedad tromboembólica venosa y cirrosis hepática.

OBJECTIVE: despite the endogenous coagulopathy of cirrhosis, some patients do experience thrombophilic states. The American College of Chest Physicians failed to address the prevention and treatment of venous thromboembolism (VTE) occurring among these patients. This study aims to describe the characteristics of cirrhotics patients hospitalized in the last 15 years, and to use the experience gained. MATERIAL AND METHOD: we retrospectively reviewed all admissions for cirrhosis in our hospital from 1992 to 2007. A total of 17 patients had non-portal venous thromboembolic disease. We recorded risk factors, epidemiological and laboratory data, thrombosis characteristics, and treatment complications. RESULTS AND CONCLUSIONS: approximately 0.8% of all hospitalized patients with cirrhosis had a non-portal VTE despite the elevated INR and low platelet count. We found low serum albumin, acquired antithrombin III, protein C and protein S deficiency, presence of antiphospholipid antibodies, and hyperhomocisteinemia in blood tests. Many patients had hemorragic complications during anticoagulation therapy, and 35% needed blood transfusions.

Catastrophic antiphospholipid syndrome related to severe ovarian hyperstimulation.

Antiphospholipid syndrome (APS) is a cause of infertility and fetal loss. Ovarian stimulation can induce previously unknown APS. Ovarian hyperstimulation syndrome (OHS) is uncommon but potentially life-threatening, as well as catastrophic APS. A woman that simultaneously developed a severe OHS and a catastrophic APS is described in this paper. Both entities produced thrombotic cardiac and brain thrombosis. A peculiar mechanism of cardiac ischemia is also described. In spite of the life-threatening risk of this situation, the indication for preventive anti-aggregation and/or anticoagulation is not clear.

Biochemical and functional evidence of supersensitive platelet alpha 2-adrenoceptors in major affective disorder. Effect of long-term lithium carbonate treatment.

The hypothesis that depressive illness is related to supersensitive alpha 2-adrenoceptors in the brain has been tested indirectly in blood platelets. The binding of tritiated clonidine hydrochloride to platelet membranes, a ligand that labels only the high-affinity state of the alpha 2-adrenoceptor that is coupled with cell functions, and the aggregation response induced by epinephrine hydrochloride, which is the result of the activation of the high-affinity state, were measured and correlated in 13 patients with major affective disorder. Both the number of high-affinity binding sites and the aggregation response were increased in depressed patients. There was a negative and significant correlation between both measures in the same depressed patients. Treatment with lithium carbonate (Plenur [Spain]; Linthane, comparable US product) was associated with a decrease in the high-affinity state and with an increase in the aggregation response. Thus, major effective disorder may be related to a dysfunction of the high-affinity state of the alpha 2-adrenoceptor that recognizes agonists and mediates physiological effects.

Hippocampal cell fate regulation by chronic cocaine during periods of adolescent vulnerability: Consequences of cocaine exposure during adolescence on behavioral despair in adulthood.

Given that adolescence represents a critical moment for shaping adult behavior and may predispose to disease vulnerability later in life, the aim of this study was to find a vulnerable period during adolescence in which hippocampal cell fate regulation was altered by cocaine exposure, and to evaluate the long-term consequences of a cocaine experience during adolescence in affecting hippocampal plasticity and behavioral despair in adulthood. Study I: Male rats were treated with cocaine (15mg/kg, i.p.) or saline for 7 consecutive days during adolescence (early post-natal day (PND) 33-39, mid PND 40-46, late PND 47-53). Hippocampal plasticity (i.e., cell fate regulation, cell genesis) was evaluated 24h after the last treatment dose during the course of adolescence (PND 40, PND 47, PND 54). Study II: The consequences of cocaine exposure during adolescence (PND 33-39 or PND 33-46; 7 or 14days) were measured in adulthood at the behavioral (i.e., forced swim test, PND 62-63) and molecular (hippocampal cell markers, PND 64) levels. Chronic cocaine during early adolescence dysregulated FADD forms only in the hippocampus (HC), as compared to other brain regions, and during mid adolescence, impaired cell proliferation (Ki-67) and increased PARP-1 cleavage (a cell death maker) in the HC. Interestingly, chronic cocaine exposure during adolescence did not alter the time adult rats spent immobile in the forced swim test. These results suggest that this paradigm of chronic cocaine administration during adolescence did not contribute to the later manifestation of behavioral despair (i.e., one pro-depressive symptom) as measured by the forced swim test in adulthood.

Chronic morphine induces up-regulation of the pro-apoptotic Fas receptor and down-regulation of the anti-apoptotic Bcl-2 oncoprotein in rat brain.

1. This study was designed to assess the influence of activation and blockade of the endogenous opioid system in the brain on two key proteins involved in the regulation of programmed cell death: the pro-apoptotic Fas receptor and the anti-apoptotic Bcl-2 oncoprotein. 2. The acute treatment of rats with the mu-opioid receptor agonist morphine (3-30 mg x kg(-1), i.p., 2 h) did not modify the immunodensity of Fas or Bcl-2 proteins in the cerebral cortex. Similarly, the acute treatment with low and high doses of the antagonist naloxone (1 and 100 mg x kg(-1), i.p., 2 h) did not alter Fas or Bcl-2 protein expression in brain cortex. These results discounted a tonic regulation through opioid receptors on Fas and Bcl-2 proteins in rat brain. 3. Chronic morphine (10-100 mg x kg(-1), 5 days, and 10 mg x kg(-1), 13 days) induced marked increases (47-123%) in the immunodensity of Fas receptor in the cerebral cortex. In contrast, chronic morphine (5 and 13 days) decreased the immunodensity of Bcl-2 protein (15-30%) in brain cortex. Chronic naloxone (10 mg x kg(-1), 13 days) did not alter the immunodensities of Fas and Bcl-2 proteins in the cerebral cortex. 4. The concurrent chronic treatment (13 days) of naloxone (10 mg x kg(-1)) and morphine (10 mg x kg(-1)) completely prevented the morphine-induced increase in Fas receptor and decrease in Bcl-2 protein immunoreactivities in the cerebral cortex. 5. The results indicate that morphine, through the sustained activation of opioid receptors, can promote abnormal programmed cell death by enhancing the expression of pro-apoptotic Fas receptor protein and damping the expression of anti-apoptotic Bcl-2 oncoprotein.

Labelling of human platelet alpha 2-adrenoceptors with the full agonist [3H](-)adrenaline.

[3H](-)Adrenaline has been used to characterize alpha 2-adrenoceptors on human platelets. Although (-)adrenaline is a good substrate for the platelet enzyme MAO-B, enzymatic inhibition was not a prerequisite to quantify the specific binding of the radioligand to platelet membranes. At 25 degrees C the binding was rapid (t1/2 of association: 10.3 min), reversible (t1/2 of dissociation: 4.0 min) and linearly dependent on the amount of protein present in the assay. The binding sites for [3H](-)adrenaline showed the specificity required for an alpha 2-adrenoceptor. The rank order of potency of inhibitors of [3H](-)adrenaline binding was oxymetazoline greater than idazoxan congruent to phentolamine congruent to clonidine congruent to (-)adrenaline greater than (-)noradrenaline greater than yohimbine much much greater than phenylephrine much greater than prazosin greater than (+)propranolol. Moreover, the nucleotide guanosine triphosphate (GTP) inhibited in a concentration-dependent manner (10(-9)-10(-4) M) the specific binding of [3H](-)adrenaline, suggesting that the radioligand preferentially labelled the high affinity state of the alpha 2-adrenoceptor. Linear (Scatchard) and non-linear analyses of [3H](-)adrenaline binding indicated the existence of a single population of non-interacting sites (KD = 2.5-2.7 nM; Bmax = 49-53 fmol/mg protein). The binding characteristics for [3H](-)adrenaline were not affected by age and sex of the donors or by freezing of platelet-rich plasma. In the same subjects alpha 2-adrenoceptor density (Bmax) for the full agonist [3H](-)adrenaline was 2.9-fold lower than that quantitated by the selective antagonist [3H]yohimbine. The inhibition constants (Ki) of adrenergic drugs and of various antidepressant drugs in competing with [3H](-)adrenaline were correlated with the inhibition constants of these drugs in competing with [3H]clonidine (r = 0.96; P less than 0.001) which suggests that both radioligands labelled the same alpha 2-adrenoceptor on the human platelet. The binding of the full agonist [3H](-)adrenaline to human platelet membranes might be a useful tool for the study of dysfunctions related to the high affinity state of the alpha 2-adrenoceptor.

The arterial system of the abdominal viscera and the pelvis of the dormouse, Eliomys quercinus (Gliridae, Rodentia).

This paper deals with the origin, arrangement and variations of the abdominal and pelvic arteries in the garden dormouse, Eliomys quercinus. Fourteen latex-injected specimens (10 males, 4 females) were analysed by dissection. Measurements from the aortic bifurcation to the origin of the major arterial trunks were taken. The results obtained are compared with those reported for other myomorph rodents. The general arterial system of the dormouse basically agrees with the patterns observed in other rodent species. However, Eliomys quercinus shows some distinguishing features, such as the particular origin of the left and right gastric arteries, the distal arrangement of the deep circumflex iliac arteries, especially the right one, and the source of the medial femoral circumflex artery as a branch of the femoral artery.

Arterial vascularization of the abdominal and pelvic regions in the degu, Octodon degus (Rodentia, Octodontidae).

The abdominal and the pelvic arterial supply of the degu, Octodon degus, were described in 19 specimens (10 males and 9 females) from a laboratory strain. Animals were injected through the left ventricle of the heart with coloured latex solution and subsequently dissected under a surgical microscope. The arrangement and variations of the visceral and muscular arteries were described. Comparative analysis among rodents revealed that, even though there was a wide range of interspecific variation in the characters considered, there were several constant anatomical features with phylogenetic value. In this sense, results on the degu and the guinea pig, Cavia porcellus, showed that these hystricognaths share particular features that differentiate them from the sciurognaths analysed to date. The distinguishing characteristics between these two groups of rodents were found in the arrangement of the coeliacomesenteric trunk, and in the cranial abdominal, right gastric, caudal mesenteric, and deep circumflex iliac arteries. The phylogenetic meaning of particular angiological features in rodents were commented.

[Axillo-subclavian effort thrombosis: main characteristics]. / Trombosis de esfuerzo axilosubclavia. Características más relevantes.

OBJECTIVE: Effort related thrombosis of the axillo-subclavian vein is a disabling disorder that occurs primarily in healthy young individuals. The aim of this study is to show our experience in diagnosis and therapy of this entity. METHODS: During a 5 years period (1994 to 1998) we studied 7 patients (6 woman and 1 man), with an average age of 26 years old. All patients underwent Doppler ultrasound examinations and, later, venography of the affected upper extremity. All of them were treated at the outset with systemic infusion of fibrinolytic agents. RESULTS: Only one patient manifested successfully clinic outcome. Five patients were treated with surgical decompression resulting in excellent function. One patient refused surgical treatment, and he was treated with warfarin sodium showing a poor clinic response. CONCLUSION: Although systemic fibrinolytic therapy can restore axillo-subclavian vein patency, surgical approach is necessary to relieve the external compression.

[Pneumocystis carinii pneumonia]. / La neumonía por Pneumocystis carinii.

We present twelve cases of Pneumocystis Carinii Pneumonia (PCP) hospitalized at the Internal Medicine Service of the Hospital Clínico de Valencia between 1989 and 1990. All patients were infected by HIV-1, with ages between 25 and 32 years, with circulating CD4 lymphocytes lower than 25% or 200 cells per cubic millimeter and with positive p24 antigen. Ten of them were parenterally drug addicts and two of them, homosexuals. Diagnosis was made by fibrobronchoscopy (FB) with bronchoaspiration (BAS) and bronchoalveolar lavage (BAL), or sputum induced by physiological serum aerosol at three per cent, using in both cases blue tinction with toluidine 0 of the samples obtained. Given the foreseeable increase of this disease in our country, we stress the risk of a potential change in its clinical spectrum, affecting new population groups, mainly the elderly, as well as the development of new early diagnosis techniques and the emergence of new treatments, including corticotherapy.

FADD adaptor and PEA-15/ERK1/2 partners in major depression and schizophrenia postmortem brains: basal contents and effects of psychotropic treatments.

Enhanced brain apoptosis (neurons and glia) may be involved in major depression (MD) and schizophrenia (SZ), mainly through the activation of the intrinsic (mitochondrial) apoptotic pathway. In the extrinsic death pathway, pro-apoptotic Fas-associated death domain (FADD) adaptor and its non-apoptotic p-Ser194 FADD form have critical roles interacting with other death regulators such as phosphoprotein enriched in astrocytes of 15 kDa (PEA-15) and extracellular signal-regulated kinase (ERK). The basal status of FADD (protein and messenger RNA (mRNA)) and the effects of psychotropic drugs (detected in blood/urine samples) were first assessed in postmortem prefrontal cortex of MD and SZ subjects (including a non-MD/SZ suicide group). In MD, p-FADD, but not total FADD (and mRNA), was increased (26%, n=24; all MD subjects) as well as p-FADD/FADD ratio (a pro-survival marker) in antidepressant-free MD subjects (50%, n=10). In contrast, cortical FADD (and mRNA), p-FADD, and p-FADD/FADD were not altered in SZ brains (n=21) regardless of antipsychotic medications (except enhanced mRNA in treated subjects). Similar negative results were quantified in the non-MD/SZ suicide group. In MD, the regulation of multifunctional PEA-15 (i.e., p-Ser116 PEA-15 blocks pro-apoptotic FADD and PEA-15 prevents pro-survival ERK action) and the modulation of p-ERK1/2 were also investigated. Cortical p-PEA-15 was not changed whereas PEA-15 was increased mainly in antidepressant-treated subjects (16-20%). Interestingly, cortical p-ERK1/2/ERK1/2 ratio was reduced (33%) in antidepressant-free when compared to antidepressant-treated MD subjects. The neurochemical adaptations of brain FADD (increased p-FADD and pro-survival p-FADD/FADD ratio), as well as its interaction with PEA-15, could play a major role to counteract the known activation of the mitochondrial apoptotic pathway in MD.

Differential impact of a complex environment on positive affect in an animal model of individual differences in emotionality.

Anhedonia, or the inability to experience positive feelings is a hallmark of depression. However, few animal models have relied on decreased positive affect as an index of susceptibility to depression. Rats emit frequency-modulated ultrasonic vocalizations (USVs), designated as "positive" calls in the 50-kHz range. USVs have been associated with pharmacological activation of motivational reward circuits. Here we utilized selectively-bred rats differing in "emotionality" to ask whether there are associated differences in USVs. Rats bred based on locomotor response to novelty and classified as bred High Responders (bHRs) or bred Low Responders (bLRs) exhibit inborn differences in response to environmental cues, stress responsiveness, and depression-like behavior. These animals also exhibit differences in anxiety-like behavior, which are reversed by exposure to environmental complexity (EC). Finally, these animals exhibit unique profiles of responsiveness to rewarding stimuli accompanied with distinct patterns of dopamine regulation. We investigated whether acute and chronic environmental manipulations impacted USVs in bHRs and bLRs. We found that, relative to bLRs, bHRs emitted significantly more 50-kHz USVs. However, if a bLR is accompanied by another bLR, there is a significant increase in 50-kHZ USVs emitted by this phenotype. bHRs emitted increases in 50-kHZ UVSs upon first exposure to EC, whereas bLRs showed a similar increase only after repeated exposure. bLRs' increase in positive affect after chronic EC was coupled with significant positive correlations between corticosterone levels and c-fos mRNA in the accumbens. Conversely, a decline in the rate of positive calls in bHRs after chronic EC was associated with a negative correlation between corticosterone and accumbens c-fos mRNA. These studies demonstrate that inborn differences in emotionality interact with the environment to influence positive affect and underscore the potential interaction between glucocorticoids and the mesolimbic reward circuitry in modulating 50-kHz calls.

The melanin-concentrating hormone (MCH) system in an animal model of depression-like behavior.

Selective breeding for divergence in locomotion in a novel environment (bHR, bred High-Responder; bLR, bred Low-Responder) correlates with stress-reactivity, spontaneous anxiety-like behaviors and predicts vulnerability in a rodent model of depression. Identifying genetic factors that may account for such vulnerability are key determinants not only for the illness outcome but also for the development of better-tailored treatment options. Melanin-concentrating hormone (MCH) is a neuropeptide that exhibits some of the hallmarks of a regulator of affective states. The aim of this study was to ascertain the role of the MCH system in depression-like behaviors in bHR vs. bLR rats. bLR rats showed a 44% increase in hypothalamic pMCH mRNA and a 14% decrease in hippocampal CA1 MCH1R mRNA when compared to bHR rats. Interestingly, the amount of time that rats spent immobile in the FST (depressive-like behavior) correlated positively with the amount of hypothalamic pMCH mRNA and negatively with that of hippocampal CA1 MCH1R. The results indicate that the bLR-bHR is a useful rat model to investigate individual basal genetic differences that participate in the monitoring of emotional responsiveness (i.e., depression- and anxiety-like behaviors). They also point to the MCH system (i.e., chronically higher pMCH expression and consequently receptor down-regulation) as a candidate biomarker for the severity of depressive-like behavior. The data indicate that MCH1R participates in the modulation of depression-like behavior through a process that involves the CA1 region of the hippocampus, supporting the possible use of MCH1R antagonists in the treatment of depression.