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Contagious depression is a phenomenon that is yet to be fully recognized and this stems from insufficient material on the subject. At the moment, there is no existing format for studying the mechanism of action, prevention, containment, and treatment of contagious depression. The purpose of this study, therefore, was to establish the first animal model of contagious depression. Healthy rats can contract depressive behaviors if exposed to depressed rats. Depression is induced in rats by subjecting them to several manipulations of chronic unpredictable stress (CUS) over 5 weeks, as described in the protocol. A successful sucrose preference test confirmed the development of depression in the rats. The CUS-exposed rats were then caged with naïve rats from the contagion group (1 naïve rat/2 depressed rats in a cage) for an additional 5 weeks. 30 social groups were created from the combination of CUS-exposed rats and naïve rats. This proposed depression-contagion protocol in animals consists mainly of cohabiting CUS-exposed and healthy rats for 5 weeks. To ensure that this method works, a series of tests are carried out - first, the sucrose preference test upon inducing depression to rats, then, the sucrose preference test, alongside the open field and forced-swim tests at the end of the cohabitation period. Throughout the experiment, rats are given tags and are always returned to their cages after each test. A few limitations to this method are the weak differences recorded between the experimental and control groups in the sucrose preference test and the irreversible traumatic outcome of the forced swim test. These may be worth considering for suitability before any future application of the protocol. Nonetheless, following the experiment, naïve rats developed contagion depression after 5 weeks of sharing the same cage with the CUS-exposed rats.

The UFC analysis supports the behavioral analysis and thus, lends validity to our results.

Cadmiumclassified as a major carcinogen is considered a poisonous and unwanted heavy metal to a lot of tissues in many organisms. Of many publications already available, the general consensus is that the cadmium attenuating element is metallothionein (MT) through its interchangeable mechanism with Zn triggered by the presence of Cd, providing binding sites for Cd ions. MT was first discovered in the kidney cortex of the horse; it represents a low molecular weight protein, rich in cysteine residues which effectively bind with metals. Its functions consist in detoxification of heavy metals like mercury, arsenic, cadmium, homeostasis of essential metals including copper and zinc, anti-oxidation against reactive oxygen species, protection against DNA damage, oxidative stress, cell survival, angiogenesis, apoptosis, and increase of proliferation. In this work, we sought to highlight the protective function of MT in the brain and serum of rats by means of detoxification under induced effects of controlled Cd doses. We have done this by exposing Wistar rats to Cd at different doses in drinking water at different time intervals. In two independent experiments, 58 rats were subjected to 0.1 or 1.0 µg Cd2+/kg of body weight for 15 or 36 days under different conditions. The obtained data indicates the different functioning systems for the brain and the blood for MT metabolism under Cd effect. Our results indicate significant loss of metallothionein level in the brain and important increases in the amount of MT in serum proving that even minimal ingestion of toxic Cd is enough to trigger the release of MT protein in blood.

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In this research, we investigated the effect of pituitrin-izadrin induced injury on the levels of metallothionein (MT) and soluble and filament forms of glial fibrillary acidic protein (GFAP) in the hippocampusA strocytes are amongst the earliest and prominent to express changes under attacks [1]. They are the most numerous nonneuronal cell types in the central nervous system (CNS) and make up about 50% of the volume of the human brain [1,2]. Their functions are known to be critical, such as scavenge transmitters released during synaptic activity, control ion and water homeostasis, release neurotrophic factors, shuttle metabolite, and waste products, and to participate in the formation of the blood-brain-barrier [3,4]. Failure of any of these supportive functions of astrocytes will constitute a threat to neuronal survival. Astrocytes are home to a number of essential proteins of the CNS, including metallothionein and glial fibrillary acidic protein, which presumably carry out some astrocyte functions.Metallothioneins (MTs) are cysteine-rich, low molecular weight, heat stable proteins firstly described by Margoshes [5]. They are largely synthesized in the liver and the kidney in humans but are found at a number of other sites. In the CNS, MT-I and MT-II are conspicuously absent from neuronal populations, yet abundant in fibrous and protoplasmic astrocytes. MT is detectable in the extracellular fluid of the injured brain and astrocytes are capable of secreting MT in a regulatable manner [6].MTs have been implicated as regulatory molecules in gene expression, homeostatic control of cellular metabolism of metals, and cellular adaptation to stress. Thus, they fulfill a regulatory capacity and influence transcription, replication, protein synthesis, metabolism, as well as other zinc-dependent biological processes [7]. It has been shown that the ability of animals to recover from CNS injuries or degenerative diseases depends on the deficiency or excess availability of MT-I/-II [7][8][9][10][11]. MT has equally been demonstrated to be down-regulated in cases of induced intoxication [12] and infection [13] but its correlated effect to other astrocyte proteins has yet to be tested.GFAP is expressed in mature astrocytes in the CNS [14]. It is a member of the family of cytoskeletal proteins and is the primary intermediate filament with a size of 8-9 nm, highly specific to the CNS. However, it has been found outside the CNS in relatively low amounts [15]. It has two physicochemical GFAP forms: water-soluble (sGFAP) and filament (fGFAP) [16]. The sGFAP is unevenly distributed in various brain regions, with the maximum con-