A review of behavioral methods for the evaluation of cognitive performance in animal models: Current techniques and links to human cognition.

INTRODUCTION: Memory is defined as the ability to store, maintain and retrieve information. Learning is the acquisition of information that changes behavior and memory. Stress, dementia, head trauma, amnesia, Alzheimer's, Huntington, Parkinson's, Wernicke-Korsakoff syndrome (WKS) may be mentioned among the diseases in which memory and learning are affected. The task of understanding deficits in memory and learning in humans is daunting due to the complexity of neural and cognitive mechanisms in the nervous system. This job is made more difficult for clinicians and researchers by the fact that many techniques used to research memory are not ethically acceptable or technically feasible for use in humans. Thus, animal models have been necessary alternative for studying normal and disordered learning and memory. This review attempts to bridge these domains to allow biomedical researchers to have a firm grasp of "memory" and "learning" as constructs in humans whereby they may then select the proper animal cognitive test. RESULTS AND CONCLUSION: Various tests (open field habituation test, Y-maze test, passive avoidance test, step-down inhibitory avoidance test, active avoidance test, 8-arms radial maze test, Morris water maze test, radial arm water maze, novel object recognition test and gait function test) have been designed to evaluate different kinds of memory. Each of these tests has their strengths and limits. Abnormal results obtained using these tasks in non-human animals indicate malfunctions in memory which may be due to several physiological and psychological diseases of nervous system. Further studies by using the discussed tests can be very beneficial for achieving a therapeutic answer to these diseases.

The possible role of CREB-BDNF signaling pathway in neuroprotective effects of minocycline against alcohol-induced neurodegeneration: molecular and behavioral evidences.

Abuse of alcohol triggers neurodegeneration in human brain. Minocycline has characteristics conferring neuroprotection. Current study evaluates the role of the CREB-BDNF signaling pathway in mediating minocycline's neuroprotective effects against alcohol-induced neurodegeneration. Seventy adult male rats were randomly split into groups 1 and 2 that received saline and alcohol (2 g/kg/day by gavage, once daily), respectively, and groups 3, 4, 5, and 6 were treated simultaneously with alcohol and minocycline (10, 20, 30 and 40 mg/kg I.P, respectively) for 21 days. Group 7 received minocycline alone (40 mg/kg, i.p) for 21 days. Morris water maze (MWM) has been used to assess cognitive activity. Hippocampal neurodegenerative and histological parameters as well as cyclic AMP response element-binding protein (CREB) and brain-derived neurotrophic factor (BDNF) levels were assessed. Alcohol impaired cognition, and concurrent therapy with various minocycline doses attenuated alcohol-induced cognition disturbances. Additionally, alcohol administration boosted lipid peroxidation and levels of glutathione in oxidized form (GSSG), tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1ß), and Bax protein, while decreased reducing type of glutathione (GSH), Bcl-2 protein, phosphorylated CREB, and BDNF levels in rat hippocampus. Alcohol also decreased the activity in the hippocampus of superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GR). In comparison, minocycline attenuated alcohol-induced neurodegeneration; elevating expression levels of P-CREB and BDNF and inhibited alcohol induced histopathological changes in both dentate gyrus (DG) and CA1 of hippocampus. Thus, minocycline is likely to provide neuroprotection against alcohol-induced neurodegeneration through mediation of the P-CREB/BDNF signaling pathway.