Learning-induced survival of new neurons depends on the cognitive status of aged rats.
نویسندگان
چکیده
Aging is accompanied by an alteration of spatial memory, which has been related to an alteration in hippocampal plasticity. Within the dentate gyrus, new neurons are generated throughout the entire life of an individual. This neurogenesis seems to play a role in hippocampal-mediated learning and learning-induced changes in neurogenesis have been proposed to be involved in memory. However, in aged rats, little is known on the influence of learning on the early development of the adult-born neurons and on the possible involvement of learning-induced changes in neurogenesis in age-related memory deficits. To address this issue, we took advantage of the existence of spontaneous individual differences for performances observed in aged subjects in the water maze. In this task, learning can be divided into two phases, an early phase during which performances quickly improve, and a late phase during which asymptotic levels of performances are reached. We show that the influence of spatial learning on the survival of the newly born cells depends on their birth date and the memory abilities of the aged rats. In aged rats with preserved spatial memory, learning increases the survival of cells generated before learning whereas it decreases survival of cells produced during the early phase of learning. These results highlight the importance of learning-induced changes in adult-born cell survival in memory. Furthermore, they provide new insights on the possible neural mechanisms of aging of cognitive functions and show that an alteration to the steps leading to neurogenesis may be involved in the determination of individual memory abilities.
منابع مشابه
The Implication of Androgens in the Presence of Protein Kinase C to Repair Alzheimer’s Disease-Induced Cognitive Dysfunction
Aging, as a major risk factor of memory deficiency, affects neural signaling pathways in hippocampus. In particular, age-dependent androgens deficiency causes cognitive impairments. Several enzymes like protein kinase C (PKC) are involved in memory deficiency. Indeed, PKC regulatory process mediates α-secretase activation to cleave APP in β-amyloid cascade and tau proteins phosphorylation mecha...
متن کاملNeuroprotective role of curcumin on the hippocampus against the structural and serological alterations of streptozotocin-induced diabetes in sprague dawely rats
Objective(s): Diabetes mellitus causes impaired memory and cognitive functions. The hippocampus plays a key role in memory and learning. Curcumin attenuates diabetic nephropathy in vivo. Curcumin has shown a neurogenic effect and cognition-enhancing potential in aged rats. The aim of this study is to evaluate the possible protective role of curcumin on the histological and serologicalchanges of...
متن کاملDipeptidyl peptidase-4 inhibitor ameliorates status epilepticus seizures and cognitive disturbances in a rat model of temporal lobe epilepsy
Background and Objective: In temporal lobe epilepsy (TLE), recurrent seizures accompany with cognitive deficit. In some patients, the current medications cannot provide satisfactory control of seizures, therefore new drugs that act through different mechanisms are required. In the present study, the useful effect of dipeptidyl peptidase-4 inhibitor was evaluated in experimental model of tempora...
متن کاملCrocin Improved Learning and Memory Impairments in Streptozotocin-Induced Diabetic Rats
Objective(s): Crocin influences many biological functions including memory and learning. The present study was aimed to investigate the effects of crocin on learning and memory impairments in streptozotocine-induced diabetic rats. Materials and Methods: Diabetes was induced by intraperitoneal (IP) injection of streptozotocin (STZ, 45 mg/kg). Transfer latency (TL) paradigm in elevated plus-maze ...
متن کاملAllicin attenuates tunicamycin-induced cognitive deficits in rats via its synaptic plasticity regulatory activity
Objective(s): To illuminate the functional effects of allicin on rats with cognitive deficits induced by tunicamycin (TM) and the molecular mechanism of this process. Materials and Methods: 200–250 g male SD rats were divided into three groups at random: control group (n=12), TM group (5 μl, 50 μM, i.c.v, n=12), and allicin treatment group (180 mg/kg/d with chow diet, n=12). After 16 weeks of a...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- The Journal of neuroscience : the official journal of the Society for Neuroscience
دوره 27 22 شماره
صفحات -
تاریخ انتشار 2007