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Synaptic Changes (synaptic + change)

Distribution by Scientific Domains

Medical Sciences	50%
Life Sciences	37%

Selected Abstracts

AGE-RELATED SYNAPTIC CHANGES IN THE CA1 STRATUM RADIATUM AND SPATIAL LEARNING IMPAIRMENT IN RATS

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2009
Li-Hong Long
SUMMARY 1Age-related impairments in hippocampus-dependent spatial learning and memory are not associated with a loss of neurons, but may be related to synaptic changes. In the present study, we analysed the behavioural performance of adult, middle-aged and old Wistar rats using the Morris water maze, as well as the structure of synapses and the expression of autophosphorylated Ca2+/calmodulin-dependent protein kinase II at threonine 286 (pThr286-,CaMKII), a key post-synaptic protein in the CA1 stratum radiatum, in the same rats. 2Old Wistar rats showed significant cognitive deficits. Synaptic density, the area of post-synaptic densities and the total number of synapses in the CA1 stratum radiatum of old rats were significantly decreased compared with adult rats. The decrease in autophosphorylated pThr286-,CaMKII was age dependent. 3These findings reveal that age-related impairments in learning and memory are associated with synaptic atrophy. The decreased expression of pThr286-CaMKII may result in reduced synaptic function with ageing. [source]

Soleus T reflex modulation in response to spinal and tendinous adaptations to unilateral lower limb suspension in humans

ACTA PHYSIOLOGICA, Issue 3 2008
O. R. Seynnes
Abstract Aim:, To investigate the influence of tendinous and synaptic changes induced by unilateral lower limb suspension (ULLS) on the tendon tap reflex. Methods:, Eight young men underwent a 23-day period of ULLS. Muscle cross-sectional area (CSA), torque and electromyographic (EMG) activity of the plantar flexor muscles (normalized to the M wave), Achilles tendon,aponeurosis mechanical properties, soleus (SOL) H and T reflexes and associated peak twitch torques were measured at baseline, after 14 and 23 days of ULLS, and 1 week after resuming ambulatory activity. Results:, Significant decreases in muscle CSA (,9%), in maximal voluntary torque (,10%) and in the associated SOL EMG activity (,16%) were found after ULLS (P < 0.05). In addition to a 36% (P < 0.01) decrease in tendon,aponeurosis stiffness, normalized H reflex increased by 35% (P < 0.05). An increase in the slope (28%, P < 0.05) and intercept (85%, P < 0.05) of the T reflex recruitment curve pointed to an increase in the gain and to a decrease in the sensitivity of this reflex, possibly resulting from the decrease in the tendon,aponeurosis stiffness at low forces. Following ULLS, changes in tendinous stiffness correlated with changes in neuromuscular efficiency (peak twitch torque to reflex ratio) at higher tendon tap forces. Conclusion:, These findings point out the dual and antagonistic influences of spinal and tendinous adaptations upon the tendon tap reflex in humans under conditions of chronic unloading. These observations have potential implications for the sensitivity of the short-latency Ia stretch response involved in rapid compensatory contractions to unexpected postural perturbations. [source]

Influence of parental deprivation on the behavioral development in Octodon degus: Modulation by maternal vocalizations

DEVELOPMENTAL PSYCHOBIOLOGY, Issue 3 2003
Katharina Braun
Abstract Repeated separation from the family during very early stages of life is a stressful emotional experience which induces a variety of neuronal and synaptic changes in limbic cortical areas that may be related to behavioral alterations. First, we investigated whether repeated parental separation and handling, without separation from the family, leads to altered spontaneous exploratory behavior in a novel environment (open field test) in 8-day-old Octodon degus. Second, we tested whether the parentally deprived and handled animals display different stimulus-evoked exploratory behaviors in a modified open field version, in which a positive emotional stimulus, the maternal call, was presented. In the open field test a significant influence of previous emotional experience was found for the parameters of running, rearing, and vocalization. Parentally deprived degus displayed increased horizontal (running) and vertical (rearing) motoric activities, but decreased vocalization, compared to normal and handled controls. The presentation of maternal vocalizations significantly modified running, vocalization, and grooming activities, which in the case of running activity was dependent on previous emotional experience. Both deprivation-induced locomotor hyperactivity together with the reduced behavioral response towards a familiar acoustic emotional signal are similar to behavioral disturbances observed in human attachment disorders. © 2003 Wiley Periodicals, Inc. Dev Psychobiol 42: 237,245, 2003. [source]

Role for glia in synaptogenesis

GLIA, Issue 3 2004
Erik M. Ullian
Abstract Nearly one-half of the cells in a human brain are astrocytes, but the function of these little cells remains a great mystery. Astrocytes form an intimate association with synapses throughout the adult CNS, where they help regulate ion and neurotransmitter concentrations. Recent in vitro studies, however, have found that astrocytes also exert powerful control over the number of CNS synapses that form, are essential for postsynaptic function, and are required for synaptic stability and maintenance. Moreover, recent studies increasingly implicate astrocytes in vivo as participants in activity-dependent structural and functional synaptic changes throughout the nervous system. Taken together, these data force us to rethink the role of glia. We propose that astrocytes should not be viewed primarily as support cells, but rather as cells that actively control the structural and functional plasticity of synapses in developing and adult organisms. © 2004 Wiley-Liss, Inc. [source]

Ischemia-induced modifications in hippocampal CA1 stratum radiatum excitatory synapses

HIPPOCAMPUS, Issue 10 2006
Tatiana Kovalenko
Abstract Relatively mild ischemic episode can initiate a chain of events resulting in delayed cell death and significant lesions in the affected brain regions. We studied early synaptic modifications after brief ischemia modeled in rats by transient vessels' occlusion in vivo or oxygen,glucose deprivation in vitro and resulting in delayed death of hippocampal CA1 pyramidal cells. Electron microscopic analysis of excitatory spine synapses in CA1 stratum radiatum revealed a rapid increase of the postsynaptic density (PSD) thickness and length, as well as formation of concave synapses with perforated PSD during the first 24 h after ischemic episode, followed at the long term by degeneration of 80% of synaptic contacts. In presynaptic terminals, ischemia induced a depletion of synaptic vesicles and changes in their spatial arrangement: they became more distant from active zones and had larger intervesicle spacing compared to controls. These rapid structural synaptic changes could be implicated in the mechanisms of cell death or adaptive plasticity. Comparison of the in vivo and in vitro model systems used in the study demonstrated a general similarity of these early morphological changes, confirming the validity of the in vitro model for studying synaptic structural plasticity. © 2006 Wiley-Liss, Inc. [source]

Modulation of synaptic plasticity by stress and antidepressants

BIPOLAR DISORDERS, Issue 3 2002
Maurizio Popoli
Recent preclinical and clinical studies have shown that mechanisms underlying neuronal plasticity and survival are involved in both the outcome of stressful experiences and the action of antidepressants. Whereas most antidepressants predominantly affect the brain levels of monoamine neurotransmitters, it is increasingly appreciated that they also modulate neurotransmission at synapses using the neurotransmitter glutamate (the most abundant in the brain). In the hippocampus, a main area of the limbic system involved in cognitive functions as well as attention and affect, specific molecules enriched at glutamatergic synapses mediate major changes in synaptic plasticity induced by stress paradigms or antidepressant treatments. We analyze here the modifications induced by stress or antidepressants in the strength of synaptic transmission in hippocampus, and the molecular modifications induced by antidepressants in two main mediators of synaptic plasticity: the N -methyl- D -aspartate (NMDA) receptor complex for glutamate and the Ca2+/calmodulin-dependent protein kinase II (CaM kinase II). Both stress and antidepressants induce alterations in long-term potentiation of hippocampal glutamatergic synapses, which may be partly accounted for by the influence of environmental or drug-induced stimulation of monoaminergic pathways projecting to the hippocampus. In the course of antidepressant treatments significant changes have been described in both the NMDA receptor and CaM kinase II, which may account for the physiological changes observed. A central role in these synaptic changes is exerted by brain-derived neurotrophic factor (BDNF), which modulates both synaptic plasticity and its molecular mediators, as well as inducing morphological synaptic changes. The role of these molecular effectors in synaptic plasticity is discussed in relation to the action of antidepressants and the search for new molecular targets of drug action in the therapy of mood disorders. [source]