Home About us Contact
|
Home About us Contact | ||
|
|
||
Long-term Spatial Memory (long-term + spatial_memory)
Selected AbstractsSeizures in the Developing Brain Cause Adverse Long-term Effects on Spatial Learning and AnxietyEPILEPSIA, Issue 12 2004Umit Sayin Summary:,Purpose: Seizures in the developing brain cause less macroscopic structural damage than do seizures in adulthood, but accumulating evidence shows that seizures early in life can be associated with persistent behavioral and cognitive impairments. We previously showed that long-term spatial memory in the eight-arm radial-arm maze was impaired in rats that experienced a single episode of kainic acid (KA)-induced status epilepticus during early development (postnatal days (P) 1,14). Here we extend those findings by using a set of behavioral paradigms that are sensitive to additional aspects of learning and behavior. Methods: On P1, P7, P14, or P24, rats underwent status epilepticus induced by intraperitoneal injections of age-specific doses of KA. In adulthood (P90,P100), the behavioral performance of these rats was compared with that of control rats that did not receive KA. A modified version of the radial-arm maze was used to assess short-term spatial memory; the Morris water maze was used to evaluate long-term spatial memory and retrieval; and the elevated plus maze was used to determine anxiety. Results: Compared with controls, rats with KA seizures at each tested age had impaired short-term spatial memory in the radial-arm maze (longer latency to criterion and more reference errors), deficient long-term spatial learning and retrieval in the water maze (longer escape latencies and memory for platform location), and a greater degree of anxiety in the elevated plus maze (greater time spent in open arms). Conclusions: These findings provide additional support for the concept that seizures early in life may be followed by life-long impairment of certain cognitive and behavioral functions. These results may have clinical implications, favoring early and aggressive control of seizures during development. [source] 5-HT1A and NMDA receptors interact in the rat medial septum and modulate hippocampal-dependent spatial learningHIPPOCAMPUS, Issue 12 2009Elin Elvander-Tottie Abstract Cholinergic and GABAergic neurons in the medial septum/vertical limb of the diagonal band of Broca (MS/vDB) projecting to the hippocampus, constitute the septohippocampal projection, which is important for hippocampal-dependent learning and memory. There is also evidence for an extrinsic as well as an intrinsic glutamatergic network within the MS/vDB. GABAergic and cholinergic septohippocampal neurons express the serotonergic 5-HT1A receptor and most likely also glutamatergic NMDA receptors. The aim of the present study was to examine whether septal 5-HT1A receptors are important for hippocampal-dependent long-term memory and whether these receptors interact with glutamatergic NMDA receptor transmission in a manner important for hippocampal-dependent spatial memory. Intraseptal infusion of the 5-HT1A receptor agonist (R)-8-OH-DPAT (1 or 4 ,g/rat) did not affect spatial learning in the water maze task but impaired emotional memory in the passive avoidance task at the higher dose tested (4 ,g/rat). While intraseptal administration of (R)-8-OH-DPAT (4 ,g) combined with a subthreshold dose of the NMDA receptor antagonist D-AP5 (1 ,g) only marginally affected spatial acquisition, it produced a profound impairment in spatial memory. In conclusion, septal 5-HT1A receptors appears to play a more prominent role in emotional than in spatial memory. Importantly, septal 5-HT1A and NMDA receptors appear to interact in a manner, which is particularly critical for the expression or retrieval of hippocampal-dependent long-term spatial memory. It is proposed that NMDA receptor hypofunction in the septal area may unmask a negative effect of 5-HT1A receptor activation on memory, which may be clinically relevant. © 2009 Wiley-Liss, Inc. [source] A single application of MK801 causes symptoms of acute psychosis, deficits in spatial memory, and impairment of synaptic plasticity in ratsHIPPOCAMPUS, Issue 2 2008Denise Manahan-Vaughan Abstract Schizophrenia is mostly a progressive psychiatric illness. Although cognitive changes in chronic schizophrenia have been investigated, little is known about the consequences of a single psychotic episode on memory mechanisms and formation. We investigated changes in hippocampal long-term potentiation (LTP) and spatial memory in a rat model of an acute psychotic episode. Application of NMDA receptor antagonists, such as MK801 (dizolcilpine) in rats, have been shown to give rise to an acute and short-lasting behavioral state, which mirrors many symptoms of schizophrenia. Furthermore, NMDA antagonist-intake in humans elicits symptoms of schizophrenia such as hallucinations, delusions, and affective blunting. We therefore treated animals with a single systemic injection of MK801 (5 mg/kg). Increased stereotypy, locomotion, and ataxia were evident immediately after MK801-treatment, with effects disappearing within 24 h. MK801-treatment caused a disruption of prepulse inhibition of the acoustic startle reflex, 1 day but not 7 or 28 days after treatment. These effects were consistent with the occurrence of an acute psychotic episode. LTP was profoundly impaired in freely moving rats 7 days after MK801 application. Four weeks after treatment, a slight recovery of LTP was seen, however marked deficits in long-term spatial memory were evident. These data suggest that treatment with MK801 to generate an acute psychotic episode in rats, gives rise to grave disturbances in synaptic plasticity and is associated with lasting impairments with the ability to form spatial memory. © 2007 Wiley-Liss, Inc. [source] Influence of predator stress on the consolidation versus retrieval of long-term spatial memory and hippocampal spinogenesisHIPPOCAMPUS, Issue 7 2006David M. Diamond Abstract We have studied the influence of predator stress (30 min of cat exposure) on long-term (24 h) spatial memory and the density of spines in basilar dendrites of CA1 neurons. Predator stress occurred either immediately before water maze training (Stress Pre-Training) or before the 24 h memory test (Stress Pre-Retrieval). The Control (nonstress) group exhibited excellent long-term spatial memory and a robust increase in the density of stubby, but not mushroom, shaped spines. The Stress Pre-Training group had impaired long-term memory and did not exhibit any changes in spine density. The Stress Pre-Retrieval group was also impaired in long-term memory performance, but this group exhibited an increase in the density of stubby, but not mushroom, shaped spines, which was indistinguishable from the control group. These findings indicate that: (1) A single day of water maze training under control conditions produced intact long-term memory and an increase in the density of stubby spines in CA1; (2) Stress before training interfered with the consolidation of information into long-term memory and suppressed the training-induced increase in spine density; and (3) Stress immediately before the 24 h memory test trial impaired the retrieval of the stored memory, but did not reverse the training-induced increase in CA1 spine density. Overall, this work provides evidence of structural plasticity in dendrites of CA1 neurons which may be involved in the consolidation process, and how spinogenesis and memory are modulated by stress. © 2006 Wiley-Liss, Inc. [source] Sequestration of serum response factor in the hippocampus impairs long-term spatial memoryJOURNAL OF NEUROCHEMISTRY, Issue 2 2005Pramod K. Dash Abstract The formation of long-term memory has been shown to require protein kinase-mediated gene expression. One such kinase, mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK), can lead to the phosphorylation of serum response factor (SRF) and Elk-1, enhancing the expression of target genes. However, a direct involvement of these transcription factors in memory storage has not been demonstrated. We have employed an oligonucleotide decoy technique to interrogate SRF and Elk-1. Previously, it has been shown that intra-amygdalal infusion of small double-stranded decoy oligonucleotides for nuclear factor-kappaB (NFkappaB) can impair long-term memory for fear-potentiated startle. Using this approach, we found that intra-hippocampal infusion of NFkappaB decoy oligonucleotides also impairs long-term spatial memory, consistent with a role for this factor in long-term memory storage. Decoy oligonucleotides containing the binding site for SRF, as confirmed by shift-western, did not influence memory acquisition but impaired long-term spatial memory. Analysis of search behavior during the transfer test revealed deficits consistent with a loss of precise platform location information. In contrast, oligonucleotides with a binding site for either Elk-1 or another target of ERK activity, SMAD3/SMAD4, did not interfere with memory formation or storage. These findings suggest that SRF-mediated gene expression is required for long-term spatial memory. [source] Hyperglycemia not hypoglycemia alters neuronal dendrites and impairs spatial memoryPEDIATRIC DIABETES, Issue 6 2008John I Malone Background/Objective:, We previously reported that chronic hyperglycemia, but not hypoglycemia, was associated with the reduction of neuronal size in the rat brain. We hypothesized that hyperglycemia-induced changes in neuronal structure would have negative consequences, such as impaired learning and memory. We therefore assessed the effects of hyperglycemia and hypoglycemia on neuronal dendritic structure and cognitive functioning in young rats. Design/Methods:, Experimental manipulations were conducted on male Wistar rats for 8 wk, beginning at 4 wk of age. At the completion of the treatments, all rats were trained in the radial-arm water maze, a spatial (hippocampus-dependent) learning and memory task. Three groups of rats were tested: an untreated control group, a streptozotocin-induced diabetic (STZ-D) group, and an intermittent hypoglycemic group. Following behavioral training, the brains of all animals were examined with histologic and biochemical measurements. Results:, Peripheral hyperglycemia was associated with significant increases in brain sorbitol (7.5 ± 1.6 vs. 5.84 ± 1.0 ,M/mg) and inositol (9.6 ± 1.4 vs. 7.1 ± 1.1 ,M/mg) and reduced taurine (0.65 ± 0.1 vs. 1.3 ± 0.1 mg/mg). Histologic evaluation revealed neurons with reduced dendritic branching and spine density in STZ-D rats but not in control or hypoglycemic animals. In addition, the STZ-D group exhibited impaired performance on the water maze memory test. Conclusions:, Hyperglycemia, but not hypoglycemia, was associated with adverse effects on the brain polyol pathway activity, neuronal structural changes, and impaired long-term spatial memory. This finding suggests that the hyperglycemic component of diabetes mellitus has a greater adverse effect on brain functioning than does intermittent hypoglycemia. [source] A prospective study of severe hypoglycemia and long-term spatial memory in children with type 1 diabetesPEDIATRIC DIABETES, Issue 2 2004Tamara Hershey Abstract:, In a previous retrospective study, severe hypoglycemia (SH) was associated with decreased long-term spatial memory in children with type 1 diabetes mellitus (T1DM). In this study, we tested the hypothesis that prospectively ascertained SH would also be associated with decreased spatial long-term memory over time. Children with T1DM (n = 42) and sibling controls (n = 25) performed a spatial delayed response (SDR) task with short and long delays and other neuropsychological tests at baseline and after 15 months of monitoring. Extreme glycemic events and other medical complications were recorded prospectively during follow-up. Fourteen T1DM children experienced at least one episode of SH during the follow-up period (range = 1,5). After controlling for long-delay SDR performance at baseline, age, gender, and age of onset, the presence of SH during the prospective period was statistically associated with decreased long-delay SDR performance at follow-up (semipartial r = ,0.38, p = 0.017). This relationship was not seen with short-delay SDR or with verbal or object memory, attention, or motor speed. These results, together with previously reported data, support the hypothesis that SH has specific, negative effects on spatial memory skills in T1DM children. [source] | |||||||||||||