Independence of Short- and Long-Term Memory: A Neural System Analysis

Kesner, Raymond P.; Conner, Hubert S.

doi:10.1126/science.176.4033.432

Cited by 49 publications

(18 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A traditional view is that STM grades into LTM and is essential for its formation (Squire et al, 1993;Kandel, 2001). However, there are studies in many species including humans supporting the view that different phases of memory are based on parallel, independent processes (Kesner and Connor, 1972;Frieder and Allweis, 1978;Menzel, 1979;Sullivan and Sagar, 1991;Emptage and Carew, 1993;Botzer et al, 1998;Izquierdo et al, 1998;Izquierdo et al, 1999;Xia et al, 1999;Izquierdo et al, 2000;Waddell and Quinn, 2001). In addition, studies in Aplysia clearly indicate that short-term facilitation and long-term facilitation are not serially linked (Emptage and Carew, 1993;Muller and Carew, 1998).…”

Section: Discussionmentioning

confidence: 94%

Early Activation of Extracellular Signal-Regulated Kinase Signaling Pathway in the Hippocampus is Required for Short-Term Memory Formation of a Fear-Motivated Learning

et al. 2006

View full text Add to dashboard Cite

1. According to its duration there are, at least, two major forms of memory in mammals: short term memory (STM) which develops in a few seconds and lasts several hours and long-term memory (LTM) lasting days, weeks and even a lifetime. In contrast to LTM, very little is known about the neural, cellular and molecular requirements for mammalian STM formation. 2. Here we show that early activation of extracellular signal-regulated kinases 1/2 (ERK1/2) in the hippocampus is required for the establishment of STM for a one-trial inhibitory avoidance task in the rat. Immediate posttraining infusion of U0126 (a selective inhibitor of ERK kinase) into the CA1 region of the dorsal hippocampus blocked STM formation. 3. Reversible inactivation of the entorhinal cortex through muscimol infusion produced deficits in STM and a selective and rapid decrease in hippocampal ERK2 activation.4. Together with our previous findings showing a rapid decrease in ERK2 activation and impaired STM after blocking BDNF function, the present results strongly suggest that ERK2 signaling in the hippocampus is a critical step in STM processing.

show abstract

Section: Discussionmentioning

confidence: 94%

Early Activation of Extracellular Signal-Regulated Kinase Signaling Pathway in the Hippocampus is Required for Short-Term Memory Formation of a Fear-Motivated Learning

et al. 2006

View full text Add to dashboard Cite

show abstract

“…The hippocampus regulates the generation of long term memory (Kesner and Connor, 1972) and spatial learning (Morris et al, 1986). First, we investigated if there was in fact any change in the expression of hippocampal plasticity-related genes during memory consolidation (Fig.…”

Section: Resultsmentioning

confidence: 99%

Regulation of Cyclic AMP Response Element Binding and Hippocampal Plasticity-Related Genes by Peroxisome Proliferator-Activated Receptor α

et al. 2013

View full text Add to dashboard Cite

Peroxisome proliferator-activated receptor (PPAR) α is a transcription factor that regulates genes involved in fatty acid catabolism. Here we provide evidence that PPARα is constitutively expressed in nuclei of hippocampal neurons and surprisingly controls calcium influx and the expression of various plasticity-related genes via direct transcriptional regulation of CREB. Accordingly, Ppara-null, but not Pparb-null, mice are deficient in CREB and memory-associated genes, and have decreased spatial learning and memory. While shRNA knockdown of PPARα in the hippocampus suppressed CREB and NR2A rendering wild type animals markedly poor in consolidating spatial memory, introduction of PPARα to the hippocampus of Ppara-null mice increased hippocampal CREB and NR2A and improved spatial learning and memory. These results together with detailed analyses of CREB, NR2A and spatial learning and memory in bone marrow chimeric animals lacking PPARα in the CNS describe a novel mechanism for transcriptional control of Creb and associated plasticity genes by PPARα.

show abstract

“…The hippocampus regulates the generation of long term memory44 and spatial learning45 and has been shown to be critical for spatial memory in human subjects with hippocampal damage (reviewed in46). Together, the presented memory tests suggest an essential role of hippocampal α 3 Na+/K+-ATPase in consolidating particularly long-term spatial memory and fear-dependent memory, whereas short-term memory seemed less affected.…”

Section: Discussionmentioning

confidence: 99%

Cognitive deficits caused by a disease-mutation in the α3 Na+/K+-ATPase isoform

Holm

Isaksen

Glerup

et al. 2016

Sci Rep

View full text Add to dashboard Cite

The Na+/K+-ATPases maintain Na+ and K+ electrochemical gradients across the plasma membrane, a prerequisite for electrical excitability and secondary transport in neurons. Autosomal dominant mutations in the human ATP1A3 gene encoding the neuron-specific Na+/K+-ATPase α3 isoform cause different neurological diseases, including rapid-onset dystonia-parkinsonism (RDP) and alternating hemiplegia of childhood (AHC) with overlapping symptoms, including hemiplegia, dystonia, ataxia, hyperactivity, epileptic seizures, and cognitive deficits. Position D801 in the α3 isoform is a mutational hotspot, with the D801N, D801E and D801V mutations causing AHC and the D801Y mutation causing RDP or mild AHC. Despite intensive research, mechanisms underlying these disorders remain largely unknown. To study the genotype-to-phenotype relationship, a heterozygous knock-in mouse harboring the D801Y mutation (α3+/D801Y) was generated. The α3+/D801Y mice displayed hyperactivity, increased sensitivity to chemically induced epileptic seizures and cognitive deficits. Interestingly, no change in the excitability of CA1 pyramidal neurons in the α3+/D801Y mice was observed. The cognitive deficits were rescued by administration of the benzodiazepine, clonazepam, a GABA positive allosteric modulator. Our findings reveal the functional significance of the Na+/K+-ATPase α3 isoform in the control of spatial learning and memory and suggest a link to GABA transmission.

show abstract

Independence of Short- and Long-Term Memory: A Neural System Analysis

Cited by 49 publications

References 11 publications

Early Activation of Extracellular Signal-Regulated Kinase Signaling Pathway in the Hippocampus is Required for Short-Term Memory Formation of a Fear-Motivated Learning

Early Activation of Extracellular Signal-Regulated Kinase Signaling Pathway in the Hippocampus is Required for Short-Term Memory Formation of a Fear-Motivated Learning

Regulation of Cyclic AMP Response Element Binding and Hippocampal Plasticity-Related Genes by Peroxisome Proliferator-Activated Receptor α

Cognitive deficits caused by a disease-mutation in the α3 Na+/K+-ATPase isoform

Contact Info

Product

Resources

About