Study of long-term potentiation (LTP) in the song bird brain regions essential for vocal learning using multi-electrode dish (MED)

2007 ◽  
Vol 58 ◽  
pp. S172
Author(s):  
Chikafusa Bessho ◽  
Tatsuya Yamamoto
Keyword(s):  
Vocal Learning ◽  
Long Term Potentiation ◽  
Brain Regions ◽  
Song Bird ◽  
Term Potentiation

scholarly journals The evidence for hippocampal long-term potentiation as a basis of memory for simple tasks

2008 ◽  
Vol 80 (1) ◽  
pp. 115-127 ◽  
Author(s):  
Iván Izquierdo ◽  
Martín Cammarota ◽  
Weber C. Da Silva ◽  
Lia R.M. Bevilaqua ◽  
Janine I. Rossato ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Brain Regions ◽  
Memory Formation ◽  
Long Term Memory ◽  
Ca1 Region ◽  
Term Potentiation ◽  
The One ◽  
Similar Task ◽  
Stimulation Of

Long-term potentiation (LTP) is the enhancement of postsynaptic responses for hours, days or weeks following the brief repetitive afferent stimulation of presynaptic afferents. It has been proposed many times over the last 30 years to be the basis of long-term memory. Several recent findings finally supported this hypothesis: a) memory formation of one-trial avoidance learning depends on a series of molecular steps in the CA1 region of the hippocampus almost identical to those of LTP in the same region; b)hippocampal LTP in this region accompanies memory formation of that task and of another similar task. However, CA1 LTP and the accompanying memory processes can be dissociated, and in addition plastic events in several other brain regions(amygdala, entorhinal cortex, parietal cortex) are also necessary for memory formation of the one-trial task, and perhaps of many others.

scholarly journals Plasticity of Neuron-Glial Transmission: Equipping Glia for Long-Term Integration of Network Activity

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Wayne Croft ◽  
Katharine L. Dobson ◽  
Tomas C. Bellamy
Keyword(s):  
Long Term Potentiation ◽  
Brain Regions ◽  
Neuronal Firing ◽  
Network Activity ◽  
Neuronal Function ◽  
Term Potentiation ◽  
Bidirectional Communication ◽  
Long Time ◽  
Activity Dependent

The capacity of synaptic networks to express activity-dependent changes in strength and connectivity is essential for learning and memory processes. In recent years, glial cells (most notably astrocytes) have been recognized as active participants in the modulation of synaptic transmission and synaptic plasticity, implicating these electrically nonexcitable cells in information processing in the brain. While the concept of bidirectional communication between neurons and glia and the mechanisms by which gliotransmission can modulate neuronal function are well established, less attention has been focussed on the computational potential of neuron-glial transmission itself. In particular, whether neuron-glial transmission is itself subject to activity-dependent plasticity and what the computational properties of such plasticity might be has not been explored in detail. In this review, we summarize current examples of plasticity in neuron-glial transmission, in many brain regions and neurotransmitter pathways. We argue that induction of glial plasticity typically requires repetitive neuronal firing over long time periods (minutes-hours) rather than the short-lived, stereotyped trigger typical of canonical long-term potentiation. We speculate that this equips glia with a mechanism for monitoring average firing rates in the synaptic network, which is suited to the longer term roles proposed for astrocytes in neurophysiology.

Evidence for the Role of Endogenous Carbon Monoxide in Memory Processing

2007 ◽  
Vol 19 (4) ◽  
pp. 557-562 ◽  
Author(s):  
M. C. Cutajar ◽  
T. M. Edwards
Keyword(s):  
Carbon Monoxide ◽  
Long Term Potentiation ◽  
Brain Regions ◽  
Memory Research ◽  
Memory Processing ◽  
Important Target ◽  
Term Potentiation ◽  
Per Se

For a decade and a half, nitric oxide (NO) has been implicated in memory processing across a wide variety of tasks and species. Comparatively, endogenously produced carbon monoxide (CO) has lagged behind as a target for research into the pharmacological processes underlying memory formation. This is surprising given that CO is formed in memory-associated brain regions, is structurally similar to NO, and along with NO can activate guanylate cyclase, which is an enzyme well characterized in memory processing. Nevertheless, a limited number of electrophysiological investigations have concluded that endogenous CO is involved in long-term potentiation. Although not evidence for a role in memory per se, these studies did point to the possible importance of CO in memory processing. In addition, there is now evidence to suggest that endogenous CO is important in avoidance learning and possible for other tasks. This review therefore seeks to promote endogenous CO as a potentially important target for memory research.

scholarly journals Ablation of STAT3 in Purkinje cells reorganizes cerebellar synaptic plasticity in long-term fear memory network

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Jeong-Kyu Han ◽  
Sun-Ho Kwon ◽  
Yong Gyu Kim ◽  
Jaeyong Choi ◽  
Jong-Il Kim ◽  
...  
Keyword(s):  
Purkinje Cells ◽  
Long Term Potentiation ◽  
Fear Memory ◽  
Emotional Memory ◽  
Brain Regions ◽  
Cellular Mechanisms ◽  
Term Potentiation ◽  
Memory Network ◽  
Cerebellar Purkinje Cells

Emotional memory processing engages a large neuronal network of brain regions including the cerebellum. However, the molecular and cellular mechanisms of the cerebellar cortex modulating the fear memory network are unclear. Here, we illustrate that synaptic signaling in cerebellar Purkinje cells (PCs) via STAT3 regulates long-term fear memory. Transcriptome analyses revealed that PC-specific STAT3 knockout (STAT3PKO) results in transcriptional changes that lead to an increase in the expression of glutamate receptors. The amplitude of AMPA receptor-mediated excitatory postsynaptic currents at parallel fiber (PF) to PC synapses was larger in STAT3PKO mice than in wild-type (WT) littermates. Fear conditioning induced long-term depression of PF–PC synapses in STAT3PKO mice while the same manipulation induced long-term potentiation in WT littermates. STAT3PKO mice showed an aberrantly enhanced long-term fear memory. Neuronal activity in fear-related regions increased in fear-conditioned STAT3PKO mice. Our data suggest that STAT3-dependent molecular regulation in PCs is indispensable for proper expression of fear memory.

scholarly journals Hippocampal Neuropeptide Y2 receptor blockade improves spatial memory retrieval and modulates limbic brain metabolism

2021 ◽  
Author(s):  
Marta Mendez-Couz ◽  
Hector Gonzalez-Pardo ◽  
Jorge L Arias ◽  
Nelida M Conejo
Keyword(s):  
Spatial Memory ◽  
Brain Metabolism ◽  
Drugs Of Abuse ◽  
Dorsal Hippocampus ◽  
Long Term Potentiation ◽  
Brain Regions ◽  
Memory Recall ◽  
Y2 Receptor ◽  
Term Potentiation

Introduction: The neuropeptide Y (NPY) is broadly distributed in the central nervous system (CNS), and it has been related to neuroprotective functions. NPY seems to be an important component to counteract brain damage and cognitive impairment mediated by drugs of abuse and neurodegenerative diseases, and both NPY and its Y2 receptor (Y2R) are highly expressed in the hippocampus, critical for learning and memory. We have recently demonstrated its influence on cognitive functions; however, the specific mechanism and involved brain regions where NPY modulates spatial memory by acting on Y2R remain unclear. Methods: Here, we examined the involvement of the hippocampal NPY Y2R in spatial memory and associated changes in brain metabolism by bilateral administration of the selective antagonist BIIE0246 into the rat dorsal hippocampus. To further evaluate the relationship between memory functions and neuronal activity, we analysed the regional expression of the mitochondrial enzyme cytochrome c oxidase (CCO) as an index of oxidative metabolic capacity in limbic and non-limbic brain regions. Results: The acute blockade of NPY Y2R significantly improved spatial memory recall in rats trained in the Morris water maze that matched metabolic activity changes in spatial memory processing regions. Specifically, CCO activity changes were found in the dentate gyrus of the dorsal hippocampus and CA1 subfield of the ventral hippocampus, the infralimbic region of the PFC and the mammillary bodies. Conclusions: These findings suggest that the NPY hippocampal system, through its Y2R receptor, influences spatial memory recall (retrieval) and exerts control over patterns of brain activation that are relevant for associative learning, probably mediated by Y2R modulation of long-term potentiation and long-term depression.

scholarly journals Long-term potentiation prevents ketamine-induced aberrant neurophysiological dynamics in the hippocampus-prefrontal cortex pathway in vivo

2019 ◽  
Author(s):  
Cleiton Lopes-Aguiar ◽  
Rafael N. Ruggiero ◽  
Matheus T. Rossignoli ◽  
Ingrid de Miranda Esteves ◽  
José Eduardo Peixoto Santos ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Synaptic Plasticity ◽  
Animal Models ◽  
Long Term Potentiation ◽  
Brain Regions ◽  
High Frequency Stimulation ◽  
Evoked Responses ◽  
Term Potentiation

ABSTRACTN-methyl-D-aspartate receptor (NMDAr) antagonists such as ketamine (KET) produce psychotic-like behavior in both humans and animal models. NMDAr hypofunction affects normal oscillatory dynamics and synaptic plasticity in key brain regions related with schizophrenia, particularly in the hippocampus and the prefrontal cortex. In contrast, long-term potentiation (LTP) induction is known to increase glutamatergic transmission. Thus, we hypothesized that LTP could mitigate the electrophysiological changes promoted by KET. We recorded HPC-PFC local field potentials and evoked responses in urethane anesthetized rats, before and after KET administration, preceded or not by LTP induction. Our results show that KET promotes an aberrant delta-high-gamma crossfrequency coupling in the PFC and an enhancement in HPC-PFC evoked responses. LTP induction prior to KET attenuates changes in synaptic efficiency and prevents the increase in cortical gamma amplitude comodulation. These findings are consistent with evidence that increased efficiency of glutamatergic receptors attenuates cognitive impairment in animal models of psychosis. Therefore, high-frequency stimulation in HPC may be a useful tool to better understand how to prevent NMDAr hypofunction effects on synaptic plasticity and oscillatory coordination in cortico-limbic circuits.

scholarly journals Satb2 determines miRNA expression and long-term memory in the adult central nervous system

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Clemens Jaitner ◽  
Chethan Reddy ◽  
Andreas Abentung ◽  
Nigel Whittle ◽  
Dietmar Rieder ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Long Term Potentiation ◽  
Brain Regions ◽  
Memory Formation ◽  
Adult Brain ◽  
Synaptic Activity ◽  
Long Term Memory ◽  
Term Potentiation ◽  
Chromatin Configuration

SATB2 is a risk locus for schizophrenia and encodes a DNA-binding protein that regulates higher-order chromatin configuration. In the adult brain Satb2 is almost exclusively expressed in pyramidal neurons of two brain regions important for memory formation, the cerebral cortex and the CA1-hippocampal field. Here we show that Satb2 is required for key hippocampal functions since deletion of Satb2 from the adult mouse forebrain prevents the stabilization of synaptic long-term potentiation and markedly impairs long-term fear and object discrimination memory. At the molecular level, we find that synaptic activity and BDNF up-regulate Satb2, which itself binds to the promoters of coding and non-coding genes. Satb2 controls the hippocampal levels of a large cohort of miRNAs, many of which are implicated in synaptic plasticity and memory formation. Together, our findings demonstrate that Satb2 is critically involved in long-term plasticity processes in the adult forebrain that underlie the consolidation and stabilization of context-linked memory.

Long term potentiation: Attending to levels of organization of learning and memory mechanisms

1997 ◽  
Vol 20 (4) ◽  
pp. 631-632
Author(s):  
Matthew Shapiro ◽  
Eric Hargreaves
Keyword(s):  
Learning And Memory ◽  
Long Term Potentiation ◽  
Brain Regions ◽  
Task Demands ◽  
Memory Storage ◽  
Storage Mechanism ◽  
Levels Of Organization ◽  
Term Potentiation ◽  
Set Up

Shors & Matzel set up a straw man, that LTP is a memory storage mechanism, and knock him down without due consideration of the important relations among different levels of organization and analysis regarding LTP, learning, and memory. Assessing these relationships requires analysis and hypotheses linking specific brain regions, neural circuits, plasticity mechanisms, and task demands. The issue addressed by the authors is important, but their analysis is off target.

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