scholarly journals Hippocampal CA1 pyramidal cells do not receive monosynaptic input from thalamic nucleus reuniens

2021 ◽  
Author(s):  
Lilya Andrianova ◽  
Erica S Brady ◽  
Gabriella Margetts-Smith ◽  
Shivali Kohli ◽  
Chris J McBain ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Thalamic Nucleus ◽  
Critical Role ◽  
Pyramidal Cells ◽  
Brain Regions ◽  
Thalamic Nuclei ◽  
Nucleus Reuniens ◽  
Ca1 Pyramidal Cells ◽  
Local Inhibition ◽  
The Many

Midline thalamic nuclei play a critical role in cognitive functions such as memory, decision-making and spatial navigation, by facilitating communication between the many brain regions involved in these processes. One canonical feature of thalamic interactions with the cortex or hippocampus appears to be that the thalamus receives input from, and projects to, excitatory neurons. Thalamic nucleus reuniens (NRe) is located on the midline and is viewed primarily as a relay from prefrontal cortex to hippocampal and entorhinal areas, although these connections are poorly defined at the cellular and synaptic level. Using electrophysiology and monosynaptic circuit-tracing, we found that pyramidal cells in CA1 receive no direct input from NRe. This contrasts starkly with prefrontal cortex, subiculum and entorhinal cortex, and indicates that NRe inputs to CA1 primarily drive local inhibition and not excitation they do in the other regions. The NRe to CA1 projection is thus a unique thalamic projection and as such is raising important questions about the function of NRe-mediated prefrontal control of the hippocampus.

Distance-Dependent Ni2+-Sensitivity of Synaptic Plasticity in Apical Dendrites of Hippocampal CA1 Pyramidal Cells

2002 ◽  
Vol 87 (2) ◽  
pp. 1169-1174 ◽  
Author(s):  
Yoshikazu Isomura ◽  
Yoko Fujiwara-Tsukamoto ◽  
Michiko Imanishi ◽  
Atsushi Nambu ◽  
Masahiko Takada
Keyword(s):  
Calcium Influx ◽  
Critical Role ◽  
Field Potential ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Apical Dendrite ◽  
Excitatory Postsynaptic Potential ◽  
Distal Dendrite ◽  
Ca1 Pyramidal Cells ◽  
Hippocampal Ca1

Low concentration of Ni2+, a T- and R-type voltage-dependent calcium channel (VDCC) blocker, is known to inhibit the induction of long-term potentiation (LTP) in the hippocampal CA1 pyramidal cells. These VDCCs are distributed more abundantly at the distal area of the apical dendrite than at the proximal dendritic area or soma. Therefore we investigated the relationship between the Ni2+-sensitivity of LTP induction and the synaptic location along the apical dendrite. Field potential recordings revealed that 25 μM Ni2+ hardly influenced LTP at the proximal dendritic area (50 μm distant from the somata). In contrast, the same concentration of Ni2+ inhibited the LTP induction mildly at the middle dendritic area (150 μm) and strongly at the distal dendritic area (250 μm). Ni2+ did not significantly affect either the synaptic transmission at the distal dendrite or the burst-firing ability at the soma. However, synaptically evoked population spikes recorded near the somata were slightly reduced by Ni2+ application, probably owing to occlusion of dendritic excitatory postsynaptic potential (EPSP) amplification. Even when the stimulating intensity was strengthened sufficiently to overcome such a reduction in spike generation during LTP induction, the magnitude of distal LTP was not significantly recovered from the Ni2+-dependent inhibition. These results suggest that Ni2+ may inhibit the induction of distal LTP directly by blocking calcium influx through T- and/or R-type VDCCs. The differentially distributed calcium channels may play a critical role in the induction of LTP at dendritic synapses of the hippocampal pyramidal cells.

scholarly journals Nucleus reuniens is required for encoding and retrieving precise, hippocampal-dependent contextual fear memories in rats

2018 ◽  
Author(s):  
Karthik R. Ramanathan ◽  
Reed L. Ressler ◽  
Jingji Jin ◽  
Stephen Maren
Keyword(s):  
Prefrontal Cortex ◽  
Spatial Memory ◽  
Fear Conditioning ◽  
Medial Prefrontal Cortex ◽  
Thalamic Nucleus ◽  
Nmda Receptor Antagonist ◽  
Pavlovian Fear Conditioning ◽  
Contextual Memory ◽  
Nucleus Reuniens ◽  
Contextual Fear

AbstractThe nucleus reuniens (RE) is a ventral midline thalamic nucleus that interconnects the medial prefrontal cortex (mPFC) and hippocampus (HPC). Considerable data indicate that HPC-mPFC circuits are involved in contextual and spatial memory; however, it is not clear whether the RE mediates the acquisition or retrieval of these memories. To examine this question, we inactivated the RE with muscimol before either the acquisition or retrieval of Pavlovian fear conditioning in rats; freezing served as the index of fear. We found that RE inactivation before conditioning impaired the acquisition of contextual freezing, whereas inactivation of the RE prior to retrieval testing increased the generalization of freezing to a novel context; inactivation of the RE did not affect either the acquisition or expression of auditory fear conditioning. Interestingly, contextual conditioning impairments were absent when retrieval testing was also conducted after RE inactivation. Contextual memories acquired under RE inactivation were hippocampal-independent, insofar as contextual freezing in rats conditioned under RE inactivation was insensitive to intra-hippocampal infusions of the NMDA receptor antagonist, D,L-amino-5-phosophonovaleric acid (APV). Together, these data reveal that the RE supports hippocampal-dependent encoding of precise contextual memories that allow discrimination of dangerous from safe contexts. When the RE is inactive, however, alternate neural systems acquire an impoverished contextual memory that is only expressed when the RE is offline.SIGNIFICANCE STATEMENTThe midline thalamic nucleus reuniens (RE) coordinates communication between the hippocampus and medial prefrontal cortex, brain areas critical for contextual and spatial memory. Here we show that temporary pharmacological inactivation of RE impairs the acquisition and precision of contextual fear memories after Pavlovian fear conditioning in rats. However, inactivating the RE prior to retrieval testing restored contextual memory in rats conditioned after RE inactivation. Critically, we show that imprecise contextual memories acquired under RE inactivation are learned independently of the hippocampus. These data reveal that the RE is required for hippocampal-dependent encoding of precise contextual memories to support the discrimination of safe and dangerous contexts.

scholarly journals Distributed interactive brain circuits for object-in-place memory: A place for time?

2020 ◽  
Vol 4 ◽  
pp. 239821282093347 ◽  
Author(s):  
John P. Aggleton ◽  
Andrew J.D. Nelson
Keyword(s):  
Object Recognition ◽  
Brain Regions ◽  
Object Location ◽  
Thalamic Nuclei ◽  
Nucleus Reuniens ◽  
Individual Object ◽  
Dorsal Nucleus ◽  
Place Memory ◽  
Behavioural Test ◽  
The Individual

Rodents will spontaneously learn the location of an individual object, an ability captured by the object-in-place test. This review considers the network of structures supporting this behavioural test, as well as some potential confounds that may affect interpretation. A hierarchical approach is adopted, as we first consider those brain regions necessary for two simpler, ‘precursor’ tests (object recognition and object location). It is evident that performing the object-in-place test requires an array of areas additional to those required for object recognition or object location. These additional areas include the rodent medial prefrontal cortex and two thalamic nuclei (nucleus reuniens and the medial dorsal nucleus), both densely interconnected with prefrontal areas. Consequently, despite the need for object and location information to be integrated for the object-in-place test, for example, via the hippocampus, other contributions are necessary. These contributions stem from how object-in-place is a test of associative recognition, as none of the individual elements in the test phase are novel. Parallels between the structures required for object-in-place and for recency discriminations, along with a re-examination of the demands of the object-in-place test, signal the integration of temporal information within what is usually regarded as a spatial-object test.

EPS Mid-Career Award 2006: Understanding anterograde amnesia: Disconnections and hidden lesions

2008 ◽  
Vol 61 (10) ◽  
pp. 1441-1471 ◽  
Author(s):  
John P. Aggleton
Keyword(s):  
Anterograde Amnesia ◽  
Functional System ◽  
Brain Regions ◽  
Retrosplenial Cortex ◽  
Thalamic Nuclei ◽  
Neural Basis ◽  
Lesion Effect ◽  
Anterior Thalamic Nuclei ◽  
Colloid Cysts ◽  
The Many

Three emerging strands of evidence are helping to resolve the causes of the anterograde amnesia associated with damage to the diencephalon. First, new anatomical studies have refined our understanding of the links between diencephalic and temporal brain regions associated with amnesia. These studies direct attention to the limited numbers of routes linking the two regions. Second, neuropsychological studies of patients with colloid cysts confirm the importance of at least one of these routes, the fornix, for episodic memory. By combining these anatomical and neuropsychological data strong evidence emerges for the view that damage to hippocampal—mammillary body—anterior thalamic interactions is sufficient to induce amnesia. A third development is the possibility that the retrosplenial cortex provides an integrating link in this functional system. Furthermore, recent evidence indicates that the retrosplenial cortex may suffer “covert” pathology (i.e., it is functionally lesioned) following damage to the anterior thalamic nuclei or hippocampus. This shared indirect “lesion” effect on the retrosplenial cortex not only broadens our concept of the neural basis of amnesia but may also help to explain the many similarities between temporal lobe and diencephalic amnesia.

scholarly journals Stratum Lacunosum-moleculare Interneurons of the Hippocampus Coordinate Memory Encoding and Retrieval

2021 ◽  
Author(s):  
Jun Guo ◽  
Heankel Cantu Oliveros ◽  
So Jung Oh ◽  
Bo Liang ◽  
Ying Li ◽  
...  
Keyword(s):  
Pyramidal Cells ◽  
Brain Regions ◽  
Cellular Level ◽  
Memory Encoding ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1 ◽  
Stratum Lacunosum Moleculare ◽  
Encoding And Retrieval

Encoding and retrieval of memory are two processes serving distinct biological purposes but operating in highly overlapping brain circuits. It is unclear how the two processes are coordinated in the same brain regions, especially in the hippocampal CA1 region where the two processes converge at the cellular level. Here we find that the neuron-derived neurotrophic factor (NDNF)-positive interneurons at stratum lacunosum-moleculare (SLM) in CA1 play opposite roles in memory encoding and retrieval. These interneurons show high activities in learning and low activities in recall. Increasing their activity facilitates learning but impairs recall. They inhibit the entorhinal- but dis-inhibit the CA3- inputs to CA1 pyramidal cells and thereby either suppress or elevate CA1 pyramidal cells′ activity depending on animal′s behavioral states. Thus, by coordinating entorhinal- and CA3- dual inputs to CA1, these SLM interneurons are key to switching the hippocampus between encoding and retrieval modes.

Dual medial prefrontal cortex and hippocampus projecting neurons in the paraventricular nucleus of the thalamus

2021 ◽  
Author(s):  
Tatiana D. Viena ◽  
Gabriela E. Rasch ◽  
Timothy A. Allen
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Paraventricular Nucleus ◽  
Calcium Binding ◽  
Integration Site ◽  
Critical Role ◽  
Emotional Memory ◽  
Nucleus Reuniens ◽  
Reward Seeking ◽  
Midline Thalamus

AbstractThe paraventricular nucleus (PVT) of the midline thalamus is a critical higher-order cortico-thalamo-cortical integration site that plays a critical role in various behaviors including reward seeking, cue saliency, and emotional memory. Anatomical studies have shown that PVT projects to both medial prefrontal cortex (mPFC) and hippocampus (HC). However, dual mPFC-HC projecting neurons which could serve a role in synchronizing mPFC and HC activity during PVT-dependent behaviors, have not been explored. Here we used a dual retrograde adenoassociated virus (AAV) tracing approach to characterize the location and proportion of different projection populations that send collaterals to mPFC and/or ventral hippocampus (vHC). Additionally, we examined the distribution of calcium binding proteins calretinin (CR) and calbindin (CB) with respect to these projection populations PVT. We found that PVT contains separate populations of cells that project to mPFC, vHC, and those that innervate both regions. Interestingly, dual mPFC-HC projecting cells expressed neither CR or CB. Topographically, mPFC- and vHC-projecting CB+ and CR+ cells clustered around dual projecting neurons in PVT. These results are consistent with the features of dual mPFC-vHC projecting cells in the nucleus reuniens (RE) and suggestive of a functional mPFC-PVT-vHC system that may support mPFC-vHC interactions in PVT-dependent behaviors.

scholarly journals Cell assemblies in the cortico-hippocampal-reuniens network during slow oscillations

2018 ◽  
Author(s):  
David Angulo-Garcia ◽  
Maëva Ferraris ◽  
Antoine Ghestem ◽  
Lauriane Nallet-Khosrofian ◽  
Christophe Bernard ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Information Exchange ◽  
Brain Regions ◽  
Nucleus Reuniens ◽  
Slow Oscillations ◽  
Neuronal Assemblies ◽  
Up States ◽  
Sequential Activation ◽  
The Stability

AbstractThe nucleus reuniens (NR) is an important anatomical and functional relay between the medial prefrontal cortex (mPFC) and the hippocampus (HPC). Whether the NR controls neuronal assemblies, a hallmark of information exchange between the HPC and mPFC for memory transfer/consolidation, is not known. Using simultaneous LFP and unit recordings in NR, HPC and mPFC in rats during slow oscillations under anesthesia, we identified a reliable sequential activation of NR neurons at the beginning of UP states, which preceded mPFC ones. NR sequences were spatially organized, from dorsal to ventral NR. Chemical inactivation of the NR disrupted mPFC sequences at the onset of UP states as well as HPC sequences present during sharp-wave ripples. We conclude that the NR contributes to the coordination and stabilization of mPFC and HPC neuronal sequences during slow oscillations, possibly via the early activation of its own sequences.Significance StatementNeuronal assemblies are believed to be instrumental to code/encode/store information. They can be recorded in different brain regions, suggesting that widely distributed networks of networks are involved in such information processing. The prefrontal cortex, the hippocampus and the thalamic nucleus reuniens constitute a typical example of a complex network involved in memory consolidation. In this study, we show that spatially organized cells assemblies are recruited in the nucleus reuniens at the UP state onset during slow oscillations. Nucleus reuniens activity appears to be necessary to the stability of prefrontal cortex and hippocampal cell assembly formation during slow oscillations. This result further highlights the role of the Nucleus Reuniens as a functional hub for exchanging and processing memories.

scholarly journals Calcium Currents Burst Back: A Possible Role for Dendrites in Epileptogenesis

2007 ◽  
Vol 7 (5) ◽  
pp. 140-141 ◽  
Author(s):  
F. Edward Dudek ◽  
Michael A. Rogawski
Keyword(s):  
Latent Period ◽  
De Novo ◽  
Critical Role ◽  
Pyramidal Cells ◽  
Calcium Currents ◽  
Single Episode ◽  
Ca1 Pyramidal Cells ◽  
Pyramidal Layer ◽  
Low Threshold ◽  
Apical Dendrites

Recruitment of Apical Dendritic T-type Ca2+Channels by Backpropagating Spikes Underlies De Novo Intrinsic Bursting in Hippocampal Epileptogenesis. Yaari Y, Yue C, Su H. J Physiol 2007;580(Pt 2):435–450. A single episode of status epilepticus (SE) induced in rodents by the convulsant pilocarpine, produces, after a latent period of 2 weeks, a chronic epileptic condition. During the latent period of epileptogenesis, most CA1 pyramidal cells that normally fire in a regular pattern, acquire low-threshold bursting behaviour, generating high-frequency clusters of 3–5 spikes as their minimal response to depolarizing stimuli. Recruitment of a Ni2+- and amiloride-sensitive T-type Ca2+ current ( ICaT), shown to be up-regulated after SE, plays a critical role in burst generation in most cases. Several lines of evidence suggest that ICaT driving bursting is located in the apical dendrites. Thus, bursting was suppressed by focally applying Ni2+ to the apical dendrites, but not to the soma. It was also suppressed by applying either tetrodotoxin or the KV7/M-type K+ channel agonist retigabine to the apical dendrites. Severing the distal apical dendrites 150 μM from the pyramidal layer also abolished this activity. Intradendritic recordings indicated that evoked bursts are associated with local Ni2+-sensitive slow spikes. Blocking persistent Na+ current did not modify bursting in most cases. We conclude that SE-induced increase in ICaT density in the apical dendrites facilitates their depolarization by the backpropagating somatic spike. The ICaT-driven dendritic depolarization, in turn, spreads towards the soma, initiating another backpropagating spike, and so forth, thereby creating a spike burst. The early appearance and predominance of ICaT-driven low-threshold bursting in CA1 pyramidal cells that experienced SE most probably contribute to the emergence of abnormal network discharges and may also play a role in the circuitry reorganization associated with epileptogenesis.

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