scholarly journals Selective lesion of the hippocampus increases the differentiation of immature neurons in the monkey amygdala

2016 ◽  
Vol 113 (50) ◽  
pp. 14420-14425 ◽  
Author(s):  
Loïc J. Chareyron ◽  
David G. Amaral ◽  
Pierre Lavenex

A large population of immature neurons is present in the ventromedial portion of the adult primate amygdala, a region that receives substantial direct projections from the hippocampal formation. Here, we show the effects of neonatal (n = 8) and adult (n = 6) hippocampal lesions on the populations of mature and immature neurons in the paralaminar, lateral, and basal nuclei of the adult monkey amygdala. Compared with unoperated controls (n = 7), the number of mature neurons was about 70% higher in the paralaminar nucleus of neonate- and adult-lesioned monkeys, and 40% higher in the lateral and basal nuclei of neonate-lesioned monkeys. The number of immature neurons in the paralaminar nucleus was 40% higher in neonate-lesioned monkeys and 30% lower in adult-lesioned monkeys. Similar changes in neuron numbers were also found in two monkeys with nonexperimental, selective, bilateral hippocampal damage. These changes in neuron numbers following hippocampal lesions appear to reflect the differentiation of immature neurons present in the paralaminar nucleus. After adult lesions, the differentiation of immature neurons was essentially restricted to the paralaminar nucleus and was associated with a decrease in the population of immature neurons. In contrast, after neonatal lesions, the differentiation of immature neurons involved the paralaminar, lateral, and basal nuclei. It was associated with an increase in the population of immature neurons in the paralaminar nucleus. Such lesion-induced neuronal plasticity sheds new light on potential mechanisms that may facilitate functional recovery following focal brain injury.

2021 ◽  
Vol 22 (13) ◽  
pp. 6691
Author(s):  
Loïc J. Chareyron ◽  
Pamela Banta Lavenex ◽  
David G. Amaral ◽  
Pierre Lavenex

In recent years, a large population of immature neurons has been documented in the paralaminar nucleus of the primate amygdala. A substantial fraction of these immature neurons differentiate into mature neurons during postnatal development or following selective lesion of the hippocampus. Notwithstanding a growing number of studies on the origin and fate of these immature neurons, fundamental questions about the life and death of these neurons remain. Here, we briefly summarize what is currently known about the immature neurons present in the primate ventral amygdala during development and in adulthood, as well as following selective hippocampal lesions. We provide evidence confirming that the distribution of immature neurons extends to the anterior portions of the entorhinal cortex and layer II of the perirhinal cortex. We also provide novel arguments derived from stereological estimates of the number of mature and immature neurons, which support the view that the migration of immature neurons from the lateral ventricle accompanies neuronal maturation in the primate amygdala at all ages. Finally, we propose and discuss the hypothesis that increased migration and maturation of neurons in the amygdala following hippocampal dysfunction may be linked to behavioral alterations associated with certain neurodevelopmental disorders.


2004 ◽  
Vol 91 (2) ◽  
pp. 1036-1049 ◽  
Author(s):  
Brigitte van Zundert ◽  
Francisco J. Alvarez ◽  
Juan Carlos Tapia ◽  
Hermes H. Yeh ◽  
Emilio Diaz ◽  
...  

Microtubules have been proposed to interact with gephyrin/glycine receptors (GlyRs) in synaptic aggregates. However, the consequence of microtubule disruption on the structure of postsynaptic GlyR/gephyrin clusters is controversial and possible alterations in function are largely unknown. In this study, we have examined the physiological and morphological properties of GlyR/gephyrin clusters after colchicine treatment in cultured spinal neurons during development. In immature neurons (5-7 DIV), disruption of microtubules resulted in a 33 ± 4% decrease in the peak amplitude and a 72 ± 15% reduction in the frequency of spontaneous glycinergic miniature postsynaptic currents (mIPSCs) recorded in whole cell mode. However, similar colchicine treatments resulted in smaller effects on 10-12 DIV neurons and no effect on mature neurons (15-17 DIV). The decrease in glycinergic mIPSC amplitude and frequency reflects postsynaptic actions of colchicine, since postsynaptic stabilization of microtubules with GTP prevented both actions and similar reductions in mIPSC frequency were obtained by modifying the Cl- driving force to obtain parallel reductions in mIPSC amplitude. Confocal microscopy revealed that colchicine reduced the average length and immunofluorescence intensity of synaptic gephyrin/GlyR clusters in immature (approximately 30%) and intermediate (approximately 15%) neurons, but not in mature clusters. Thus the structural and functional changes of postsynaptic gephyrin/GlyR clusters after colchicine treatment were tightly correlated. Finally, RT-PCR, kinetic analysis and picrotoxin blockade of glycinergic mIPSCs indicated a reorganization of the postsynaptic region from containing both α2β and α1β GlyRs in immature neurons to only α1β GlyRs in mature neurons. Microtubule disruption preferentially affected postsynaptic sites containing α2β-containing synaptic receptors.


1965 ◽  
Vol 16 (3_suppl) ◽  
pp. 1277-1290 ◽  
Author(s):  
Daniel R. Snyder ◽  
Robert L. Isaacson

Ten rats with large bilateral hippocampectomies, 10 rats with smaller amounts of damage of the dorsal hippocampus, 10 rats with destruction of postero-lateral neocortex, and 15 normal animals were trained in two types of passive-avoidance situations. One passive-avoidance task required inhibition of drinking while thirsty, the other required an animal to refrain from entering a small compartment after i: had been trained to enter, while hungry, for a food reward. Animals with the largest amounts of hippocampal destruction were impaired in both types of problems. Animals with smaller degrees of hippocampal damage were not different from normal animals in their ability to inhibit licking but were impaired in the other task. Animals with neocortical destruction showed impairment only in the licking situation.


2019 ◽  
Vol 93 (24) ◽  
Author(s):  
Jane X. Yeh ◽  
Eunhye Park ◽  
Kimberly L. W. Schultz ◽  
Diane E. Griffin

ABSTRACT Alphaviruses are enveloped, positive-sense RNA viruses that are important causes of viral encephalomyelitis. Sindbis virus (SINV) infects the neurons of rodents and is a model for studying factors that regulate infection of neuronal cells. The outcome of alphavirus infection of the central nervous system is dependent on neuronal maturation status. Differentiated mature neurons survive and control viral replication better than undifferentiated immature neurons. The cellular factors involved in age-dependent susceptibility include higher levels of antiapoptotic and innate immune factors in mature neurons. Because NF-κB pathway activation is required for the initiation of both apoptosis and the host antiviral response, we analyzed the role of NF-κB during SINV infection of differentiated and undifferentiated rat neuronal cells. SINV infection induced canonical NF-κB activation, as evidenced by the degradation of IκBα and the phosphorylation and nuclear translocation of p65. Inhibition or deletion of the upstream IκB kinase substantially reduced SINV replication in differentiated but not in undifferentiated neuronal cells or mouse embryo fibroblasts. NF-κB inhibition did not affect the establishment of infection, replication complex formation, the synthesis of nonstructural proteins, or viral RNA synthesis in differentiated neurons. However, the translation of structural proteins was impaired, phosphorylation of the α subunit of eukaryotic translation initiation factor 2 (eIF2α) was decreased, and host protein synthesis was maintained, suggesting that NF-κB activation was involved in the regulation of translation during infection of mature neurons. Inhibition or deletion of double-stranded RNA-activated protein kinase (PKR) also decreased eIF2α phosphorylation, the translation of viral structural proteins, and virus production. Therefore, canonical NF-κB activation synergizes with PKR to promote SINV replication in differentiated neurons by facilitating viral structural protein translation. IMPORTANCE Mosquito-borne alphaviruses are a significant and growing cause of viral encephalomyelitis worldwide. The outcome of alphaviral neuronal infections is host age dependent and greatly affected by neuronal maturation status, with differentiated, mature neurons being more resistant to infection than undifferentiated, immature neurons. The biological factors that change during neuronal maturation and that influence the outcome of viral infection are currently only partially defined. These studies investigated the role of NF-κB in determining the outcome of alphaviral infection in mature and immature neurons. Inhibition of canonical NF-κB activation decreased alphavirus replication in mature neurons by regulating protein synthesis and limiting the production of the viral structural proteins but had little effect on viral replication in immature neurons or fibroblasts. Therefore, NF-κB is a signaling pathway that influences the maturation-dependent outcome of alphaviral infection in neurons and that highlights the importance of cellular context in determining the effects of signal pathway activation.


1996 ◽  
Vol 19 (4) ◽  
pp. 770-771
Author(s):  
Dave G. Mumby

AbstractEichenbaum et al. (1994a) hypothesized that perceptually distinct items and the relations among them are processed sequentially by the parahippocampal region and the hippocampal formation, respectively. Predictions based solely on their model's sequential-processing feature might prove easier to disconfirm than those based on its representational features. Two such predictions are discussed: (1) double dissociations should be impossible following hippocampal vs. parahippocampal lesions, and (2) hippocampal lesions should not exacerbate impairments that follow complete parahippocampal lesions.


eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Chiara La Rosa ◽  
Francesca Cavallo ◽  
Alessandra Pecora ◽  
Matteo Chincarini ◽  
Ugo Ala ◽  
...  

The adult mammalian brain is mainly composed of mature neurons. A limited amount of stem cell-driven neurogenesis persists in postnatal life and is reduced in large-brained species. Another source of immature neurons in adult brains is cortical layer II. These cortical immature neurons (cINs) retain developmentally undifferentiated states in adulthood, though they are generated before birth. Here, the occurrence, distribution and cellular features of cINs were systematically studied in 12 diverse mammalian species spanning from small-lissencephalic to large-gyrencephalic brains. In spite of well-preserved morphological and molecular features, the distribution of cINs was highly heterogeneous, particularly in neocortex. While virtually absent in rodents, they are present in the entire neocortex of many other species and their linear density in cortical layer II generally increased with brain size. These findings suggest an evolutionary developmental mechanism for plasticity that varies among mammalian species, granting a reservoir of young cells for the cerebral cortex.


2018 ◽  
Author(s):  
Milenna T. van Dijk ◽  
Zejia Angel Yu ◽  
Younghun Lim ◽  
René Hen ◽  
André A. Fenton

ABSTRACTDiscriminating similar memories and events depends on the dentate gyrus region of the hippocampus. This region is also distinctive because neurogenesis continues in adulthood. Whether both mature and immature granule cells play a role in memory discrimination, and whether the roles are distinct is actively investigated. Here we demonstrate that manipulating either mature or immature granule cells can impair discrimination of similar active place avoidance memories, but the manipulations have different effects. We also observe that prior experience modulates which memories are compromised by inactivation of immature neurons. These data demonstrate the importance of the dentate gyrus network of cells for memory discrimination.


2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Jana Mrzílková ◽  
Matěj Patzelt ◽  
Pasquale Gallina ◽  
Zdeněk Wurst ◽  
Martin Šeremeta ◽  
...  

Micro-CT imaging is a well-established morphological method for the visualization of animal models. We used ethanol fixation of the mouse brains to perform high-resolution micro-CT scans showing in great details brain grey and white matters. It was possible to identify more than 50 neuroanatomical structures on the 5 selected coronal sections. Among white matter structures, we identified fornix, medial lemniscus, crossed tectospinal pathway, mammillothalamic tract, and the sensory root of the trigeminal ganglion. Among grey matter structures, we identified basal nuclei, habenular complex, thalamic nuclei, amygdala, subparts of hippocampal formation, superior colliculi, Edinger–Westphal nucleus, and others. We suggest that micro-CT of the mouse brain could be used for neurohistological lesions evaluation as an alternative to classical neurohistology because it does not destroy brain tissue.


1999 ◽  
Vol 11 (6) ◽  
pp. 682-697 ◽  
Author(s):  
Katharina Henke ◽  
Neal E. A. Kroll ◽  
Hamraz Behniea ◽  
David G. Amaral ◽  
Michael B. Miller ◽  
...  

We present a longitudinal neuropsychological study (31 examinations over a period of 18 months) of patient DF. DF demonstrated bilateral atrophy of the hippocampal formation and globus pallidus resulting from carbon monoxide poisoning. Eighteen months after the event, the volume of the hippocampal formation was reduced by 42% on the left side and 28% on the right. The patient initially presented with a severe global amnesia. Then, he showed a gradual, yet selective recovery of episodic memory function. Verbal free recall and spatial memory performance remained reduced, whereas immediate word recall and recognition memory, as well as picture learning and memory, improved to levels at the lower range of normal performance. Interestingly, nonspatial associative learning was never much impaired and recovered completely by the end of testing. These data are taken as evidence that the human hippocampal formation does not equally support different forms of episodic memory.


Sign in / Sign up

Export Citation Format

Share Document