Neuronal diversity and their spine density in the hippocampal complex of the House Crow (Corvus splendens), a food-storing bird

2016 ◽  
Vol 94 (8) ◽  
pp. 541-553 ◽  
Author(s):  
U.C. Srivastava ◽  
Durgesh Singh ◽  
Prashant Kumar ◽  
Sippy Singh

Hippocampus, one of the parts included in the limbic system, is involved in various functions such as learning, memory, food-storing behavior, and sexual discrimination. Neuronal classes of the hippocampal complex in food-storing birds have been also reported, but the study lacks details pertaining to neuronal characteristics and the spine density of the neurons in different subfields of the hippocampus. Hence, the present study was undertaken with the aim to explore the morphology of neurons and the spines present on their dendrites within the hippocampal complex of the House Crow (Corvus splendens Vieillot, 1817), a food-storing Indian bird, and to compare it with previously reported nonfood-storing bird species. It was observed that the hippocampus of C. splendens harbors diverse neuronal classes with substantial percentages of pyramidal neurons, well-developed local circuit neurons, and high spine density. All these neuronal specializations in C. splendens can be related with the food-storing behavior of the bird, which itself is an advantage over nonfood-storing birds.

2014 ◽  
Vol 37 (3) ◽  
pp. 233-235 ◽  
Author(s):  
Durgesh Singh ◽  
Prashant Kumar ◽  
U. C. Srivastava

1998 ◽  
Vol 1 (3) ◽  
pp. 237-242 ◽  
Author(s):  
M.I. Pérez-Vega ◽  
G. Barajas-López ◽  
A.R. del Angel-Meza ◽  
I. González-Burgos ◽  
A. Feria-Velasco

2020 ◽  
Vol 5 ◽  
pp. 68
Author(s):  
Emma Craig ◽  
Christopher M. Dillingham ◽  
Michal M. Milczarek ◽  
Heather M. Phillips ◽  
Moira Davies ◽  
...  

Background: Neuronal plasticity is thought to underlie learning and memory formation. The density of dendritic spines in the CA1 region of the hippocampus has been repeatedly linked to mnemonic processes. Both the number and spatial location of the spines, in terms of proximity to nearest neighbour, have been implicated in memory formation. To examine how spatial training impacts synaptic structure in the hippocampus, Lister-Hooded rats were trained on a hippocampal-dependent spatial task in the radial-arm maze.  Methods: One group of rats were trained on a hippocampal-dependent spatial task in the radial arm maze. Two further control groups were included: a yoked group which received the same sensorimotor stimulation in the radial-maze but without a memory load, and home-cage controls. At the end of behavioural training, the brains underwent Golgi staining. Spines on CA1 pyramidal neuron dendrites were imaged and quantitatively assessed to provide measures of density and distance from nearest neighbour.  Results: There was no difference across behavioural groups either in terms of spine density or in the clustering of dendritic spines. Conclusions: Spatial learning is not always accompanied by changes in either the density or clustering of dendritic spines on the basal arbour of CA1 pyramidal neurons when assessed using Golgi imaging.


2016 ◽  
Author(s):  
Tharkika Nagendran ◽  
Rylan S. Larsen ◽  
Rebecca L. Bigler ◽  
Shawn B. Frost ◽  
Benjamin D. Philpot ◽  
...  

AbstractInjury of CNS nerve tracts remodels circuitry through dendritic spine loss and hyper-excitability, thus influencing recovery. Due to the complexity of the CNS, a mechanistic understanding of injury-induced synaptic remodeling remains unclear. Using microfluidic chambers to separate and injure distal axons, we show that axotomy causes retrograde dendritic spine loss at directly injured pyramidal neurons followed by retrograde presynaptic hyper-excitability. These remodeling events require activity at the site of injury, axon-to-soma signaling, and transcription. Similarly, directly injured corticospinal neurons in vivo also exhibit a specific increase in spiking following axon injury. Axotomy-induced hyper-excitability of cultured neurons coincides with elimination of inhibitory inputs onto injured neurons, including those formed onto dendritic spines. Netrin-1 downregulation occurs following axon injury and exogenous netrin-1 applied after injury normalizes spine density, presynaptic excitability, and inhibitory inputs at injured neurons. Our findings show that intrinsic signaling within damaged neurons regulates synaptic remodeling and involves netrin-1 signaling.


2019 ◽  
Vol 13 ◽  
Author(s):  
Tamar Macharadze ◽  
Eike Budinger ◽  
Michael Brosch ◽  
Henning Scheich ◽  
Frank W. Ohl ◽  
...  

Neuron ◽  
2014 ◽  
Vol 83 (2) ◽  
pp. 431-443 ◽  
Author(s):  
Yelin Chen ◽  
Yuanyuan Wang ◽  
Ali Ertürk ◽  
Dara Kallop ◽  
Zhiyu Jiang ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Christopher A. Chapleau ◽  
Elena Maria Boggio ◽  
Gaston Calfa ◽  
Alan K. Percy ◽  
Maurizio Giustetto ◽  
...  

Alterations in dendritic spines have been documented in numerous neurodevelopmental disorders, including Rett Syndrome (RTT). RTT, an X chromosome-linked disorder associated with mutations inMECP2, is the leading cause of intellectual disabilities in women. Neurons inMecp2-deficient mice show lower dendritic spine density in several brain regions. To better understand the role of MeCP2 on excitatory spine synapses, we analyzed dendritic spines of CA1 pyramidal neurons in the hippocampus ofMecp2tm1.1Jaemale mutant mice by either confocal microscopy or electron microscopy (EM). At postnatal-day 7 (P7), well before the onset of RTT-like symptoms, CA1 pyramidal neurons from mutant mice showed lower dendritic spine density than those from wildtype littermates. On the other hand, at P15 or later showing characteristic RTT-like symptoms, dendritic spine density did not differ between mutant and wildtype neurons. Consistently, stereological analyses at the EM level revealed similar densities of asymmetric spine synapses in CA1stratum radiatumof symptomatic mutant and wildtype littermates. These results raise caution regarding the use of dendritic spine density in hippocampal neurons as a phenotypic endpoint for the evaluation of therapeutic interventions in symptomaticMecp2-deficient mice. However, they underscore the potential role of MeCP2 in the maintenance of excitatory spine synapses.


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