Circuit-Specific Dendritic Development in the Piriform Cortex

AbstractDendritic geometry is largely determined during postnatal development and has a substantial impact on neural function. In sensory processing, postnatal development of the dendritic tree is affected by two dominant circuit motifs, ascending sensory feedforward inputs and descending and local recurrent connections. In the three-layered anterior piriform cortex, neurons in the sublayers 2a and 2b display vertical segregation of these two circuit motifs. Here, we combined electrophysiology, detailed morphometry and Ca2+ imaging in acute mouse brain slices and modeling to study circuit specific aspects of dendritic development. We observed that determination of branching complexity, dendritic length increases and pruning occurred in distinct developmental phases. Layer 2a and layer 2b neurons displayed developmental phase specific differences between their apical and basal dendritic trees related to differences in circuit incorporation. We further identified functional candidate mechanisms for circuit-specific differences in postnatal dendritic growth in sublayers 2a and 2b at the meso- and microscale level. Already in the first postnatal week, functional connectivity of layer 2a and layer 2b neurons during early spontaneous network activity scales with differences in basal dendritic growth. During the early critical period of sensory plasticity in the piriform cortex, our data is consistent with a model that proposes a role for dendritic NMDA-spikes in selecting branches for survival during developmental pruning in apical dendrites. The different stages of the morphological and functional developmental pattern differences between layer 2a and layer 2b neurons demonstrate the complex interplay between dendritic development and circuit specificity.Significance StatementSensory cortices are composed of ascending sensory circuits that relay sensory information from the periphery and recurrent intracortical circuits. Dendritic trees of neurons are shaped during development and determine which circuits contribute to the neuronal input space. To date, circuit-specific aspects of dendritic development and the underlying mechanisms are poorly understood. Here, we investigate dendritic development in layer 2 of the piriform cortex, a three-layered palaeocortex that displays a clear vertical segregation of sensory and recurrent circuits. Our results suggest that dendritic development occurs in distinct developmental phases with different circuit-specific properties. We further identify candidate mechanisms for neuronal activity patterns that could determine differences in circuit-specific dendritic development.

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Faculty Opinions recommendation of GABAergic circuits control input-spike coupling in the piriform cortex.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1119482.575681 ◽

2008 ◽

Author(s):

John Hildebrand ◽

Hong Lei

Keyword(s):

Piriform Cortex ◽

Control Input ◽

Input Spike

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Faculty Opinions recommendation of Mutant ataxin-3 with an abnormally expanded polyglutamine chain disrupts dendritic development and metabotropic glutamate receptor signaling in mouse cerebellar Purkinje cells.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.718874668.793529549 ◽

2017 ◽

Author(s):

Masanobu Kano

Keyword(s):

Purkinje Cells ◽

Glutamate Receptor ◽

Metabotropic Glutamate Receptor ◽

Receptor Signaling ◽

Metabotropic Glutamate ◽

Dendritic Development ◽

Cerebellar Purkinje Cells

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Analysis of interneurons of the rat piriform cortex : morphology, innervation, calcium binding protein expression and co-expression

10.22215/etd/2007-12521 ◽

2007 ◽

Author(s):

Sabrina D'Alfonso

Keyword(s):

Protein Expression ◽

Calcium Binding ◽

Binding Protein ◽

Piriform Cortex ◽

Calcium Binding Protein

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Effects of Lacosamide Treatment on Epileptogenesis, Neuronal Damage and Behavioral Comorbidities in a Rat Model of Temporal Lobe Epilepsy

International Journal of Molecular Sciences ◽

10.3390/ijms22094667 ◽

2021 ◽

Vol 22 (9) ◽

pp. 4667

Author(s):

Michaela Shishmanova-Doseva ◽

Dimitrinka Atanasova ◽

Yordanka Uzunova ◽

Lyubka Yoanidu ◽

Lyudmil Peychev ◽

...

Keyword(s):

Oxidative Stress ◽

Temporal Lobe Epilepsy ◽

Temporal Lobe ◽

Basolateral Amygdala ◽

Neuronal Damage ◽

Piriform Cortex ◽

Preference Test ◽

Neuroprotective Activity ◽

Object Recognition Test ◽

Beneficial Effects

Clinically, temporal lobe epilepsy (TLE) is the most prevalent type of partial epilepsy and often accompanied by various comorbidities. The present study aimed to evaluate the effects of chronic treatment with the antiepileptic drug (AED) lacosamide (LCM) on spontaneous motor seizures (SMS), behavioral comorbidities, oxidative stress, neuroinflammation, and neuronal damage in a model of TLE. Vehicle/LCM treatment (30 mg/kg, p.o.) was administered 3 h after the pilocarpine-induced status epilepticus (SE) and continued for up to 12 weeks in Wistar rats. Our study showed that LCM attenuated the number of SMS and corrected comorbid to epilepsy impaired motor activity, anxiety, memory, and alleviated depressive-like responses measured in the elevated plus maze, object recognition test, radial arm maze test, and sucrose preference test, respectively. This AED suppressed oxidative stress through increased superoxide dismutase activity and glutathione levels, and alleviated catalase activity and lipid peroxidation in the hippocampus. Lacosamide treatment after SE mitigated the increased levels of IL-1β and TNF-α in the hippocampus and exerted strong neuroprotection both in the dorsal and ventral hippocampus, basolateral amygdala, and partially in the piriform cortex. Our results suggest that the antioxidant, anti-inflammatory, and neuroprotective activity of LCM is an important prerequisite for its anticonvulsant and beneficial effects on SE-induced behavioral comorbidities.

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