Effects of prenatal ethanol exposure on dendritic spines of layer V pyramidal neurons in the somatosensory cortex of the rat

Abstract Fetal alcohol spectrum disorder (FASD) encompasses a range of cognitive and behavioral deficits, with aberrances in the function of cerebral cortical pyramidal neurons implicated in its pathology. However, the mechanisms underlying these aberrances, including whether they persist well beyond ethanol exposure in utero, remain to be explored. We addressed these issues by employing a mouse model of FASD in which pregnant mice were exposed to binge-type ethanol from embryonic day 13.5 through 16.5. In both male and female offspring (postnatal day 28–32), whole-cell patch clamp recording of layer V/VI somatosensory cortex pyramidal neurons revealed increases in the frequency of excitatory and inhibitory postsynaptic currents. Furthermore, expressing channelrhodopsin in either GABAergic interneurons (Nkx2.1Cre-Ai32) or glutamatergic pyramidal neurons (Emx1IRES Cre-Ai32) revealed a shift in optically evoked paired-pulse ratio. These findings are consistent with an excitatory-inhibitory imbalance with prenatal ethanol exposure due to diminished inhibitory but enhanced excitatory synaptic strength. Prenatal ethanol exposure also altered the density and morphology of spines along the apical dendrites of pyramidal neurons. Thus, while both presynaptic and postsynaptic mechanisms are affected following prenatal exposure to ethanol, there is a prominent presynaptic component that contributes to altered inhibitory and excitatory synaptic transmission in the somatosensory cortex.

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Noradrenergic enhancement of GABA-induced input resistance changes in layer V regular spiking pyramidal neurons of rat somatosensory cortex

Brain Research ◽

10.1016/0006-8993(95)00060-4 ◽

1995 ◽

Vol 675 (1-2) ◽

pp. 171-182 ◽

Cited By ~ 31

Author(s):

Francis M. Sessler ◽

Weimin Liu ◽

Michael L. Kirifides ◽

Robert D. Mouradian ◽

Rick C.-S. Lin ◽

...

Keyword(s):

Somatosensory Cortex ◽

Pyramidal Neurons ◽

Input Resistance ◽

Layer V ◽

Rat Somatosensory Cortex

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Steady-state dynamics and experience-dependent plasticity of dendritic spines of layer 4/5a pyramidal neurons in somatosensory cortex

Frontiers in Systems Neuroscience ◽

10.3389/conf.fnsys.2014.05.00016 ◽

2014 ◽

Vol 8 ◽

Author(s):

Miquelajauregui Amaya ◽

Kribakaran Sahana ◽

Mostany Ricardo ◽

Badaloni Aurora ◽

Consalez Giacomo ◽

...

Keyword(s):

Steady State ◽

Somatosensory Cortex ◽

Dendritic Spines ◽

Pyramidal Neurons ◽

Dependent Plasticity ◽

Layer 4

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Plastic changes to dendritic spines on layer V pyramidal neurons are involved in the rectifying role of the prefrontal cortex during the fast period of motor learning

Behavioural Brain Research ◽

10.1016/j.bbr.2015.11.013 ◽

2016 ◽

Vol 298 ◽

pp. 261-267 ◽

Cited By ~ 8

Author(s):

David González-Tapia ◽

Nestor I. Martínez-Torres ◽

Marisela Hernández-González ◽

Miguel Angel Guevara ◽

Ignacio González-Burgos

Keyword(s):

Prefrontal Cortex ◽

Motor Learning ◽

Dendritic Spines ◽

Pyramidal Neurons ◽

Plastic Changes ◽

Layer V

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Fear extinction reverses dendritic spine formation induced by fear conditioning in the mouse auditory cortex

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1801504115 ◽

2018 ◽

Vol 115 (37) ◽

pp. 9306-9311 ◽

Cited By ~ 19

Author(s):

Cora Sau Wan Lai ◽

Avital Adler ◽

Wen-Biao Gan

Keyword(s):

Auditory Cortex ◽

Fear Conditioning ◽

Dendritic Spines ◽

Dendritic Spine ◽

Pyramidal Neurons ◽

Fear Extinction ◽

Spine Formation ◽

Synaptic Circuits ◽

Auditory Cue ◽

Layer V

Fear conditioning-induced behavioral responses can be extinguished after fear extinction. While fear extinction is generally thought to be a form of new learning, several lines of evidence suggest that neuronal changes associated with fear conditioning could be reversed after fear extinction. To better understand how fear conditioning and extinction modify synaptic circuits, we examined changes of postsynaptic dendritic spines of layer V pyramidal neurons in the mouse auditory cortex over time using transcranial two-photon microscopy. We found that auditory-cued fear conditioning induced the formation of new dendritic spines within 2 days. The survived new spines induced by fear conditioning with one auditory cue were clustered within dendritic branch segments and spatially segregated from new spines induced by fear conditioning with a different auditory cue. Importantly, fear extinction preferentially caused the elimination of newly formed spines induced by fear conditioning in an auditory cue-specific manner. Furthermore, after fear extinction, fear reconditioning induced reformation of new dendritic spines in close proximity to the sites of new spine formation induced by previous fear conditioning. These results show that fear conditioning, extinction, and reconditioning induce cue- and location-specific dendritic spine remodeling in the auditory cortex. They also suggest that changes of synaptic connections induced by fear conditioning are reversed after fear extinction.

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