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A strict correlation between dendritic and somatic plateau depolarizations in the rat prefrontal cortex pyramidal neurons.

ABSTRACT: One of the fundamental problems in neurobiology is to understand the cellular mechanism for sustained neuronal activity (neuronal UP states). Prefrontal pyramidal neurons readily switch to a long-lasting depolarized state after suprathreshold stimulation of basal dendrites. Analysis of the dendritic input-output function revealed that basal dendrites operate in a somewhat binary regimen (DOWN or UP) in regard to the amplitude of the glutamate-evoked electrical signal. Although the amplitude of the dendritic potential quickly becomes saturated (dendritic UP state), basal dendrites preserve their ability to code additional increase in glutamatergic input. Namely, after the saturation of the plateau amplitude, an additional increase in excitatory input is interpreted as an increase in plateau duration. Experiments performed in tetrodotoxin indicate that the maintenance of a stable depolarized state does not require inhibitory inputs to "balance" the excitation. In the absence of action potential-dependent (network-driven) GABAergic transmission, pyramidal neurons respond to brief (5 ms) glutamate pulses with stable long-lasting (approximately 500 ms) depolarizations. Voltage-sensitive dye recordings revealed that this somatic plateau depolarization is precisely time-locked with the regenerative dendritic plateau potential. The somatic plateau rises a few milliseconds after the onset of the dendritic transient and collapses with the breakdown of the dendritic plateau depolarization. In our in vitro model, the stable long-lasting somatic depolarization (UP state like) is a direct consequence of the local processing of a strong excitatory glutamatergic input arriving on the basal dendrite. The slow component of the somatic depolarization accurately mirrors the glutamate-evoked dendritic plateau potential (dendritic UP state).

SUBMITTER: Milojkovic BA

PROVIDER: S-EPMC5643048 | biostudies-literature | 2005 Apr

REPOSITORIES: biostudies-literature

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A strict correlation between dendritic and somatic plateau depolarizations in the rat prefrontal cortex pyramidal neurons.

Milojkovic Bogdan A BA Radojicic Mihailo S MS Antic Srdjan D SD

The Journal of neuroscience : the official journal of the Society for Neuroscience 20050401 15

One of the fundamental problems in neurobiology is to understand the cellular mechanism for sustained neuronal activity (neuronal UP states). Prefrontal pyramidal neurons readily switch to a long-lasting depolarized state after suprathreshold stimulation of basal dendrites. Analysis of the dendritic input-output function revealed that basal dendrites operate in a somewhat binary regimen (DOWN or UP) in regard to the amplitude of the glutamate-evoked electrical signal. Although the amplitude of t ...[more]

PMID: 15829646

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Project description:Exposure to unpredictable environmental stress is widely recognized as a major determinant for risk and severity in neuropsychiatric disorders such as major depressive disorder, anxiety, schizophrenia, and PTSD. The ability of ostensibly unrelated disorders to give rise to seemingly similar psychiatric phenotypes highlights a need to identify circuit-level concepts that could unify diverse factors under a common pathophysiology. Although difficult to disentangle a causative effect of stress from other factors on medial prefrontal cortex (PFC) dysfunction, a wealth of data from humans and rodents demonstrates that the PFC is a key target of stress. The present study sought to identify a model of chronic unpredictable stress (CUS) which induces affective behaviors in C57BL6J mice and once established, measure stress-related alterations in intrinsic excitability and synaptic regulation of mPFC layer 5/6 pyramidal neurons. Adult male mice received 2 weeks of 'less intense' stress or 2 or 4 weeks of 'more intense' CUS followed by sucrose preference for assessment of anhedonia, elevated plus maze for assessment of anxiety and forced swim test for assessment of depressive-like behaviors. Our findings indicate that more intense CUS exposure results in increased anhedonia, anxiety, and depressive behaviors, while the less intense stress results in no measured behavioral phenotypes. Once a behavioral model was established, mice were euthanized approximately 21 days post-stress for whole-cell patch clamp recordings from layer 5/6 pyramidal neurons in the prelimbic (PrL) and infralimbic (IL) cortices. No significant differences were initially observed in intrinsic cell excitability in either region. However, post-hoc analysis and subsequent confirmation using transgenic mice expressing tdtomato or eGFP under control of dopamine D1-or D2-type receptor showed that D1-expressing pyramidal neurons (D1-PYR) in the PrL exhibit reduced thresholds to fire an action potential (increased excitability) but impaired firing capacity at more depolarized potentials, whereas D2-expressing pyramidal neurons (D2-PYR) showed an overall reduction in excitability and spike firing frequency. Examination of synaptic transmission showed that D1-and D2-PYR exhibit differences in basal excitatory and inhibitory signaling under naïve conditions. In CUS mice, D1-PYR showed increased frequency of both miniature excitatory and inhibitory postsynaptic currents, whereas D2-PYR only showed a reduction in excitatory currents. These findings demonstrate that D1-and D2-PYR subpopulations differentially undergo stress-induced intrinsic and synaptic plasticity that may have functional implications for stress-related pathology, and that these adaptations may reflect unique differences in basal properties regulating output of these cells.

Dataset Information

A strict correlation between dendritic and somatic plateau depolarizations in the rat prefrontal cortex pyramidal neurons.

Publications

A strict correlation between dendritic and somatic plateau depolarizations in the rat prefrontal cortex pyramidal neurons.

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