Morphological homeostasis in cortical dendrites

Neurons have significant potential for the homeostatic regulation of a broad range of functional features, from gene expression to synaptic excitability. In this article, we show that dendritic morphology may also be under intrinsic homeostatic control. We present the results from a statistical analysis of a large collection of digitally reconstructed neurons, demonstrating that fluctuations in dendritic size in one given portion of a neuron are systematically counterbalanced by the remaining dendrites in the same cell. As a result, the total dendritic measure (e.g., number of branches, length, and surface area) of each neuron in a given morphological class is, on average, significantly less random than would be expected if trees (and their parts) were regulated independently during development. This observation is general across scales that range from gross basal/apical subdivisions to individual branches and bifurcations, and its statistical significance is robust among various brain regions, cell types, and experimental conditions. Given the pivotal dendritic role in signal integration, synaptic plasticity, and network connectivity, these findings add a dimension to the functional characterization of neuronal homeostasis

Dendritic but not somatic GABAergic inhibition is decreased in experimental epilepsy.

International audienceImpaired inhibition is thought to be important in temporal lobe epilepsy (TLE), the most common form of epilepsy in adult patients. We report that, in experimental TLE, spontaneous GABAergic inhibition was increased in the soma but reduced in the dendrites of pyramidal neurons. The former resulted from the hyperactivity of somatic projecting interneurons, whereas the latter was probably due to the degeneration of a subpopulation of dendritic projecting interneurons. A deficit in dendritic inhibition could reduce seizure threshold, whereas enhanced somatic inhibition would prevent the continuous occurrence of epileptiform activity

Effects of Age and Acute Ethanol on Glutamatergic Neurotransmission in the Medial Prefrontal Cortex of Freely Moving Rats Using Enzyme-Based Microelectrode Amperometry

Ethanol abuse during adolescence may significantly alter development of the prefrontal cortex which continues to undergo structural remodeling into adulthood. Glutamatergic neurotransmission plays an important role during these brain maturation processes and is modulated by ethanol. In this study, we investigated glutamate dynamics in the medial prefrontal cortex of freely moving rats, using enzyme-based microelectrode amperometry. We analyzed the effects of an intraperitoneal ethanol injection (1 g/kg) on cortical glutamate levels in adolescent and adult rats. Notably, basal glutamate levels decreased with age and these levels were found to be significantly different between postnatal day (PND) 28-38 vs PND 44-55 (p<0.05) and PND 28-38 vs adult animals (p<0.001). We also observed spontaneous glutamate release (transients) throughout the recordings. The frequency of transients (per hour) was significantly higher in adolescent rats (PND 28-38 and PND 44-55) compared to those of adults. In adolescent rats, post-ethanol injection, the frequency of glutamate transients decreased within the first hour (p<0.05), it recovered slowly and in the third hour there was a significant rebound increase of the frequency (p<0.05). Our data demonstrate age-dependent differences in extracellular glutamate levels in the medial prefrontal cortex and suggest that acute ethanol injections have both inhibitory and excitatory effects in adolescent rats. These effects of ethanol on the prefrontal cortex may disturb its maturation and possibly limiting individuals´ control over addictive behaviors