Glycinergic Neurotransmission: A Potent Regulator of Embryonic Motor Neuron Dendritic Morphology and Synaptic Plasticity

Fogarty, Matthew J.; Kanjhan, Refik; Bellingham, Mark C.; Noakes, Peter G.

doi:10.1523/jneurosci.1576-15.2016

Cited by 34 publications

(38 citation statements)

References 55 publications

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“…A persistent increase in the excitatory synaptic drive onto mPFC LVPNs and their input resistance is likely to relate to changes in the somatodendritic surface area and volume of individual mPFC LVPNs after ethanol consumption (van Zundert et al, 2008; Fogarty et al, 2016). We therefore investigated the dendritic morphology of the mPFC LVPNs in response to these altered synaptic inputs.…”

Section: Resultsmentioning

confidence: 99%

Increased Synaptic Excitation and Abnormal Dendritic Structure of Prefrontal Cortex Layer V Pyramidal Neurons following Prolonged Binge-Like Consumption of Ethanol

Klenowski

Fogarty

Shariff

et al. 2016

eNeuro

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Long-term alcohol use causes a multitude of neurochemical changes in cortical regions that facilitate the transition to dependence. Therefore, we used a model of long-term, binge-like ethanol consumption in rats to determine the effects on morphology and synaptic physiology of medial prefrontal cortex (mPFC) layer V pyramidal neurons. Following 10 weeks of ethanol consumption, we recorded synaptic currents from mPFC neurons and used neurobiotin filling to analyze their morphology. We then compared these data to measurements obtained from age-matched, water-drinking control rats. We found that long-term ethanol consumption caused a significant increase in total dendrite arbor length of mPFC layer V pyramidal neurons. Dendritic restructuring was primarily observed in basal dendrite arbors, with mPFC neurons from animals engaged in long-term ethanol drinking having significantly larger and more complex basal arbors compared with controls. These changes were accompanied by significantly increased total spine densities and spontaneous postsynaptic excitatory current frequency, suggesting that long-term binge-like ethanol consumption enhances basal excitatory synaptic transmission in mPFC layer V pyramidal neurons. Our results provide insights into the morphological and functional changes in mPFC layer V pyramidal neuronal physiology following prolonged exposure to ethanol and support changes in mPFC activity during the development of alcohol dependence.

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Section: Resultsmentioning

confidence: 99%

Increased Synaptic Excitation and Abnormal Dendritic Structure of Prefrontal Cortex Layer V Pyramidal Neurons following Prolonged Binge-Like Consumption of Ethanol

Klenowski

Fogarty

Shariff

et al. 2016

eNeuro

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show abstract

“…GABA is the main inhibitory neurotransmitter in the adult forebrain, whereas glycine mediates inhibitory neurotransmission mainly in the brainstem and spinal cord (Fogarty et al . ).…”

Section: Synapse Structure and Functionmentioning

confidence: 97%

“…The most abundant excitatory neurotransmitter in the central nervous system is glutamate. GABA is the main inhibitory neurotransmitter in the adult forebrain, whereas glycine mediates inhibitory neurotransmission mainly in the brainstem and spinal cord (Fogarty et al 2016).…”

mentioning

confidence: 99%

Synaptopathies: synaptic dysfunction in neurological disorders – A review from students to students

Lepeta

Lourenco

Schweitzer

et al. 2016

Journal of Neurochemistry

264

220

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Synapses are essential components of neurons and allow information to travel coordinately throughout the nervous system to adjust behavior to environmental stimuli and to control body functions, memories, and emotions. Thus, optimal synaptic communication is required for proper brain physiology, and slight perturbations of synapse function can lead to brain disorders. In fact, increasing evidence has demonstrated the relevance of synapse dysfunction as a major determinant of many neurological diseases. This notion has led to the concept of synaptopathies as brain diseases with synapse defects as shared pathogenic features. In this review, which was initiated at the 13th International Society for Neurochemistry Advanced School, we discuss basic concepts of synapse structure and function, and provide a critical view of how aberrant synapse physiology may contribute to neurodevelopmental disorders (autism, Down syndrome, startle disease, and epilepsy) as well as neurodegenerative disorders (Alzheimer and Parkinson disease). We finally discuss the appropriateness and potential implications of gathering synapse diseases under a single term. Understanding common causes and intrinsic differences in diseaseassociated synaptic dysfunction could offer novel clues toward synapse-based therapeutic intervention for neurological and neuropsychiatric disorders.

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“…They provide synaptic input to motoneurons of the ventral spinal cord or the respiratory-related motor nuclei, thereby shaping the signaling to motoneurons [44,45]). Central glycinergic synaptic activity also plays a vital role in regulating motoneuron morphology and glutamatergic central synaptic inputs to these neurons during late embryonic development [46]. The activity of GlyT2 is essential for maintaining diverse aspects of the motor function.…”

Section: Movement Diseases: Hyperekplexiamentioning

confidence: 99%

Glycinergic transmission: glycine transporter GlyT2 in neuronal pathologies

2016

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Glycinergic neurons are major contributors to the regulation of neuronal excitability, mainly in caudal areas of the nervous system. These neurons control fluxes of sensory information between the periphery and the CNS and diverse motor activities like locomotion, respiration or vocalization. The phenotype of a glycinergic neuron is determined by the expression of at least two proteins: GlyT2, a plasma membrane transporter of glycine, and VIAAT, a vesicular transporter shared by glycine and GABA. In this article, we review recent advances in understanding the role of GlyT2 in the pathophysiology of inhibitory glycinergic neurotransmission. GlyT2 mutations are associated to decreased glycinergic function that results in a rare movement disease termed hyperekplexia (HPX) or startle disease. In addition, glycinergic neurons control pain transmission in the dorsal spinal cord and their function is reduced in chronic pain states. A moderate inhibition of GlyT2 may potentiate glycinergic inhibition and constitutes an attractive target for pharmacological intervention against these devastating conditions.

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Glycinergic Neurotransmission: A Potent Regulator of Embryonic Motor Neuron Dendritic Morphology and Synaptic Plasticity

Cited by 34 publications

References 55 publications

Increased Synaptic Excitation and Abnormal Dendritic Structure of Prefrontal Cortex Layer V Pyramidal Neurons following Prolonged Binge-Like Consumption of Ethanol

Increased Synaptic Excitation and Abnormal Dendritic Structure of Prefrontal Cortex Layer V Pyramidal Neurons following Prolonged Binge-Like Consumption of Ethanol

Synaptopathies: synaptic dysfunction in neurological disorders – A review from students to students

Glycinergic transmission: glycine transporter GlyT2 in neuronal pathologies

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