Distribution of GABAA receptor subunit mRNAs in rat lumbar spinal cord

Wisden, William; Gundlach, Andrew L.; Barnard, Eric A.; Seeburg, Peter H.; Hunt, S. P.

doi:10.1016/0169-328x(91)90109-b

Cited by 92 publications

(62 citation statements)

References 22 publications

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“…We show that at P1, only the GABA A R␣2 and GABA A R␣3 remain expressed on the surface of TS motoneurons. During the first postnatal week, the expression of both subunits decreases but they are still observed at P12, in agreement with in situ hybridization in adult rat lumbar spinal cord (Wisden et al, 1991). At P7, mixed GABA/glycine events represented 18% of the miniature IPSCs.…”

Section: Postnatal Development Of Glyr and Gaba A R In Ts Motoneuronssupporting

confidence: 61%

Differential Plasticity of the GABAergic and Glycinergic Synaptic Transmission to Rat Lumbar Motoneurons after Spinal Cord Injury

Sadlaoud

Tazerart²,

Brocard³

et al. 2010

J. Neurosci.

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Maturation of inhibitory postsynaptic transmission onto motoneurons in the rat occurs during the perinatal period, a time window during which pathways arising from the brainstem reach the lumbar enlargement of the spinal cord. There is a developmental switch in miniature IPSCs (mIPSCs) from predominantly long-duration GABAergic to short-duration glycinergic events. We investigated the effects of a complete neonatal [postnatal day 0 (P0)] spinal cord transection (SCT) on the expression of Glycine and GABA A receptor subunits (GlyR and GABA A R subunits) in lumbar motoneurons. In control rats, the density of GlyR increased from P1 to P7 to reach a plateau, whereas that of GABA A R subunits dropped during the same period. In P7 animals with neonatal SCT (SCT-P7), the GlyR densities were unchanged compared with controls of the same age, while the developmental downregulation of GABA A R was prevented. Whole-cell patch-clamp recordings of mIPSCs performed in lumbar motoneurons at P7 revealed that the decay time constant of miniature IPSCs and the proportion of GABAergic events significantly increased after SCT. After daily injections of the 5-HT 2 R agonist DOI, GABA A R immunolabeling on SCT-P7 motoneurons dropped down to values reported in control-P7, while GlyR labeling remained stable. A SCT made at P5 significantly upregulated the expression of GABA A R 1 week later with little, if any, influence on GlyR. We conclude that the plasticity of GlyR is independent of supraspinal influences whereas that of GABA A R is markedly influenced by descending pathways, in particular serotoninergic projections.

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Section: Postnatal Development Of Glyr and Gaba A R In Ts Motoneuronssupporting

confidence: 61%

Differential Plasticity of the GABAergic and Glycinergic Synaptic Transmission to Rat Lumbar Motoneurons after Spinal Cord Injury

Sadlaoud

Tazerart²,

Brocard³

et al. 2010

J. Neurosci.

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“…GABA A receptors containing the ␣4-subunit are insensitive to benzodiazepines (Wisden et al, 1991), so we examined ␣4-subunit expression and localization using Western analysis of BLA tissue. There was no treatment-related change in total ␣4-subunit protein expression ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Chronic Ethanol and Withdrawal Differentially Modulate Lateral/Basolateral Amygdala Paracapsular and Local GABAergic Synapses

Diaz

Christian²,

Anderson³

et al. 2011

J Pharmacol Exp Ther

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Withdrawal-related anxiety is cited as a major contributor to relapse in recovering alcoholics. Changes in lateral/basolateral amygdala (BLA) neurotransmission could directly influence anxiety-like behaviors after chronic ethanol exposure and withdrawal. We have shown that these treatments enhance BLA glutamatergic function and neurotransmission. However, the BLA GABAergic system tightly controls the expression of anxiety-like behavior, and additional neuroadaptations in this system are potentially important as well. The intrinsic BLA GABAergic system consists of at least two populations of interneurons: local feed-back interneurons scattered throughout the region and feed-forward interneurons concentrated within groups found in the lateral/paracapsular region of the BLA. In the present study, we found that withdrawal from chronic ethanol robustly decreased presynaptic function at feed-forward GABA synapses but did not alter neurotransmitter release from local interneurons. Differential presynaptic changes at these synapses were complemented by decreased zolpidem sensitivity at feed-forward synapses and decreased midazolam sensitivity at local synapses. Consistent with this, chronic ethanol/ withdrawal decreased expression of GABA ␣1-subunit total protein and increased surface expression of ␣4-subunit protein. We also found transient increases in GABA-receptor-associated protein levels and persistent increases in ␥2-subunit and gephyrin proteins that would suggest alterations in GABA A receptor trafficking that might help regulate changes in ␣4-subunit localization. These data together suggest that chronic ethanol and withdrawal differentially modulate local and lateral paracapsular cell GABAergic synapses via distinct presynaptic and postsynaptic mechanisms. These findings extend our understanding of the neurobiological mechanisms governing changes in anxiety-like behavior after chronic ethanol exposure and withdrawal.

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“…This pharmacological diversity is further exacerbated by the neuroanatomical heterogeneity of the distribution of these different GABA A receptor subtypes. Thus, although the cortex and hippocampus contain ␣ 1 , ␣ 2 , ␣ 3 , ␣ 4 , and ␣ 5 subunits, more restricted localizations are found in the cerebellum (primarily ␣ 1 and ␣ 6 ), spinal cord (primarily ␣ 2 and ␣ 3 ), and thalamus (primarily ␣ 1 and ␣ 4 ) (Wisden et al 1991(Wisden et al , 1992Fritschy and Mohler 1995). Consistent with this anatomical distribution, in vitro pharmacological analysis of cerebellum and spinal cord GABA A receptors (Villiger 1984;Watanabe et al 1985;Langer and Arbilla 1988;Benavides et al 1988Benavides et al , 1992 suggests that the benzodiazepine pharmacology of the cerebellum and spinal cord are dictated largely by the ␣ 1 and ␣ 2 and ␣ 3 subunits, respectively.…”

mentioning

confidence: 99%

Regional Differences in the Inhibition of Mouse In Vivo [3H]Ro 15-1788 Binding Reflect Selectivity for α1 versus α2 and α3 Subunit-Containing GABAA Receptors

Atack

Smith

Emms

et al. 1999

Neuropsychopharmacology

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Distribution of GABAA receptor subunit mRNAs in rat lumbar spinal cord

Cited by 92 publications

References 22 publications

Differential Plasticity of the GABAergic and Glycinergic Synaptic Transmission to Rat Lumbar Motoneurons after Spinal Cord Injury

Differential Plasticity of the GABAergic and Glycinergic Synaptic Transmission to Rat Lumbar Motoneurons after Spinal Cord Injury

Chronic Ethanol and Withdrawal Differentially Modulate Lateral/Basolateral Amygdala Paracapsular and Local GABAergic Synapses

Regional Differences in the Inhibition of Mouse In Vivo [3H]Ro 15-1788 Binding Reflect Selectivity for α1 versus α2 and α3 Subunit-Containing GABAA Receptors

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