scholarly journals Regulation of dendritic calcium release in striatal spiny projection neurons

2013 ◽  
Vol 110 (10) ◽  
pp. 2325-2336 ◽  
Author(s):  
Joshua L. Plotkin ◽  
Weixing Shen ◽  
Igor Rafalovich ◽  
Luke E. Sebel ◽  
Michelle Day ◽  
...  
Keyword(s):  
Action Potentials ◽  
Metabotropic Glutamate Receptors ◽  
Glutamate Release ◽  
Brain Slices ◽  
Long Term Potentiation ◽  
Laser Scanning Microscopy ◽  
Projection Neurons ◽  
Indirect Pathway ◽  
Group I

The induction of corticostriatal long-term depression (LTD) in striatal spiny projection neurons (SPNs) requires coactivation of group I metabotropic glutamate receptors (mGluRs) and L-type Ca2+ channels. This combination leads to the postsynaptic production of endocannabinoids that act presynaptically to reduce glutamate release. Although the necessity of coactivation is agreed upon, why it is necessary in physiologically meaningful settings is not. The studies described here attempt to answer this question by using two-photon laser scanning microscopy and patch-clamp electrophysiology to interrogate the dendritic synapses of SPNs in ex vivo brain slices from transgenic mice. These experiments revealed that postsynaptic action potentials induce robust ryanodine receptor (RYR)-dependent Ca2+-induced-Ca2+ release (CICR) in SPN dendritic spines. Depolarization-induced opening of voltage-gated Ca2+ channels was necessary for CICR. CICR was more robust in indirect pathway SPNs than in direct pathway SPNs, particularly in distal dendrites. Although it did not increase intracellular Ca2+ concentration alone, group I mGluR activation enhanced CICR and slowed Ca2+ clearance, extending the activity-evoked intraspine transient. The mGluR modulation of CICR was sensitive to antagonism of inositol trisphosphate receptors, RYRs, src kinase, and Cav1.3 L-type Ca2+ channels. Uncaging glutamate at individual spines effectively activated mGluRs and facilitated CICR induced by back-propagating action potentials. Disrupting CICR by antagonizing RYRs prevented the induction of corticostriatal LTD with spike-timing protocols. In contrast, mGluRs had no effect on the induction of long-term potentiation. Taken together, these results make clearer how coactivation of mGluRs and L-type Ca2+ channels promotes the induction of activity-dependent LTD in SPNs.

Activation of Group I mGluRs Is Necessary for Induction of Long-Term Depression at Striatal Synapses

2001 ◽  
Vol 86 (5) ◽  
pp. 2405-2412 ◽  
Author(s):  
Ki-Wug Sung ◽  
Sukwoo Choi ◽  
David M. Lovinger
Keyword(s):  
Synaptic Transmission ◽  
Metabotropic Glutamate Receptors ◽  
Brain Slices ◽  
High Frequency Stimulation ◽  
Long Term Depression ◽  
Selective Antagonist ◽  
Group I ◽  
Group Ii ◽  
Mglur Antagonist

Activation of metabotropic glutamate receptors (mGluRs), which are coupled to G proteins, has important roles in certain forms of synaptic plasticity including corticostriatal long-term depression (LTD). In the present study, extracellular field potential and whole cell voltage-clamp recording techniques were used to investigate the effect of mGluR antagonists with different subtype specificity on high-frequency stimulation (HFS)-induced LTD of synaptic transmission in the striatum of brain slices obtained from 15-to 25-day-old rats. Induction of LTD was prevented during exposure to the nonselective mGluR antagonist (RS)-α-methyl-4-carboxyphenylglycine (500 μM). The group I mGluR-selective antagonists ( S)-4-carboxy-phenylglycine (50 μM) and (RS)-1-aminoindan-1,5-dicarboxylic acid (100 μM) prevented induction of LTD when applied before and during HFS. The mGluR1-selective antagonist 7-(Hydroxyimino) cyclopropa[b]chromen-1a-carboxylate ethyl ester (80 μM) also blocked LTD induction. Unexpectedly, the mGluR5-selective antagonist 2-methyl-6-(phenylethyl)-pyridine (10 μM) also prevented LTD induction. The group II mGluR antagonist LY307452 (10 μM) did not block LTD induction at corticostriatal synapses, but LY307452 was able to block transient synaptic depression induced by the group II agonist LY314593. None of the antagonists had any effect on basal synaptic transmission at the concentrations used, and mGluR antagonists did not reverse LTD when applied beginning 20 min after HFS. These results suggest that both group I mGluR subtypes contribute to the induction of LTD at corticostriatal synapses.

scholarly journals Long-term potentiation in hippocampal oriens interneurons: postsynaptic induction, presynaptic expression and evaluation of candidate retrograde factors

2014 ◽  
Vol 369 (1633) ◽  
pp. 20130133 ◽  
Author(s):  
Elizabeth Nicholson ◽  
Dimitri M. Kullmann
Keyword(s):  
Ampa Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Long Term Potentiation ◽  
Metabotropic Glutamate ◽  
Ca1 Region ◽  
Group I ◽  
Term Potentiation ◽  
Trpv1 Receptors ◽  
Retrograde Signalling

Several types of hippocampal interneurons exhibit a form of long-term potentiation (LTP) that depends on Ca 2+ -permeable AMPA receptors and group I metabotropic glutamate receptors. Several sources of evidence point to a presynaptic locus of LTP maintenance. The retrograde factor that triggers the expression of LTP remains unidentified. Here, we show that trains of action potentials in putative oriens-lacunosum-moleculare interneurons of the mouse CA1 region can induce long-lasting potentiation of stimulus-evoked excitatory postsynaptic currents that mimics LTP elicited by high-frequency afferent stimulation. We further report that blockers of nitric oxide production or TRPV1 receptors failed to prevent LTP induction. The present results add to the evidence that retrograde signalling underlies N -methyl- d -aspartate (NMDA) receptor-independent LTP in oriens interneurons, mediated by an unidentified factor.

scholarly journals Age-Related Alterations in the Expression of Genes and Synaptic Plasticity Associated with Nitric Oxide Signaling in the Mouse Dorsal Striatum

2015 ◽  
Vol 2015 ◽  
pp. 1-14 ◽  
Author(s):  
Aisa N. Chepkova ◽  
Susanne Schönfeld ◽  
Olga A. Sergeeva
Keyword(s):  
Nitric Oxide ◽  
Synaptic Plasticity ◽  
Metabotropic Glutamate Receptors ◽  
Dorsal Striatum ◽  
Long Term Potentiation ◽  
Striatal Slices ◽  
Expression Of Genes ◽  
Age Related ◽  
Group I

Age-related alterations in the expression of genes and corticostriatal synaptic plasticity were studied in the dorsal striatum of mice of four age groups from young (2-3 months old) to old (18–24 months of age) animals. A significant decrease in transcripts encoding neuronal nitric oxide (NO) synthase and receptors involved in its activation (NR1 subunit of the glutamate NMDA receptor and D1 dopamine receptor) was found in the striatum of old mice using gene array and real-time RT-PCR analysis. The old striatum showed also a significantly higher number of GFAP-expressing astrocytes and an increased expression of astroglial, inflammatory, and oxidative stress markers. Field potential recordings from striatal slices revealed age-related alterations in the magnitude and dynamics of electrically induced long-term depression (LTD) and significant enhancement of electrically induced long-term potentiation in the middle-aged striatum (6-7 and 12-13 months of age). Corticostriatal NO-dependent LTD induced by pharmacological activation of group I metabotropic glutamate receptors underwent significant reduction with aging and could be restored by inhibition of cGMP hydrolysis indicating that its age-related deficit is caused by an altered NO-cGMP signaling cascade. It is suggested that age-related alterations in corticostriatal synaptic plasticity may result from functional alterations in receptor-activated signaling cascades associated with increasing neuroinflammation and a prooxidant state.

scholarly journals Environmental Enrichment Rescues Endocannabinoid-Dependent Synaptic Plasticity Lost in Young Adult Male Mice after Ethanol Exposure during Adolescence

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 825
Author(s):  
Irantzu Rico-Barrio ◽  
Sara Peñasco ◽  
Leire Lekunberri ◽  
Maitane Serrano ◽  
Jon Egaña-Huguet ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Metabotropic Glutamate Receptors ◽  
Transient Receptor Potential ◽  
Long Term Potentiation ◽  
Perforant Path ◽  
Health Concern ◽  
Adolescent Male ◽  
Transient Receptor Potential Vanilloid ◽  
Group I

Binge drinking (BD) is a serious health concern in adolescents as high ethanol (EtOH) consumption can have cognitive sequelae later in life. Remarkably, an enriched environment (EE) in adulthood significantly recovers memory in mice after adolescent BD, and the endocannabinoid, 2-arachydonoyl-glycerol (2-AG), rescues synaptic plasticity and memory impaired in adult rodents upon adolescent EtOH intake. However, the mechanisms by which EE improves memory are unknown. We investigated this in adolescent male C57BL/6J mice exposed to a drinking in the dark (DID) procedure four days per week for a duration of 4 weeks. After DID, the mice were nurtured under an EE for 2 weeks and were subjected to the Barnes Maze Test performed the last 5 days of withdrawal. The EE rescued memory and restored the EtOH-disrupted endocannabinoid (eCB)-dependent excitatory long-term depression at the dentate medial perforant path synapses (MPP-LTD). This recovery was dependent on both the cannabinoid CB1 receptor and group I metabotropic glutamate receptors (mGluRs) and required 2-AG. Also, the EE had a positive effect on mice exposed to water through the transient receptor potential vanilloid 1 (TRPV1) and anandamide (AEA)-dependent MPP long-term potentiation (MPP-LTP). Taken together, EE positively impacts different forms of excitatory synaptic plasticity in water- and EtOH-exposed brains.

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