ACD can configure probes for the various manual and automated assays for INS for RNAscope Assay, or for Basescope Assay compatible for your species of interest.
Neuroscience
2021 Oct 11
McMeekin, LJ;Joyce, KL;Jenkins, LM;Bohannon, BM;Patel, KD;Bohannon, AS;Patel, A;Fox, SN;Simmons, MS;Day, JJ;Kralli, A;Crossman, DK;Cowell, RM;
PMID: 34648866 | DOI: 10.1016/j.neuroscience.2021.10.007
eNeuro
2023 Jun 22
Paliarin, F;Duplantis, C;Jones, AF;Cucinello-Ragland, J;Basavanhalli, S;Blaze, E;Doré, E;Neel, AI;Sun, H;Chen, R;Edwards, S;Gilpin, NW;Messing, RO;Maiya, R;
PMID: 37364995 | DOI: 10.1523/ENEURO.0043-23.2023
Molecular Metabolism (2019)
2019 Jan 24
Pan W, Allison MB, Sabatini P, Rupp A, Adams J, Patterson C, Jones JC, Olson DP, Myers MG.
| DOI: doi:10.1016/j.molmet.2019.01.007
Molecular psychiatry
2023 May 02
Lavertu-Jolin, M;Chattopadhyaya, B;Chehrazi, P;Carrier, D;Wünnemann, F;Leclerc, S;Dumouchel, F;Robertson, D;Affia, H;Saba, K;Gopal, V;Patel, AB;Andelfinger, G;Pineyro, G;Di Cristo, G;
PMID: 37131076 | DOI: 10.1038/s41380-023-02085-0
eNeuro
2017 Mar 17
Samineni VK, Grajales-Reyes JG, Copits BA, O’Brien DE, Trigg SL, Gomez AM, Bruchas MR, Gereau RW.
PMID: - | DOI: 10.1523/ENEURO.0129-16.2017
The ventrolateral periaqueductal gray (vlPAG) constitutes a major descending pain modulatory system and is a crucial site for opioid-induced analgesia. A number of previous studies have demonstrated that glutamate and GABA play critical opposing roles in nociceptive processing in the vlPAG. It has been suggested that glutamatergic neurotransmission exerts antinociceptive effects, whereas GABAergic neurotransmission exert pro-nociceptive effects on pain transmission, through descending pathways. The inability to exclusively manipulate subpopulations of neurons in the PAG has prevented direct testing of this hypothesis. Here we demonstrate the different contributions of genetically-defined glutamatergic and GABAergic vlPAG neurons in nociceptive processing by employing cell type-specific chemogenetic approaches in mice. Global chemogenetic manipulation of vlPAG neuronal activity suggests that vlPAG neural circuits exert tonic suppression of nociception, consistent with previous pharmacological and electrophysiological studies. However, selective modulation of GABAergic or glutamatergic neurons demonstrates an inverse regulation of nociceptive behaviors by these cell populations. Selective chemogenetic activation of glutamatergic neurons, or inhibition of GABAergic neurons, in vlPAG suppresses nociception. In contrast, inhibition of glutamatergic neurons, or activation of GABAergic neurons, in vlPAG facilitates nociception. Our findings provide direct experimental support for a model in which excitatory and inhibitory neurons in the PAG bidirectionally modulate nociception.
Significance Statement The PAG is a midbrain region critical for the modulation of pain. However, the roles played by the distinct cell types within the PAG in nociceptive processing are poorly understood. This work addresses the divergent roles of glutamatergic and GABAergic PAG neuronal subpopulations in nociceptive processing. We demonstrate that activation of glutamatergic neurons or inhibition of GABAergic neurons suppresses nociception. Whereas inhibition of glutamatergic neuronal activity or activation of GABAergic neuronal activity potentiates nociception. This report identifies distinct roles for these neuronal populations in modulating nociceptive processing.
J Neurosci.
2019 Apr 01
Baho E, Chattopadhyaya B, Lavertu-Jolin M, Mazziotti R, Awad PN, Chehrazi P, Groleau M, Jahannault-Talignani C, Vaucher E, Ango F, Pizzorusso T, Baroncelli L, Di Cristo G.
PMID: 30936240 | DOI: 10.1523/JNEUROSCI.2881-18.2019
By virtue of their extensive axonal arborisation and perisomatic synaptic targeting, cortical inhibitory Parvalbumin (PV) cells strongly regulate principal cell output and plasticity and modulate experience-dependent refinement of cortical circuits during development. An interesting aspect of PV cell connectivity is its prolonged maturation time course, which is completed only by end of adolescence. The p75 neurotrophin receptor (p75NTR) regulates numerous cellular functions, however its role on cortical circuit development and plasticity remains elusive, mainly because localizing p75NTR expression with cellular and temporal resolution has been challenging.By using RNAscope and a modified version of the Proximity Ligation Assay, we found that p75NTR expression in PV cells decreases between the second and fourth postnatal week, at a time when PV cell synapse numbers increase dramatically. Conditional knockout of p75NTR in single PV neurons in vitro and in PV cell networks in vivo causes precocious formation of PV cell perisomatic innervation and perineural nets around PV cell somata, therefore suggesting that p75NTR expression modulates the timing of maturation of PV cell connectivity in the adolescent cortex.Remarkably, we found that PV cells still express p75NTR in adult mouse cortex of both sexes and that its activation is sufficient to destabilize PV cell connectivity and to restore cortical plasticity following monocular deprivation in vivo. Altogether, our results show that p75NTR activation dynamically regulates PV cell connectivity, and represents a novel tool to foster brain plasticity in adults.SIGNIFICANCE STATEMENTIn the cortex, inhibitory, GABA-releasing neurons control the output and plasticity of excitatory neurons. Within this diverse group, parvalbumin-expressing (PV) cells form the larger inhibitory system. PV cell connectivity develops slowly, reaching maturity only at the end of adolescence, however the mechanisms controlling the timing of its maturation are not well understood. We discovered that the expression of the neurotrophin receptor p75NTR in PV cells inhibits the maturation of their connectivity in a cell autonomous fashion, both in vitro and in vivo and that p75NTR activation in adult PV cells promotes their remodelling and restores cortical plasticity. These results reveal a new p75NTR function in the regulation of the time course of PV cell maturation and in limiting cortical plasticity.
J Neurosci.
2019 Apr 08
Parekh PK, Logan RW, Ketchesin KD, Becker-Krail D, Shelton MA, Hildebrand MA, Barko K, Huang YH, McClung CA.
PMID: 30962277 | DOI: 10.1523/JNEUROSCI.2233-18.2019
The circadian transcription factor neuronal PAS domain 2 (NPAS2) is linked to psychiatric disorders associated with altered reward sensitivity. The expression of Npas2 is preferentially enriched in the mammalian forebrain, including the nucleus accumbens (NAc), a major neural substrate of motivated and reward behavior. Previously, we demonstrated that down-regulation of NPAS2 in the NAc reduces the conditioned behavioral response to cocaine in mice. We also showed that Npas2 is preferentially enriched in dopamine receptor 1 containing medium spiny neurons (D1R-MSNs) of the striatum. To extend these studies, we investigated the impact of NPAS2 disruption on accumbal excitatory synaptic transmission and strength, along with the behavioral sensitivity to cocaine reward in a cell-type specific manner. Viral-mediated knockdown of Npas2 in the NAc of male and female C57BL/6J mice increased the excitatory drive onto MSNs. Using Drd1a-tdTomato mice in combination with viral knockdown, we determined these synaptic adaptations were specific to D1R-MSNs relative to non-D1R-MSNs. Interestingly, NAc-specific knockdown of Npas2 blocked cocaine-induced enhancement of synaptic strength and glutamatergic transmission specifically onto D1R-MSNs. Lastly, we designed, validated, and employed a novel Cre-inducible short-hairpin RNA virus for MSN-subtype specific knockdown of Npas2 Cell-type specific Npas2 knockdown in D1R-MSNs, but not D2R-MSNs, in the NAc reduced cocaine conditioned place preference. Together, our results demonstrate that NPAS2 regulates excitatory synapses of D1R-MSNs in the NAc and cocaine reward-related behavior.SIGNIFICANCE STATEMENTDrug addiction is a widespread public health concern often comorbid with other psychiatric disorders. Disruptions of the circadian clock can predispose or exacerbate substance abuse in vulnerable individuals. We demonstrate a role for the core circadian protein, NPAS2, in mediating glutamatergic neurotransmission at medium spiny neurons (MSNs) in the nucleus accumbens (NAc), a region critical for reward processing. We find that NPAS2 negatively regulates functional excitatory synaptic plasticity in the NAc and is necessary for cocaine-induced plastic changes in MSNs expressing the dopamine 1 receptor (D1R). We further demonstrate disruption of NPAS2 in D1R-MSNs produces augmented cocaine preference. These findings highlight the significance of cell-type specificity in mechanisms underlying reward regulation by NPAS2 and extend our knowledge of its function.
Cell Reports
2017 Aug 29
Wyeth MS, Pelkey KA, Yuan X, Vargish G, Johnston AD, Hunt S, Fang C, Abebe D, Mahadevan V, Fisahn A, Salter MW, McInnes RR, Chittajallu R, McBain CJ.
PMID: 28854365 | DOI: 10.1016/j.celrep.2017.08.017
Although Netos are considered auxiliary subunits critical for kainate receptor (KAR) function, direct evidence for their regulation of native KARs is limited. Because Neto KAR regulation is GluK subunit/Neto isoform specific, such regulation must be determined in cell-type-specific contexts. We demonstrate Neto1/2 expression in somatostatin (SOM)-, cholecystokinin/cannabinoid receptor 1 (CCK/CB1)-, and parvalbumin (PV)-containing interneurons. KAR-mediated excitation of these interneurons is contingent upon Neto1 because kainate yields comparable effects in Neto2 knockouts and wild-types but fails to excite interneurons or recruit inhibition in Neto1 knockouts. In contrast, presynaptic KARs in CCK/CB1 interneurons are dually regulated by both Neto1 and Neto2. Neto association promotes tonic presynaptic KAR activation, dampening CCK/CB1 interneuron output, and loss of this brake in Neto mutants profoundly increases CCK/CB1 interneuron-mediatedinhibition. Our results confirm that Neto1 regulates endogenous somatodendritic KARs in diverse interneurons and demonstrate Neto regulation of presynaptic KARs in mature inhibitory presynaptic terminals.
Physiol Behav. 2014 Apr 2. pii: S0031-9384(14)00173-5.
Smith JA, Wang L, Hiller H, Taylor CT, de Kloet AD, Krause EG.
PMID: 24704193 | DOI: 10.1016/j.physbeh.2014.03.027.
Acta neuropathologica communications
2023 Apr 28
Davis, SE;Cook, AK;Hall, JA;Voskobiynyk, Y;Carullo, NV;Boyle, NR;Hakim, AR;Anderson, KM;Hobdy, KP;Pugh, DA;Murchison, CF;McMeekin, LJ;Simmons, M;Margolies, KA;Cowell, RM;Nana, AL;Spina, S;Grinberg, LT;Miller, BL;Seeley, WW;Arrant, AE;
PMID: 37118844 | DOI: 10.1186/s40478-023-01571-4
The Journal of comparative neurology
2023 May 21
Biancardi, V;Yang, X;Ding, X;Passi, D;Funk, GD;Pagliardini, S;
PMID: 37211631 | DOI: 10.1002/cne.25497
eNeuro
2021 Sep 29
Gould, NL;Kolatt Chandran, S;Kayyal, H;Edry, E;Rosenblum, K;
PMID: 34518366 | DOI: 10.1523/ENEURO.0152-21.2021
Description | ||
---|---|---|
sense Example: Hs-LAG3-sense | Standard probes for RNA detection are in antisense. Sense probe is reverse complent to the corresponding antisense probe. | |
Intron# Example: Mm-Htt-intron2 | Probe targets the indicated intron in the target gene, commonly used for pre-mRNA detection | |
Pool/Pan Example: Hs-CD3-pool (Hs-CD3D, Hs-CD3E, Hs-CD3G) | A mixture of multiple probe sets targeting multiple genes or transcripts | |
No-XSp Example: Hs-PDGFB-No-XMm | Does not cross detect with the species (Sp) | |
XSp Example: Rn-Pde9a-XMm | designed to cross detect with the species (Sp) | |
O# Example: Mm-Islr-O1 | Alternative design targeting different regions of the same transcript or isoforms | |
CDS Example: Hs-SLC31A-CDS | Probe targets the protein-coding sequence only | |
EnEm | Probe targets exons n and m | |
En-Em | Probe targets region from exon n to exon m | |
Retired Nomenclature | ||
tvn Example: Hs-LEPR-tv1 | Designed to target transcript variant n | |
ORF Example: Hs-ACVRL1-ORF | Probe targets open reading frame | |
UTR Example: Hs-HTT-UTR-C3 | Probe targets the untranslated region (non-protein-coding region) only | |
5UTR Example: Hs-GNRHR-5UTR | Probe targets the 5' untranslated region only | |
3UTR Example: Rn-Npy1r-3UTR | Probe targets the 3' untranslated region only | |
Pan Example: Pool | A mixture of multiple probe sets targeting multiple genes or transcripts |
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