References

Related publications for ATS products and services
2914 entries

Lesions of the patch compartment of dorsolateral striatum disrupt stimulus-response learning.

Jenrette TA, Logue JB, Horner KA (2019) Lesions of the patch compartment of dorsolateral striatum disrupt stimulus-response learning. Neuroscience 415:161-172. doi: 10.1016/j.neuroscience.2019.07.033

Objective: To investigate whether enhanced activation of the patch compartment contributes to habitual behavior.

Summary: The dorsolateral patch compartment may mediate habit formation by altering information flow through basal ganglia circuits.

Usage: A volume of 2 ul of Dermorphin-SAP (17 ng/ul or an equivalent amount of unconjugated SAP (as a control) was infused bilaterally, at a rate of 0.5 ul/min.

Related Products: Dermorphin-SAP / MOR-SAP (Cat. #IT-12), Saporin (Cat. #PR-01)

Hindbrain glucoregulatory mechanisms: Critical role of catecholamine neurons in the ventrolateral medulla.

Ritter S, Li A-J, Wang Q (2019) Hindbrain glucoregulatory mechanisms: Critical role of catecholamine neurons in the ventrolateral medulla. Physiol Behav 208:112568. doi: 10.1016/j.physbeh.2019.112568

Objective: To explore circuitry and potential glucose-sensing mechanisms that contribute to the functions of glucoregulatory catecholamine neurons in the ventrolateral medulla

Summary: Selective lesion of hindbrain catecholamine neurons abolishes glucoprivic elicitation of key counterregulatory responses. Selective chemogenetic activation of specific catecholamine populations elicits these responses.

Related Products: Anti-DBH-SAP (Cat. #IT-03), NPY-SAP (Cat. #IT-28)

Partial depletion of septohippocampal cholinergic cells reduces seizure susceptibility, but does not mitigate hippocampal neurodegeneration in the kainate model of epilepsy.

Soares JI, Da Costa C, Ferreira MH, Andrade PA, Maia GH, Lukoyanov NV (2019) Partial depletion of septohippocampal cholinergic cells reduces seizure susceptibility, but does not mitigate hippocampal neurodegeneration in the kainate model of epilepsy. Brain Res 1717:235-246. doi: 10.1016/j.brainres.2019.04.027

Objective: To examine how the inhibition of epilepsy-related cholinergic plasticity may be reflected in seizure susceptibility and/or in the development of chronic epilepsy and its neurological consequences.

Summary: These data suggest that seizure-induced plasticity of cholinergic cells may indeed enhance seizure susceptibility and contribute to epileptogenic processes. They do not support the hypothesis that epilepsy-related hypertrophy of cholinergic neurons may potentiate hippocampal cell loss and respective behavioral impairments.

Usage: Bilateral lesions of cholinergic cells were made by infusing 0.5 μl of 192-IgG-saporin (0.08 μg/μl saline solution) into the hippocampus.

Related Products: 192-IgG-SAP (Cat. #IT-01)

The undeveloped properties of GABA neurons in the ventral tegmental area promote energy intake for growth in juvenile rats.

Maejima Y, Yokota S, Horita S, Shimomura K (2019) The undeveloped properties of GABA neurons in the ventral tegmental area promote energy intake for growth in juvenile rats. Sci Rep 9(1):11848. doi: 10.1038/s41598-019-48336-5

Objective: To determine the underlying mechanisms that induce high energy intake (EI) per body weight (BW).

Summary: Undeveloped properties of VTA GABA neurons in juvenile rats can promote higher EI regardless of high or less palatable feeding, and contribute to growth promotion.

Usage: GAT1-SAP or control, Rabbit IgG-SAP, was bilaterally injected (0.025 μg/0.5 μl) into the VTA in eight-week-old adult rats.

Related Products: GAT1-SAP (Cat. #IT-32), Rabbit IgG-SAP (Cat. #IT-35)

Role of nociceptor toll-like receptor 4 (TLR4) in opioid-induced hyperalgesia and hyperalgesic priming.

Araldi D, Bogen O, Green PG, Levine JD (2019) Role of nociceptor toll-like receptor 4 (TLR4) in opioid-induced hyperalgesia and hyperalgesic priming. J Neurosci 39(33):6414-6424. doi: 10.1523/JNEUROSCI.0966-19.2019

Objective: To evaluate the hypothesis that hyperalgesia and priming induced by opioids are mediated by similar nociceptor mechanisms.

Summary: Treatment with isolectin B4 (IB4)-saporin or SSP-saporin (which deplete IB4! and peptidergic nociceptors, respectively), or their combination, prevented systemic LDM-induced hyperalgesia, but not priming. HDM-induced priming, but not analgesia, was markedly attenuated in both saporin-treated groups.

Usage: IB4-SAP was diluted in saline and a dose of 3.2 μg in a volume of 20 μl administered intrathecally. SSP-SAP was diluted in saline and a dose of 100 ng in a volume of 20 μl was administered intrathecally.

Related Products: IB4-SAP (Cat. #IT-10), SSP-SAP (Cat. #IT-11)

Selective role of neurokinin B in IL-31–induced itch response in mice.

Sakata D, Uruno T, Matsubara K, Andoh T, Yamamura K, Magoshi Y, Kunimura K, Kamikaseda Y, Furue M, Fukui Y (2019) Selective role of neurokinin B in IL-31–induced itch response in mice. J Allergy Clin Immunol 144(4):1130-1133. doi: 10.1016/j.jaci.2019.06.031

Objective: To examine the physiological significance of neurokinin B in IL-31–induced itch sensation.

Summary: IL-31–induced scratching was unaffected by intrathecal injection of Nppb-SAP. In contrast,treatment with Bombesin-SAP reduced IL-31–induced scratching. Neurokinin B acts upstream of GRP to transmit IL-31–induced itch sensation.

Usage: Intrathecal injection

Related Products: Bombesin-SAP (Cat. #IT-40), Nppb-SAP (Cat. #IT-69), Blank-SAP (Cat. #IT-21), NKB-SAP (Cat. #IT-63)

Human FAM173A is a mitochondrial lysine-specific methyltransferase that targets adenine nucleotide translocase and affects mitochondrial respiration.

Małecki JM, Willemen HLDM, Pinto R, Ho AYY, Moen A, Eijkelkamp N, Falnes PØ (2019) Human FAM173A is a mitochondrial lysine-specific methyltransferase that targets adenine nucleotide translocase and affects mitochondrial respiration. J Biol Chem 294(31):11654-11664. doi: 10.1074/jbc.RA119.009045 PMID: 31213526

Usage: Western blot

Related Products: Tri-methyl Lysine Rabbit Polyclonal (Cat. #AB-265)

Neuropeptide Y release in the rat spinal cord measured with Y1 receptor internalization is increased after nerve injury.

Marvizon JC, Chen W, Fu W, Taylor BK (2019) Neuropeptide Y release in the rat spinal cord measured with Y1 receptor internalization is increased after nerve injury. Neuropharmacology 158:107732. doi: 10.1016/j.neuropharm.2019.107732

Summary: NPY is released from dorsal horn interneurons or primary afferent terminals by electrical stimulation and by activation of TRPV1, PKA or NMDA receptors in. Release evoked by noxious and tactile stimuli increases after peripheral nerve injury. Ablation of Y1-expressing dorsal horn neurons with NPY-saporin produced antinociception (Lemons and Wiley) and reduced mechanical and cold hypersensitivity in the spared nerve injury model (Nelson et al.), suggesting that they are pro-nociceptive neurons.

Related Products: NPY-SAP (Cat. #IT-28)

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Mixed vehicle emissions induces angiotensin ii and cerebral microvascular angiotensin receptor expression in C57Bl/6 mice and promotes alterations in integrity in a blood-brain barrier coculture model.

Suwannasual U, Lucero J, Davis G, McDonald JD, Lund AK (2019) Mixed vehicle emissions induces angiotensin ii and cerebral microvascular angiotensin receptor expression in C57Bl/6 mice and promotes alterations in integrity in a blood-brain barrier coculture model. Toxicol Sci 170(2):525-535. doi: 10.1093/toxsci/kfz121 PMID: 31132127

Objective: To investigate the hypothesis that inhalation exposure to a mixture of gasoline and diesel vehicle engine emissions (MVE) results in altered central nervous system microvascular integrity mediated by Ang II-AT1 signaling.

Summary: Inhalation exposure to traffic-generated pollutants results in altered BBB integrity, mediated through Ang II-AT1 signaling and inflammation, which is exacerbated by a high-fat diet.

Usage: Antibody was used in immunofluorescent staining of cerebral tissue. Brain sections (10 mm) were prepared for AT1 receptor (1:1000).

Related Products: Angiotensin II receptor (AT-1R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N27AP)

RGS14414 treatment induces memory enhancement and rescues episodic memory deficits.

Masmudi‐Martin M, Navarro‐Lobato I, López‐Aranda MF, Delgado G, Martín‐Montañez E, Quiros‐Ortega ME, Carretero‐Rey M, Narváez L, Garcia‐Garrido MF, Posadas S, López‐Téllez JF, Blanco E, Jiménez‐Recuerda I, Granados‐Durán P, Paez‐Rueda J, López JC and Khan ZU (2019) RGS14414 treatment induces memory enhancement and rescues episodic memory deficits. FASEB J 33:11804-11820. doi: 10.1096/fj.201900429RR

Objective: To investigate the effect of the promotion of neuronal arborization through the expression of the regulator of G-protein signaling 14 of 414 amino acids (RGS14414).

Summary: In addition to showing the potential of RGS14414 for rescuing memory deficits, our results suggest that a boost in circuit activity could facilitate memory enhancement and the reversal of memory deficits.

Usage: 0.9 mg in 1 ml was injected into the PRh.

Related Products: OX7-SAP (Cat. IT-02)

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