- Home
- Knowledge Base
- control-conjugates
control-conjugates
Inflammatory mediators of opioid tolerance: Implications for dependency and addiction.
Eidson LN, Murphy AZ (2019) Inflammatory mediators of opioid tolerance: Implications for dependency and addiction. Peptides 115:51-58. doi: 10.1016/j.peptides.2019.01.003
Objective: To determine what mediates opioid tolerance and alterations in glutamate homeostasis.
Summary: Site-specific lesions of PAG MOR-containing neurons using Dermorphin-SAP significantly reduce the antinociceptive effects of systemic morphine suggesting that PAG MOR is critical for morphine action.
Usage: Rats were injected with 3 pmol of Dermorphin-SAP (Cat. #IT-12) into the PAG. Blank-SAP (Cat. #IT-21) was used as a control.
Related Products: Dermorphin-SAP / MOR-SAP (Cat. #IT-12), Blank-SAP (Cat. #IT-21)
Tac1-expressing neurons in the periaqueductal gray facilitate the itch-scratching cycle via descending regulation
Gao ZR, Chen WZ, Liu MZ, Chen XJ, Wan L, Zhang XY, Yuan L, Lin JK, Wang M, Zhou L, Xu XH, Sun YG (2019) Tac1-expressing neurons in the periaqueductal gray facilitate the itch-scratching cycle via descending regulation. Neuron 101(1):45-59.e9. doi: 10.1016/j.neuron.2018.11.010
Objective: To determine the neural mechanism promoting the itch-scratching cycle.
Summary: Ablation of Tac1+ but not SST+ neurons decreases itch-induced scratching behavior. l/vlPAG Tac1+ neurons Induce Scratching Behavior via a Descending Pathway.
Usage: To ablate the spinal GRPR+ neurons, mice were intrathecally injected with Bombesin-SAP or Control Blank-SAP (400 ng/5 mL).
Related Products: Bombesin-SAP (Cat. #IT-40), Blank-SAP (Cat. #IT-21)
Evidence that the LH surge in ewes involves both neurokinin B-dependent and -independent actions of kisspeptin
Goodman RL, Lopez JA, Bedenbaugh MN, Connors JM, Hardy SL< Hileman SM, Coolen LM, Lehman MN (2018) Evidence that the LH surge in ewes involves both neurokinin B-dependent and -independent actions of kisspeptin. Neuroscience 2018 Abstracts 773.20 / YY14. Society for Neuroscience, San Diego, CA.
Summary: It is generally recognized that kisspeptin plays a key role in induction of the LH surge in sheep and we have reported evidence that neurokinin B (NKB) does so as well. Specifically, disrupting NKB signaling in the retrochiasmatic area (RCh) using either an antagonist to its receptor, NK3R, or lesions of NK3R-containing neurons in the RCh with a saporin conjugate (NK3-SAP) reduced the amplitude of the estrogen-induced LH surge by 50%. Because a KISS1R antagonist (p271) also produced a 50% decrease in surge amplitude, we hypothesized that these two systems are organized in series with NKB actions in the RCh stimulating kisspeptin release. If this is the case, then the combination of NK3R lesions and a KISS1R antagonist should produce the same inhibition as either treatment alone. This experiment tested this prediction using a 2 x 2 design. Breeding season ewes were ovariectomized and immediately given an estradiol (E) implant sc and two progesterone implants (CIDRs) intravaginally that produced luteal phase levels of these steroids. Ewes then received bilateral injections of either NK3-SAP (n=6) or Blank-SAP (n=5) into the RCh. Three weeks later, an artificial follicular phase was produced by inserting four 3 cm long E implants 24 hrs after CIDR removal and either saline or p271 was infused into the lateral ventricle for 16-24 hrs after E implantation; LH was monitored every 2-4 hrs for two days. CIDRs were then reinserted and the protocol repeated in a cross-over design so that all ewes received saline and p271 treatment. In Blank-SAP ewes, p271 decreased the peak of the LH surge from 61.2 ± 7.6 to 27.4 ± 4.6 ng/mL and delayed it 8 hrs (from 26.5 ± 0.5 to 34.1 ± 1.2 hrs post E implantation). The NK3-SAP injections alone decreased the peak of the LH surge to 29.7 ± 10.7 ng/mL compared to Blank-SAP, but the peak was not further inhibited by p271 in these NK3-SAP-treated ewes (24.4 ± 1.4 ng/mL). However, p271 delayed the peak of the LH surge (from 28.8 ± 1.2 to 34.8 ± 2.1 hrs post E implantation) in the ewes injected with NK3-SAP. Based on these results, we propose that kisspeptin has two roles in the LH surge in ewes: it initiates the surge independent of NKB signaling in the RCh, and maintains LH secretion during the surge by a NKB-dependent system.
Related Products: NKB-SAP (Cat. #IT-63), Blank-SAP (Cat. #IT-21), Custom Conjugates
Removal of p75 neurotrophin receptor expression from cholinergic basal forebrain neurons reduces amyloid-β plaque deposition and cognitive impairment in aged APP/PS1 mice.
Qian L, Milne MR, Shepheard S, Rogers ML, Medeiros R, Coulson EJ (2019) Removal of p75 neurotrophin receptor expression from cholinergic basal forebrain neurons reduces amyloid-β plaque deposition and cognitive impairment in aged APP/PS1 mice. Mol Neurobiol 56(7):4639-4652. doi: 10.1007/s12035-018-1404-2
Objective: To investigate the contribution of CBF neuronal p75NTR to the progression of Alzheimer’s Disease
Summary: Data indicate that a direct interaction between CBF-expressed p75NTR and Aβ does not contribute significantly to the regulation of Aβ load.
Usage: To lesion CBF neurons, a single infusion of mu p75-SAP or control Rabbit IgG-SAP (0.4 mg/ml) was stereotaxically-injected into the basal forebrain.
Related Products: mu p75-SAP (Cat. #IT-16), Rabbit IgG-SAP (Cat. #IT-35)
Reduced microglial activity and enhanced glutamate transmission in the basolateral amygdala in early CNS autoimmunity
Acharjee S, Verbeek M, Gomez CD, Bisht K, Lee B, Benoit L, Sharkey KA, Benediktsson A, Tremblay M-E, Pittman QJ (2018) Reduced microglial activity and enhanced glutamate transmission in the basolateral amygdala in early CNS autoimmunity. J Neurosci 38:9019-9033. doi: 10.1523/JNEUROSCI.0398-18.2018
Objective: To identify CNS changes associated with behaviors in multiple sclerosis (MS) patients.
Summary: The data from this study reveal increased synaptic activity and spine density in early stages of experimental autoimmune encephalomyelitis (an animal model of MS) in the basolateral amygdala.
Usage: Mac-1-SAP mouse/human or Rat-IgG-SAP (control) was injected unilaterally in the BLA (1 ug/1 ul).
Related Products: Mac-1-SAP mouse/human (Cat. #IT-06), Rat IgG-SAP (Cat. #IT-17)
Orexinergic neurons are involved in the chemosensory control of breathing during the dark phase in a Parkinson’s disease model.
Oliveira LM, Falquetto B, Moreira TS, Takakura AC (2018) Orexinergic neurons are involved in the chemosensory control of breathing during the dark phase in a Parkinson’s disease model. Exp Neurol 309:107-118. doi: 10.1016/j.expneurol.2018.08.004
Objective: To determine the involvement of orexin cells from the lateral hypothalamus/perifornical area (LH/PeF) on breathing.
Summary: The degeneration of orexinergic neurons in this model of PD can be related to impaired chemoreceptor function in the dark phase.
Usage: For lesions of LH/PeF, two injections of Orexin-B-SAP or Rabbit IgG-SAP (100 ng/μl) were made into the lateral hypothalamus / perifornical area (LH/PeF).
Related Products: Orexin-B-SAP (Cat. #IT-20), Rabbit IgG-SAP (Cat. #IT-35)
Serotonin-specific lesions of the dorsal raphe disrupt maternal aggression and caregiving in postpartum rats.
Holschbach MA, Vitale EM, Lonstein JS (2018) Serotonin-specific lesions of the dorsal raphe disrupt maternal aggression and caregiving in postpartum rats. Behav Brain Res 348:53-64. doi: 10.1016/j.bbr.2018.04.008
Objective: To determine the effects of behavioral modifications associated with early motherhood by permanently disrupting serotonin signaling at one of its primary sources, the dorsal raphe (DR).
Summary: Prepartum serotonin-specific lesions of the DRdm impaired maternal aggression. Larger postpartum DR serotonin lesions affected both aggression and caregiving. DR serotonin lesions did not affect postpartum anxiety.
Usage: 1 μL of 0.1M anti-SERT-SAP or control Mouse IgG-SAP was slowly infused into the DR.
Related Products: Anti-SERT-SAP (Cat. #IT-23), Mouse IgG-SAP (Cat. #IT-18)
Cholinergic modulation targeting medial prefrontal cortex leads to behavior deficit in interval timing task
Zhang Q, De Corte B, Jung D, Kim Y, Geerling J, Narayanan N (2018) Cholinergic modulation targeting medial prefrontal cortex leads to behavior deficit in interval timing task. Neurology 90 (15 Supplement):P5.195.
Objective: To determine the effect of cholinergic lesion targeting medial prefrontal cortex on interval timing behavior.
Summary: Mice receiving medial prefrontal mu-p75-saporin injection performed poorly compared to control mice in interval timing task. Cholinergic lesion targeting medial prefrontal cortex caused interval timing behavior deficit in wild type mice.
Usage: mu-p75-SAP, a toxin targeting cholinergic neurons, into the bilateral medial prefrontal cortical regions of wild type mice pre-trained in interval timing task. Control mice (also pre-trained in interval timing task, n=8) received stereotactic injection of Rabbit IgG-SAP.
Related Products: mu p75-SAP (Cat. #IT-16), Rabbit IgG-SAP (Cat. #IT-35)
Modulation of chronic post-thoracotomy pain by NK-1 neurons in the rostral ventromedial medulla is not paralleled by changes spinal MAPKinase activation.
Strichartz G, Khasabov S, Barr T, Wang J, Simone D (2018) Modulation of chronic post-thoracotomy pain by NK-1 neurons in the rostral ventromedial medulla is not paralleled by changes spinal MAPKinase activation. J Pain 19:S14. doi: 10.1016/j.jpain.2017.12.065
Objective: To evaluate SSP-SAP in treatment of tactile hypersensitivity for Chronic Post-Thoractotomy Pain (CPTP).
Summary: SSP-SAP 3 weeks before thoracotomy and rib retraction (TRR) was able to completely prevent CPTP, assayed by tactile hypersensitivity.
Usage: Ablation of Neurokinin-1 receptor (NK-1R)- expressing neurons in the rat rostral ventromedial medulla (RVM), by micro-injection of the specific neurotoxin SSP-SAP. No effect with treatment of control, Blank-SAP (IT-21).
Related Products: SSP-SAP (Cat. #IT-11), Blank-SAP (Cat. #IT-21)
Acute down-regulation of BDNF signaling does not replicate exacerbated amyloid-β levels and cognitive impairment induced by cholinergic basal forebrain lesion
Turnbull MT, Boskovic Z, Coulson EJ (2018) Acute down-regulation of BDNF signaling does not replicate exacerbated amyloid-β levels and cognitive impairment induced by cholinergic basal forebrain lesion. Front Mol Neurosci 11:51. doi: 10.3389/fnmol.2018.00051
Objective: To determine if degeneration of BFCNs causes a decrease in neurotrophin levels in innervated brain areas, which in turn promotes the development of Amyloid beta pathology and cognitive impairment.
Summary: Lesion of septo-hippocampal BFCNs in a pre-symptomatic transgenic amyloid AD mouse model (APP/PS1 mice) increases soluble Ab levels in the hippocampus, and induces cognitive deficits in a spatial memory task that are not seen in either unlesioned APP/PS1 or non-transgenic littermate control mice. Cognitive decline and Amyloid-beta pathology induced by cholinergic basal forebrain neuron loss occur independent of dysfunctional neuronal BDNF signaling, and may therefore be directly underpinned by reduced cholinergic neurotransmission.
Usage: To lesion BFCNs, a single infusion of murine p75-SAP or control rabbit IgG-SAP (0.4 mg/ml) was stereotaxically injected into the basal forebrain.
Related Products: mu p75-SAP (Cat. #IT-16), Rabbit IgG-SAP (Cat. #IT-35)