tt2008

46 entries

Involvement of the basal cholinergic forebrain in the mediation of general (propofol) anesthesia.

Laalou FZ, de Vasconcelos AP, Oberling P, Jeltsch H, Cassel JC, Pain L (2008) Involvement of the basal cholinergic forebrain in the mediation of general (propofol) anesthesia. Anesthesiology 108:888-896. doi: 10.1097/ALN.0b013e31816d919b

Summary: The authors examined whether the basal forebrain cholinergic system is involved in mediating the effects of general anesthesia. Three different forms of 192-IgG-SAP (Cat. #IT-01) administration were used: intracerebroventricular injection of 2 µg, 0.4 µg injected into the nucleus basalis magnocellularis, and 0.8 µg into the medial septum/vertical diagonal band of Broca. The results suggest that loss of cholinergic neurons in the cortex and hippocampus leads to potentiation of the anesthetic effects of Propofol.

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

Oxytocin deficiency mediates hyperphagic obesity of Sim1 haploinsufficient mice.

Kublaoui BM, Gemelli T, Tolson KP, Wang Y, Zinn AR (2008) Oxytocin deficiency mediates hyperphagic obesity of Sim1 haploinsufficient mice. Mol Endocrinol 22(7):1723-1734. doi: 10.1210/me.2008-0067 PMID: 18451093

Summary: Central administration of neuropeptides in the paraventricular nucleus (PVN) is known to inhibit feeding. Here the authors examined altered hypothalamic expression of PVN neuropeptides in Sim1+/- mice. Hypothalamic expression of several neuropeptides, including corticotrophin releasing hormone (Crh) was measured. To do so, anti-Crh (Cat. #AB-02, 1:800) was used in immunohistochemistry. The data suggests that these neurons are involved in melanocortin feeding circuits.

Related Products: Corticotropin Releasing Hormone Rabbit Polyclonal (Cat. #AB-02)

Emergence of spatial impairment in rats following specific cholinergic depletion of the medial septum combined with chronic stress.

Craig LA, Hong NS, Kopp J, McDonald RJ (2008) Emergence of spatial impairment in rats following specific cholinergic depletion of the medial septum combined with chronic stress. Eur J Neurosci 27:2262-2271. doi: 10.1111/j.1460-9568.2008.06179.x

Summary: Although it is clear that loss of cholinergic neurons in the basal forebrain is intrinsic to Alzheimer’s disease, interaction of this loss with other factors in causing the disease symptoms has not been completely elucidated. Rats received bilateral injections of 192-IgG-SAP (Cat. #IT-01) into the medial septum and vertical limb of the diagonal band of Broca totaling 0.075 µg. Lesioned animals were not impaired in a water maze task, but lesioning combined with stress caused a significant reduction in performance.

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

Selective cholinergic lesions in the rat nucleus basalis magnocellularis with limited damage in the medial septum specifically alter attention performance in the five-choice serial reaction time task.

Harati H, Barbelivien A, Cosquer B, Majchrzak M, Cassel JC (2008) Selective cholinergic lesions in the rat nucleus basalis magnocellularis with limited damage in the medial septum specifically alter attention performance in the five-choice serial reaction time task. Neuroscience 153:72-83. doi: 10.1016/j.neuroscience.2008.01.031

Summary: The cognitive deficits reported in rats on use of 192-IgG-SAP (Cat. #IT-01) are varied. Here the authors examined the effect of lesions in the nucleus basalis magnocellularis (NBM) when septal damage was kept to a minimum. The NBM received bilateral 0.2-µg injections of 192-IgG-SAP, and the animals were then tested in a 5-choice serial reaction time task. The disruption of sustained visual attention remained, but other variables such as motivational, locomotion, and impulsivity-related biases were close to normal.

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

Selective ablation of dorsal horn NK(1) expressing cells reveals a modulation of spinal alpha2-adrenergic inhibition of dorsal horn neurones.

Rahman W, Suzuki R, Hunt SP, Dickenson AH (2008) Selective ablation of dorsal horn NK(1) expressing cells reveals a modulation of spinal alpha2-adrenergic inhibition of dorsal horn neurones. Neuropharmacology 54:1208-1214. doi: 10.1016/j.neuropharm.2008.03.014

Summary: In this work the spinal origin of the major descending noradrenergic inhibitory pathway is examined with the help of SP-SAP (Cat. #IT-07). Rats received a 10-µl infusion of 1-mM SP-SAP (saporin, Cat. #PR-01, was used as a control) into the sub-arachnoid space terminating in the L4-5 region. Results from examining neuronal responses under the influence of the alpha2-adrenoceptor antagonist atipamezole suggest that NK1 expressing cells are involved with activity in noradrenergic pathways and descending facilitation.

Related Products: SP-SAP (Cat. #IT-07), Saporin (Cat. #PR-01)

Substance P receptor-expressing dorsal horn neurons: Lessons from the targeted cytotoxin, substance P-saporin.

Wiley RG (2008) Substance P receptor-expressing dorsal horn neurons: Lessons from the targeted cytotoxin, substance P-saporin. Pain 136:7-10. doi: 10.1016/j.pain.2008.03.010

Summary: This review covers some of the more recent work utilizing SP-SAP (Cat. #IT-07) and SSP-SAP (Cat. #IT-11) in the dorsal horn. Specific answers to experimental questions are discussed, as well as some of the questions generated by the research. The potential of SP-SAP and SSP-SAP as pain therapeutics is also explored, along with potential clinical applications of other targeted toxins in pain therapy.

Related Products: SP-SAP (Cat. #IT-07), SSP-SAP (Cat. #IT-11)

Oxaliplatin acts on IB4-positive nociceptors to induce an oxidative stress-dependent acute painful peripheral neuropathy.

Joseph EK, Chen X, Bogen O, Levine JD (2008) Oxaliplatin acts on IB4-positive nociceptors to induce an oxidative stress-dependent acute painful peripheral neuropathy. J Pain 9:463-472. doi: 10.1016/j.jpain.2008.01.335

Summary: Oxaliplatin is a platinum-based chemotherapy agent. Use of this reagent produces various pathological pain states, depending on the dosage site. The authors administered 3.2-µg intrathecal injections of IB4-SAP (Cat. #IT-10), using saporin (Cat. #PR-01) as a control. Lesioning IB4-binding neurons in the dorsal horn completely prevented oxaliplatin-induced hyperalgesia, indicating that the IB4-positive nociceptor neuronal subset is crucial to this type of neuropathy.

Related Products: Saporin (Cat. #PR-01), IB4-SAP (Cat. #IT-10)

Cholinergic deafferentation of prefrontal cortex increases sensitivity to cross-modal distractors during a sustained attention task.

Newman LA, McGaughy J (2008) Cholinergic deafferentation of prefrontal cortex increases sensitivity to cross-modal distractors during a sustained attention task. J Neurosci 28:2642-2650. doi: 10.1523/JNEUROSCI.5112-07.2008

Summary: The authors injected 5 ng of 192-IgG-SAP (Cat. #IT-01) into the prefrontal cortex of rats to investigate the effect of cholinergic loss on distractors to attentional demand. Where all animals experienced impaired performance in the presence of visual distractions, lesioned animals were more sensitive to auditory distractions. While these results indicate compromised top-down processing, lesioned animals showed improved performance in bottom-up processing, possibly caused by a shift in circuit dynamics after the lesion.

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

Neuroanatomical and behavioral effects of a novel version of the cholinergic immunotoxin mu p75-saporin in mice.

Moreau PH, Cosquer B, Jeltsch H, Cassel JC, Mathis C (2008) Neuroanatomical and behavioral effects of a novel version of the cholinergic immunotoxin mu p75-saporin in mice. Hippocampus 18(6):610-622. doi: 10.1002/hipo.20422

Summary: 192-IgG-SAP (Cat. #IT-01) has been used for over a decade to examine the cholinergic system in the basal forebrain of rats. Establishing the same reagent for mice has been problematic. Here the authors describe the use of a mouse-specific lesioning agent, mu p75-SAP (Cat. #IT-16). After deciding on a dosage of 0.4 µg administered in the form of bilateral intracerebroventricular injections, mice were lesioned and tested. Lesioned animals displayed increased locomotor activity, and spatial learning and memory deficits, with minimal side effects.

Related Products: mu p75-SAP (Cat. #IT-16), 192-IgG-SAP (Cat. #IT-01)

Read the featured article in Targeting Trends.

Selective impairment of the cerebellar C1 module involved in rat hind limb control reduces step-dependent modulation of cutaneous reflexes.

Pijpers A, Winkelman BH, Bronsing R, Ruigrok TJ (2008) Selective impairment of the cerebellar C1 module involved in rat hind limb control reduces step-dependent modulation of cutaneous reflexes. J Neurosci 28:2179-2189. doi: 10.1523/JNEUROSCI.4668-07.2008

Summary: The cerebellar cortex is arranged in a series of modules. Elucidation of module-specific function has been difficult because of the closely arranged structure of these modules. Here the authors lesioned the C1/C3 hindlimb module of the rat with CTB-SAP (Cat. #IT-14). Rats received 75-125 ng injections of CTB-SAP into the C1 zone of the copula pyramidis or the paramedian lobule of the right cerebellar hemisphere. C1-injected animals displayed marked diminishment of cutaneously induced reflexes with no significant impact on walking or stepping pattern.

Related Products: CTB-SAP (Cat. #IT-14)

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