targeted-toxins

Chen L, Brown RE, McKenna JT, McCarley RW (2009) Animal models of narcolepsy. CNS Neurol Disord Drug Targets 8(4):296-308. doi: 10.2174/187152709788921717 PMID: 19689311

Objective: To provide information to enable a consensus concerning the evaluation of narcoleptic behavioral and EEG phenomenology in these models.

Related Products: Orexin-B-SAP (Cat. #IT-20)

See Also:

• Gerashchenko K et al. Effects of lateral hypothalamic lesion with the neurotoxin hypocretin-2-saporin on sleep in Long-Evans rats. Neuroscience 116:223-235, 2003.

Sun YG, Zhao ZQ, Meng XL, Yin J, Liu XY, Chen ZF (2009) Cellular basis of itch sensation. Science 325:1531-1534. doi: 10.1126/science.1174868

Summary: Whether itch and pain use separate neuronal pathways has long been a subject of debate. The authors injected 400 ng of bombesin-SAP (Cat. #IT-40) into the intrathecal space of mice and examined itch and pain behavior. Lesioned mice had dramatic deficits in all itch behavior tested regardless of the histamine dependence of the itch. All pain behaviors, however, were left intact. These data indicate that the gastrin-releasing peptide receptor-expressing neurons are essential for itch transmission.

Related Products: Bombesin-SAP (Cat. #IT-40)

Read the featured article in Targeting Trends.

Fargo KN, Foster AM, Sengelaub DR (2009) Neuroprotective effect of testosterone treatment on motoneuron recruitment following the death of nearby motoneurons. Dev Neurobiol 69:825-835. doi: 10.1002/dneu.20743

Summary: Previous work has demonstrated that testosterone treatment can prevent dendritic atrophy due to death of nearby motoneurons. This experiment examined whether this protection extends to motor activation. Rats received a 1 µg injection of CTB-SAP (Cat. #IT-14) into each of the right bulbocavernosus and levator ani muscles. Animals treated with testosterone preserved more of the activity duration than untreated animals, as well as no decrease in motoneuron recruitment.

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

Arias-Carrion O, Murillo-Rodriguez E (2009) Cell transplantation: a future therapy for narcolepsy?. CNS Neurol Disord Drug Targets 8:309-314. doi: 10.2174/187152709788921681

Summary: This review covers the current understanding of narcolepsy and discusses the potential for transplants as a therapeutic treatment. Animal models are summarized, including the use of orexin-SAP (Cat. #IT-20) in rats. The review goes on to suggest that production of orexigenic neuroblasts from stem cells may be a useful therapy.

Related Products: Orexin-B-SAP (Cat. #IT-20)

Ma J, Tai SK, Leung LS (2009) Ketamine-induced deficit of auditory gating in the hippocampus of rats is alleviated by medial septal inactivation and antipsychotic drugs. Psychopharmacology (Berl) 206:457-467. doi: 10.1007/s00213-009-1623-3

Summary: Schizophrenic patients do not experience the usual diminished response to repeated stimuli, otherwise known as gating. Gating loss can be caused by the administration of some psychotomimetic drugs. This study used 170 ng injections of 192-IgG-SAP (Cat. #IT-01) to examine the effect of ketamine on sensory gating loss. Elimination of septohippocampal cholinergic neurons alleviated the disruption of auditory gating caused by ketamine.

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

Vetrivelan R, Fuller PM, Tong Q, Lu J (2009) Medullary circuitry regulating rapid eye movement sleep and motor atonia. J Neurosci 29:9361-9369. doi: 10.1523/JNEUROSCI.0737-09.2009

Summary: Data concerning rapid-eye movement (REM) motor atonia in rats has not agreed with results seen in large amount of data from cats. Here the authors traced the medullary networks in rats involved with this REM function. 120-300 ng injections of orexin-SAP (Cat. #IT-20) were administered to 6 different sites in the medulla. Ablation of orexin receptor-expressing neurons in one site in the ventromedial medulla resulted in intermittent loss of muscle atonia, indicating that glutaminergic neurons in this area are key components of the REM atonia circuit.

Related Products: Orexin-B-SAP (Cat. #IT-20)

Kaur S, Thankachan S, Begum S, Liu M, Blanco-Centurion C, Shiromani PJ (2009) Hypocretin-2 saporin lesions of the ventrolateral periaquaductal gray (vlPAG) increase REM sleep in hypocretin knockout mice. PLoS One 4:e6346. doi: 10.1371/journal.pone.0006346

Summary: Not all connections between narcolepsy and orexin are understood, since orexin neurons are located in the lateral hypothalamus and some sleep functions are controlled by the brainstem. This experiment used 16.5 ng injections of orexin-SAP (Cat. #IT-20) into each side of the ventrolateral periaqueductal gray (v/PAG to) examine these connections. The results indicate that loss of orexin neurons in the v/PAG results in loss of inhibitory control over REM sleep, but does not cause cataplexy.

Related Products: Orexin-B-SAP (Cat. #IT-20)

Montero M, Gonzalez B, Zimmer J (2009) Featured Article: Depletion of microglia by Mac-1-SAP in mouse hippocampal slice cultures enhances ischemia-like neurodegeneration. Targeting Trends 10(3)

Related Products: Mac-1-SAP mouse/human (Cat. #IT-06)

Read the featured article in Targeting Trends.

See Also:

• Montero M et al. Immunotoxic depletion of microglia in mouse hippocampal slice cultures enhances ischemia-like neurodegeneration. Brain Res 1291:140-152, 2009.

Lopez-Aranda MF, Lopez-Tellez JF, Navarro-Lobato I, Masmudi-Martin M, Gutierrez A, Khan ZU (2009) Role of layer 6 of V2 visual cortex in object-recognition memory. Science 325:87-89. doi: 10.1126/science.1170869

Summary: The authors examined the role of the V2 visual cortex in visual memory. Working with the prediction that object-recognition memory (ORM) control is centered in the V2 visual cortex, rats received 0.9 µg injections of OX7-SAP (Cat. #IT-02) into this area. Treatment with OX7-SAP eliminated virtually all neurons in layer 6 of area V2 of the visual cortex without damaging the hippocampus. The results indicate that this area of the visual cortex is important for ORM formation, but not storage.

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

Esclassan F, Coutureau E, Di Scala G, Marchand AR (2009) A cholinergic-dependent role for the entorhinal cortex in trace fear conditioning. J Neurosci 29:8087-8093. doi: 10.1523/JNEUROSCI.0543-09.2009

Summary: Higher cognitive involvement can be modeled through the use of trace conditioning in simple associative tasks. Rats received several 20-80 ng injections of 192-IgG-SAP (Cat. #IT-01) into the entorhinal cortex (EC) in order to clarify the mechanisms that allow learning through the association of events that occur at different times. Cholinergic depletion of the EC did not result in a training deficit, indicating that these cells are not necessary for trace conditioning.

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