References

Parent M, Bedard MA, Aliaga A, Soucy JP, Landry St-Pierre E, Cyr M, Kostikov A, Schirrmacher E, Massarweh G, Rosa-Neto P (2012) PET imaging of cholinergic deficits in rats using [(18)F]fluoroethoxybenzovesamicol ([(18)F]FEOBV). Neuroimage 62(1):555-561. doi: 10.1016/j.neuroimage.2012.04.032

Summary: In order to better understand and evaluate neurodegenerative diseases imaging agents are necessary to visualize the affected systems. [18F]fluoroethoxybenzovesamicol ([18F]FEOBV) is one such agent that shows promise for labeling the vesicular acetylcholine transporter with positron emission tomography. The authors injected 0.2 μg of 192-IgG-SAP (Cat. #IT-01) into the left hemisphere of rats to model cholinergic terminal loss as seen in aged animals. Loss of these terminals was found to reduce [18F]FEOBV binding in the ventral frontal cortex on the lesioned side, and also in the homologous region of the contralateral hemisphere, allowing detection of both physiological and pathological reduction of cholinergic terminals.

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

Huang TY, Lin LS, Cho KC, Chen SJ, Kuo YM, Yu L, Wu FS, Chuang JI, Chen HI, Jen CJ (2012) Chronic treadmill exercise in rats delicately alters the Purkinje cell structure to improve motor performance and toxin resistance in the cerebellum. J Appl Physiol 113(6):889-895. doi: 10.1152/japplphysiol.01363.2011

Summary: It is known that exercise can improve motor performance, but the cellular changes that occur in the cerebellum in response to exercise are not understood. Rats were subject to exercise training and a rotarod test was used to evaluate performance. After training some animals were given a 2 μg injection of OX7-SAP (Cat. #IT-02) into the lateral ventricle. In sedentary rats OX7-SAP administration reduced rotarod performance as well as eliminated 60% of Purkinjie cells. Rats given exercise training exhibited much milder injury in the cerebellum as a result of the lesion and maintained a higher level of rotarod performance than the sedentary group.

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

Laplante F, Zhang ZW, Huppe-Gourgues F, Dufresne MM, Vaucher E, Sullivan RM (2012) Cholinergic depletion in nucleus accumbens impairs mesocortical dopamine activation and cognitive function in rats. Neuropharmacology 63(6):1075-1084. doi: 10.1016/j.neuropharm.2012.07.033

Summary: Current thought is that loss of cholinergic function in the nucleus accumbens (N.Acc) is associated with schizophrenia. This deficit is accompanied by low dopaminergic activity in the prefrontal area, which adversely affects working memory. Rats received bilateral injections totaling 500 ng of anti-ChAT-SAP (Cat. #IT-42) into the N.Acc; rabbit IgG-SAP (Cat. #IT-35) was used as a control. Lesioned animals had markedly reduced mesocortical dopamine activation, which corresponded with cognitive impairments. The data suggest that loss of cholinergic neurons in the N.Acc causes loss of dopamine function in the mesocorticolimbic system.

Related Products: Anti-ChAT-SAP (Cat. #IT-42), Rabbit IgG-SAP (Cat. #IT-35)

Coolen LM (2012) Featured Article: A pivotal role of lumbar spinothalamic cells in regulation of ejaculation via intraspinal connections. Targeting Trends 13(3)

Related Products: SSP-SAP (Cat. #IT-11), Blank-SAP (Cat. #IT-21)

Read the featured article in Targeting Trends.

See Also:

• Staudt MD et al. A Pivotal Role of Lumbar Spinothalamic Cells in the Regulation of Ejaculation via Intraspinal Connections. J Sex Med 9(9):2256-2265, 2012.

Brown RE, Basheer R, McKenna JT, Strecker RE, McCarley RW (2012) Control of sleep and wakefulness. Physiol Rev 92(3):1087-1187 . doi: 10.1152/physrev.00032.2011

Summary: This review summarizes mechanisms in the brain that control sleep and wakefulness. Areas discussed include wakefulness promoting systems, non-REM sleep and REM sleep definitions, the function of each kind of sleep, and dysfunction that occurs as a result of sleep disruption. Several targeted conjugates are mentioned, such as 192-IgG-SAP (Cat. #IT-01), anti-DBH-SAP (Cat. #IT-03), and orexin-SAP (Cat. #IT-20). The review summarizes the use of these products to better understand sleep networks.

Related Products: 192-IgG-SAP (Cat. #IT-01), Anti-DBH-SAP (Cat. #IT-03), Orexin-B-SAP (Cat. #IT-20)

Xu L, Scheenen WJ, Roubos EW, Kozicz T (2012) Peptidergic Edinger-Westphal neurons and the energy-dependent stress response. Gen Comp Endocrinol 177(3):296-304. doi: 10.1016/j.ygcen.2011.11.039

Objective: This study investigates the role of the midbrain Edinger–Westphal centrally projecting neuron population (EWcp; synonym: non-preganglionic Edinger–Westphal nucleus) in the energy-dependent stress adaptation response.

Summary: The current data indicates that the EWcp receives information about stressors and peripheral metabolic status, and responds to this information by generating various neuropeptide messengers.

Usage: Leptin-SAP was injected into the EWcp, to kill Leptin receptor-positive neurons. With this approach ~50% of the Ucn1/CART neurons of the EWcp were lost, and the weights of both brown and white adipose tissue significantly increased.

Related Products: Leptin-SAP (Cat. #IT-47)

Sikandar S, Bannister K, Dickenson AH (2012) Brainstem facilitations and descending serotonergic controls contribute to visceral nociception but not pregabalin analgesia in rats. Neurosci Lett 519(1):31-36. doi: 10.1016/j.neulet.2012.05.009

Summary: Neurons in the rostral ventromedial medulla (RVM) are classified as ON, OFF, or NEUTRAL based on firing patterns in response to noxious somatic stimulation. ON cells express μ-opioid receptors, and are therefore a target for dermorphin-SAP (Cat. #IT-12). The authors injected the RVM of rats with 3 pmol of dermorphin-SAP; Saporin (Cat. #PR-01) was used as a control. Results show the μ-opioid receptor population is not needed for the function of analgesics through the serotonergic system.

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

Mishra SK, Holzman S, Hoon MA (2012) A nociceptive signaling role for neuromedin B. J Neurosci 32(25):8686-8695. doi: 10.1523/JNEUROSCI.1533-12.2012

Summary: Previous work suggests that neuromedin B (NMB) is involved in nociception. Direct injection of the peptide causes nociceptive sensitization, while NMB antagonists attenuate sensitization in reponse to nerve stimulation with mustard oil. Specific subsets of dorsal horn interneurons were eliminated by administering either 10 μg of the custom conjugate neuromedin B-SAP, 0.13 μg of SSP-SAP (Cat. #IT-11), or 1.3 μg of bombesin-SAP (Cat. #IT-40). Blank-SAP (Cat. #IT-21) was used as a control. The data indicate that NMB may be involved in the perception of thermal sensation, but not mechanical or pruritic sensation.

Related Products: NMB-SAP (Cat. #IT-70), SSP-SAP (Cat. #IT-11), Bombesin-SAP (Cat. #IT-40), Blank-SAP (Cat. #IT-21)

Tai SK, Leung LS (2012) Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells. Behav Brain Res 232(1):174-182. doi: 10.1016/j.bbr.2012.04.013

Summary: It is known that vestibular stimulation induces acetylcholine release in the hippocampus. The authors hypothesized that this stimulation enhances long-term potentiation (LTP) in CA1 and depends on the activation of septohippocampal cholinergic neurons. Rats received 105-ng bilateral infusions of 192-IgG-SAP (Cat. #IT-01) into the medial septum. The data suggest that LTP enhancement during vestibular stimulation is mediated by cholinergic septohippocampal cells.

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

Abbott SB, Kanbar R, Bochorishvili G, Coates MB, Stornetta RL, Guyenet PG (2012) C1 neurons excite locus coeruleus and A5 noradrenergic neurons along with sympathetic outflow in rats. J Physiol 590(12):2897-2915. doi: 10.1113/jphysiol.2012.232157

Summary: C1 neurons are known to activate sympathetic tone and stimulate the hypothalamic-pituitary-adrenal axis. C1 activation is also reported to inhibit locus coeruleus (LC) neurons. Rats received 0.6 ng of SSP-SAP (Cat. #IT-11) injected under the caudal edge of the facial motor nucleus to destroy the retrotrapezoid nucleus, increasing the proportion of C1 ChR2-expressing neurons. Stimulation of C1 neurons resulted in activation of noradrenergic neurons that are involved in hypoxia and hypotension.

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