Elimination of neurokinin-1 receptor neurons in caudal nucleus reverses the effects of systemic bicuculline on c-Fos expression in rat trigeminal sensory nucleus: I. High intensity electrical stimulation of the trigeminal ganglion.
Abe T, Ohshita N, Sugiyo S, Moritani M, Kobayashi M, Takemura M.
Neuroscience 133(3):739-747, 2005.
The authors investigated the role of NK-1r + neurons in lamina 1 of the trigeminal caudal nucleus (Vc) for ora-facial nociception. After a 5 µl injection of 5 µM SP-SAP (Cat. #IT-07) into the cisterna magna, c-fos expression in the Vc was evaluated. SP-SAP treatment, along with use of bicuculline, a GABAA receptor antagonist, showed that NK-1r+ neurons in laminae I and III of the Vc are involved in nociceptive processing in the trigeminal sensory nucleus.
Autonomic brainstem nuclei are linked to the hippocampus.
Castle M, Comoli E, Loewy AD.
Neuroscience 134(2):657-669, 2005.
Stimulation of the vagal nerve has been reported to enhance memory, as well as be an effective treatment for epilepsy. The authors examined the underlying synaptic pathway. The right ventral CA1 hippocampal field of rats was lesioned with 42 ng of either anti-DBH-SAP (Cat. #IT-03), or 192-Saporin (Cat. #IT-01). The results indicate that both noradrenergic and cholinergic neurons are relay sites for this pathway.
Possible role of CRF peptides in burn-induced hypermetabolism.
Chance WT, Dayal R, Friend LA, Sheriff S.
Life Sci 78(7):694-703, 2006.
Burn trauma has been associated with hypermetabolism and anorexia. Corticotropin releasing factor (CRF) elevates metabolic rate and elicits anorexia, while neuropeptide Y (NPY) reduces metabolic rate while stimulating feeding. After burn treatment, rats were injected with 2.5 µg CRF-SAP (Cat. #IT-13) into the third ventricle. Several parameters, including resting energy expenditure, NPY concentrations in the paraventricular nucleus, and CRFr-2 density were evaluated post-treatment. The results indicate that the CRFr-2 is important in maintaining hypermetabolism resulting from burn trauma.
Compensatory changes in cortical cholinergic innervation in the rat following an immunotoxic lesion.
Hartonian I, de Lacalle S.
Restor Neurol Neurosci 23(2):87-96, 2005.
The ability of damaged axons to grow and functionally reinnervate damaged areas of the brain is well documented. Here the authors study this process in the context of rats lesioned with 192-Saporin (Cat. #IT-01). 10.5 ng of the immunotoxin was injected into the right horizontal diagonal band of Broca, and animals were examined from 2 to 24 weeks later. Although the functionality of the neuronal ingrowth was not examined, surviving neurons did extend their terminals into the denervated area.
Origin and immunolesioning of cholinergic basal forebrain innervation of cat primary auditory cortex.
Kamke MR, Brown M, Irvine DR.
Hear Res 206(1-2):89-106, 2005.
In this study the authors assessed the use of a cholinergic immunotoxin while examining cholinergic basal forebrain input to the primary auditory cortex in cat. Six 0.5 µg injections of ME20.4-SAP (Cat. #IT-15) were made into the putamen/globus pallidus, and cholinergic cell survival was examined by immunohistochemistry. The injected area showed a large reduction in number of AChE-positive fibers in the primary auditory cortex. This provides the evidence of the efficacy of ME20.4-SAP for investigating plasticity in cat auditory cortex.
Susceptibility to seizure-induced injury and acquired microencephaly following intraventricular injection of saporin-conjugated 192 IgG in developing rat brain.
Koh S, Santos TC, Cole AJ.
Exp Neurol 194(2):457-466, 2005.
It is thought that one mechanism for resistance to seizure-induced injury in immature animals is an abundance of neurotrophic growth factors. Rat pups were treated with 2 µg of 192-Saporin (Cat. #IT-01) injected into the left lateral ventricle to examine how cholinergic basal forebrain projections might affect this type of injury. The results indicate that these neurons may be critical for normal brain growth, and that they play a protective role in preventing excitotoxic neuronal injury.
Selective cholinergic immunolesioning affects synaptic plasticity in developing visual cortex.
Kuczewski N, Aztiria E, Leanza G, Domenici L.
Eur J Neurosci 21(7):1807-1814, 2005.
In this study the authors examined the role of subcortical cholinergic inputs in the regulation of plastic events in the visual cortex during early postnatal development. Four-day-old mouse pups were treated with a total of 0.4 µg of 192-Saporin (Cat. #IT-01), using bilateral injections. Analysis of muscarinic receptor mRNA, long-term potentiation of cortex slices, and theta burst stimulation indicated that synaptic transmission and plasticity of the developing visual cortex depends on cholinergic input.
Further analysis of the effects of immunotoxic lesions of the basal nucleus of Meynert reveals substantial impairment on visual discrimination learning in monkeys.
Ridley RM, Baker HF, Leow-Dyke A, Cummings RM.
Brain Res Bull 65(5):433-442, 2005.
Several studies in marmoset monkeys indicate that cholinergic projections from the NBM to specific portions of the neocortex are necessary for visual discrimination learning. By combining analysis of studies using a total of 1.4 µg of ME20.4-SAP (Cat. #IT-15) into various areas of the brain, the authors show that degeneration of cholinergic projections contributes to the loss of functions dependent on the neocortex.
Acetylcholine in the orbitofrontal cortex is necessary for the acquisition of a socially transmitted food preference.
Ross RS, McGaughy J, Eichenbaum H.
Learn Mem 12(3):302-306, 2005.
Cortical involvement in social transmission of food preference (STFP) has not been established, but the importance of the orbitofrontal cortex (OFC) in odor-guided learning is known. The OFC of rats was injected twice with 192-Saporin (Cat. #IT-01), then the rats were trained in STFP. Depletion of cholinergic neurons in the OFC impaired expression of the odor association, indicating that cholinergic function in the OFC is essential for this form of associative learning.
Spinal-supraspinal serotonergic circuits regulating neuropathic pain and its treatment with gabapentin.
Suzuki R, Rahman W, Rygh LJ, Webber M, Hunt SP, Dickenson AH.
Pain 117(3):292-303, 2005.
The anticonvulsant, gabapentin, is thought to modulate calcium channel function. In animals, it also affects abnormal pain function. 10 µl of 1 µM SP-SAP (Cat. #IT-07) was injected into the subarachnoid space of rats. It was found that the effects of gabapentin were blocked when NK-1r expressing neurons in the dorsal horn were eliminated. The results suggest that not only is the NK-1r pathway a determinant of neuronal and behavioral manifestations of neuropathy, it is also involved in the action of gabapentin.
Septal innervation regulates the function of alpha7 nicotinic receptors in CA1 hippocampal interneurons.
Thinschmidt JS, Frazier CJ, King MA, Meyer EM, Papke RL.
Exp Neurol 195(2):342-352, 2005.
The authors examined whether hippocampal innervation by medial septum/diagonal band of Broca projections is necessary for normal a7 receptor function. 1 µg of 192-Saporin (Cat. #IT-01) was injected into the medial septum of rats. Various methods, including whole-cell patch clamping and immunohistochemistry, were used to evaluate the effects of these lesions. Lesioning with 192-Saporin did not affect a7 receptor currents, indicating that cholinergic neurons are not linked to a7 function.
Ablation of vagal preganglionic neurons innervating the extra-thoracic trachea affects ventilatory responses to hypercapnia and hypoxia.
Wu M, Kc P, Mack SO, Haxhiu MA.
Respir Physiol Neurobiol 152(1):36-50, 2006.
Hypercapnia, an excess of CO2 in the blood, is thought to stimulate the release of acetylcholine by airway-related vagal preganglionic neurons (AVPNs). AVPNs in the nucleus ambiguus (NA) were lesioned with ten 1-µl injections of CTB-SAP (Cat. #IT-14) into the trachealis muscle of rats. Treated animals maintained rhythmic breathing patterns, but episodes of increased respiratory rate in response to hypercapnia were significantly reduced.
Mu opioid receptor-containing neurons mediate electroacupuncture-produced anti-hyperalgesia in rats with hind paw inflammation.
Zhang RX, Wang L, Liu B, Qiao JT, Ren K, Berman BM, Lao L.
Brain Res 1048(1-2):235-240, 2005.
Electroacupuncture has been shown to significantly reduce inflammatory hyperalgesia. To examine whether this effect is modulated by spinal mu opioid receptors, the authors injected 400 ng of dermorphin-SAP (Cat. #IT-12) into the subarachnoid space at the level of the lumbar spinal cord of rats. The anti-hyperalgesic effect of electroacupuncture was blocked by dermorphin-SAP administration, indicating that mu opioid receptor-containing neurons are involved in this pathway.