targeted-toxins

Croxson PL, Browning PG, Gaffan D, Baxter MG (2012) Acetylcholine facilitates recovery of episodic memory after brain damage. J Neurosci 32(40):13787-13795. doi: 10.1523/JNEUROSCI.2947-12.2012

Summary: Episodic memory is controlled by several interconnected brain structures. The order in which these structures sustain damage can affect the processes lost. In this work the authors performed numerous bilateral injections of ME20.4-SAP (Cat. #IT-15) into the infero-temporal cortex, the medial surface of the temporal lobe, the perirhinal and entorhinal cortex, and the temporal pole of monkeys. These injections totaled 2.2-2.5 μg of conjugate. The results indicate that loss of cortical acetylcholine function will interfere with adaptation to memory impairments caused by structural damage in episodic memory centers.

Related Products: ME20.4-SAP (Cat. #IT-15)

Daubert DL, McCowan M, Erdos B, Scheuer DA (2012) Nucleus of the solitary tract catecholaminergic neurons modulate the cardiovascular response to psychological stress in rats. J Physiol 590(Pt 19):4881-4895. doi: 10.1113/jphysiol.2012.232314

Summary: It has been proposed that the nucleus of the solitary tract (NTS) is highly involved in cardiovascular regulation. In light of the fact that catecholaminergic neurons in the NTS are part of stress-related neurocircuitry, the authors investigated whether these neurons attenuate blood pressure increases due to stress. Rats received 22 ng bilateral injections of anti-DBH-SAP (Cat. #IT-03) into the NTS. Mean arterial pressure and baseline plasma epinephrine were measured in a restraint test. Animals lesioned with anti-DBH-SAP displayed a significantly enhanced mean arterial pressure, and reduced plasma epinephrine. These data suggest that catecholaminergic neurons in the NTS inhibit the arterial pressure response to stress, but maintain the corticosteroid response.

Related Products: Anti-DBH-SAP (Cat. #IT-03)

Babalola PA, Fitz NF, Gibbs RB, Flaherty PT, Li PK, Johnson DA (2012) The effect of the steroid sulfatase inhibitor (p-O-sulfamoyl)-tetradecanoyl tyramine (DU-14) on learning and memory in rats with selective lesion of septal-hippocampal cholinergic tract. Neurobiol Learn Mem 98(3):303-310. doi: 10.1016/j.nlm.2012.09.003

Summary: Steroid sulfatase inhibitors such as dehydroepiandrosterone (DHEAS) have memory-enhancing effects. Working with both DHEAS and the steroid sulfatase inhibitor DU-14, the authors examined cholinergic function by infusing 0.2 μg of 192-IgG-SAP (Cat. #IT-01) into the medial septum of rats. The results indicate that memory associated with contextual fear is facilitated by steroid sulfatase inhibition, but acquisition of spatial memory is impaired by these same lesions.

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

Zant JC, Rozov S, Wigren HK, Panula P, Porkka-Heiskanen T (2012) Histamine release in the basal forebrain mediates cortical activation through cholinergic neurons. J Neurosci 32(38):13244-13254. doi: 10.1523/JNEUROSCI.5933-11.2012

Summary: The basal forebrain modulates many functions, among them the regulation of wakefulness and cortical arousal. Previous data has linked increases in histaminergic transmission to increases in wakefulness. In order to further investigate various facets of this system, the authors injected 230 ng of 192-IgG-SAP (Cat. #IT-01) into the horizontal diagonal band of Broca/substantia innominata/magnocellular preoptic area of rats. While control animals displayed several changes on administration of exogenous histamine, the lesioned animals had none of these changes.

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

Paolone G, Lee TM, Sarter M (2012) Time to pay attention: attentional performance time-stamped prefrontal cholinergic activation, diurnality, and performance. J Neurosci 32(35):12115-12128. doi: 10.1523/JNEUROSCI.2271-12.2012

Summary: This work examined the role that neuronal mechanisms have in cognitive performance on a fixed-time task. The authors performed bilateral 160 ng infusions of 192-IgG-SAP (Cat. #IT-01) into the nucleus basalis and substantia innominata of the basal forebrain of rats that had reached stable performance on a sustained attention task. In control animals trained in the same task, prefrontal cholinergic neurotransmission persisted at the fixed time even after the task was terminated. Both lesioning and altering the task training time impaired task performance.

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

Alvarez P, Chen X, Bogen O, Green PG, Levine JD (2012) IB4(+) nociceptors mediate persistent muscle pain induced by GDNF. J Neurophysiol 108(9):2545-2553. doi: 10.1152/jn.00576.2012

Summary: GDNF is found in skeletal muscle and can trigger mechanical hyperalgesia. The authors administered a 3.2-μg intrathecal dose of IB4-SAP (Cat. #IT-10) to rats. Loss of the IB4(+) nociceptors led to decreased hyperalgesic priming as well as a reduction in GDNF-induced hyperalgesia. These data indicate that GDNF plays a role in mediating induction of pain.

Related Products: IB4-SAP (Cat. #IT-10)

Koppen JR, Winter SS, Stuebing SL, Cheatwood JL, Wallace DG (2013) Infusion of GAT1-saporin into the medial septum/vertical limb of the diagonal band disrupts self-movement cue processing and spares mnemonic function. Brain Struct Funct 218(5):1099-1114. doi: 10.1007/s00429-012-0449-7

Summary: Both mnemonic and spatial processing are adversely affected by dementia due to Alzheimer’s disease. There is evidence to support the involvement of cholinergic systems in this deficit. In this work the authors examined how GABAergic neurons in the septohippocampus contribute to these cognitive functions. Rats received a total of 350 ng of GAT-1-SAP (Cat. #IT-32) infused into the medial septum-diagonal band of Broca. Although lesioned animals performed normally in tasks involving spatial cues, food hoarding was affected indicating that self-movement cue processing was interfered with by the loss of these GABAergic neurons.

Related Products: GAT1-SAP (Cat. #IT-32)

Lemons LL, Wiley RG (2012) Neuropeptide Y receptor-expressing dorsal horn neurons: role in nocifensive reflex and operant responses to aversive cold after CFA inflammation. Neuroscience 216:158-166. doi: 10.1016/j.neuroscience.2012.04.006 PMID: 22522467

Objective: To determine the role of dorsal horn Y1R-expressing neurons in pain.

Summary: Lumbar intrathecal NPY-SAP (1) reduced Complete Freund’s Adjuvant (CFA)-induced hyper-reflexia on the 10°C cold plate, (2) reduced cold aversion on the thermal preference and escape tasks, (3) was analgesic to noxious heat on the escape task, (4) reduced the CFA-induced allodynia to cold temperatures experienced on the thermal preference, feeding interference, and escape tasks, and (5) did not inhibit or interfere with morphine analgesia.

Related Products: NPY-SAP (Cat. #IT-28)

Savage S, Mattsson A, Olson L (2012) Cholinergic denervation attenuates phencyclidine-induced c-fos responses in rat cortical neurons. Neuroscience 216:38-45. doi: 10.1016/j.neuroscience.2012.04.064

Summary: Phenylcyclidine (PCP) has been used to model aspects of schizophrenia in animals. 81 ng of 192-IgG-SAP (Cat. #IT-01) was injected into the nucleus basalis magnocellularis of rats to assess the effects of low dose PCP in a cholinergically-deprived system. Saporin (Cat. #PR-01) was used as a control. Results demonstrate basalocortical cholinergic neurons are necessary for PCP to have full effect.

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

Gil-Bea FJ, Gerenu G, Aisa B, Kirazov LP, Schliebs R, Ramirez MJ (2012) Cholinergic denervation exacerbates amyloid pathology and induces hippocampal atrophy in Tg2576 mice. Neurobiol Dis 48(3):439-446. doi: 10.1016/j.nbd.2012.06.020

Summary: The hallmarks of Alzheimer’s disease (AD) include hippocampal cell loss, cholinergic dysfunction, amyloid plaques, and neurofibrillary tangles, among other things. This work sought to examine the interaction between cholinergic denervation, amyloid precursor protein (APP) processing, and hippocampal integrity. Tg2576 transgenic mice received 2 μg of mu p75-SAP (Cat. #IT-16) injected into the third ventricle. These mice overexpress a version of human APP. Lesioned animals displayed various aspects of AD such as hippocampal synaptic pathology and neurodegeneration, indicating that immunolesions in this mouse line produce a viable model for AD.

Related Products: mu p75-SAP (Cat. #IT-16)