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2118 entries

Lesions of the nucleus basalis magnocellularis (Meynert) induce enhanced somatosensory responses and tactile hypersensitivity in rats.

Dezawa S, Nagasaka K, Watanabe Y, Takashima I (2021) Lesions of the nucleus basalis magnocellularis (Meynert) induce enhanced somatosensory responses and tactile hypersensitivity in rats. Exp Neurol 335:113493. doi: 10.1016/j.expneurol.2020.113493

Summary: The authors used 192-IgG-SAP to produce a selective cholinergic lesion in the nucleus basalis of Meynert (NBM) of rats and investigated whether the NBM lesion led to tactile hypersensitivity in the forepaw. Results suggest that neuronal loss in the NBM diminishes acetylcholine actions in the S1, thereby enhancing the cortical representation of sensory stimuli, which may in turn lead to behavioral hypersensitivity.

Usage: The lesion group received injection of 0.3 μL of 192-IgG-SAP into the left nucleus basalis of Meynert (NBM).

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

Aberrant functional connectivity of basal forebrain subregions with cholinergic system in short-term and chronic insomnia disorder

Ma X, Fu S, Yin Y, Wu Y, Wang T, Xu G, Liu M, Xu Y, Tian J, Jiang G (2021) Aberrant functional connectivity of basal forebrain subregions with cholinergic system in short-term and chronic insomnia disorder. J Affect Disord 278:481-487. doi: 10.1016/j.jad.2020.09.103

Summary: Previous animal studies have identified the cholinergic basal forebrain (CBF) as a crucial structure in sleep-wake cycle modulation and lesion or inactivation of the BF has been found to increase delta electroencephalogram activity, disturb behavioral arousal, and reduce sleep. They reference Kaur et al. using 192-IgG-SAP to lesion the CBF to examine the role of these neurons in sleep behavior.

See: Kaur S et al. Effects of ibotenate and 192IgG-saporin lesions of the nucleus basalis magnocellularis/substantia innominata on spontaneous sleep and wake states and on recovery sleep after sleep deprivation in rats. J Neurosci 28:491-504, 2008.

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

From obesity to hippocampal neurodegeneration: Pathogenesis and non-pharmacological interventions

Lee TH, Yau SY (2021) From obesity to hippocampal neurodegeneration: Pathogenesis and non-pharmacological interventions. Int J Mol Sci 22(1):201. doi: 10.3390/ijms22010201

Summary: This review provides insights into how chronic metabolic disorders, like obesity, could impair brain health and cognitive functions in later life. The authors reference the use of CCK-SAP into the nodose ganglia to impair spatial memory and contextual episodic memory.

See: Suarez AN et al. Gut vagal sensory signaling regulates hippocampus function through multi-order pathways. Nat Commun 9(1):2181, 2018.

Related Products: CCK-SAP (Cat. #IT-31)

Measuring attention in rats with a visual signal detection task: Signal intensity vs. signal duration

Holloway Z, Koburov R, Hawkey A, Levin ED (2020) Measuring attention in rats with a visual signal detection task: Signal intensity vs. signal duration. Pharmacol Biochem Behav 199:173069. doi: 10.1016/j.pbb.2020.173069

Summary: Drug-induced effects have been used to demonstrate the construct validity of operant attention tasks, as well as to assess the pharmacological systems that underlie cognitive processes, such as attention, short-term memory and reaction time, either by interrupting or enhancing performance.

See: McGaughy J et al. Sustained attention performance in rats with intracortical infusions of 192 IgG-saporin-induced cortical cholinergic deafferentation: effects of physostigmine and FG 7142. Behav Neurosci 112(6):1519-1525, 1998.

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

Extracellular levels of the sleep homeostasis mediator, adenosine, are regulated by glutamatergic neurons during wakefulness and sleep

Sun MJ, Tang Y (2020) Extracellular levels of the sleep homeostasis mediator, adenosine, are regulated by glutamatergic neurons during wakefulness and sleep. Purinergic Signal 16(4):475-476. doi: 10.1007/s11302-020-09758-3

Summary: Blanco-Centurion et al. investigated the role of cholinergic neurons in the BF by administering 192–IgG–SAP to lesion them, but surprisingly the results indicated that adenosine from cholinergic neurons in BF are not essential to sleep induction.

See: Blanco-Centurion C et al. Adenosine and sleep homeostasis in the Basal forebrain. J Neurosci 26(31):8092-8100, 2006.

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

Exercise is neuroprotective to motoneuron dendrites following partial motoneuron depletion via a mechanism dependent on androgen receptors at the target muscle

Chew C (2020) Exercise is neuroprotective to motoneuron dendrites following partial motoneuron depletion via a mechanism dependent on androgen receptors at the target muscle. Indiana Univ, Dept Psychol & Brain Sci Thesis.

See: Chew C et al. Exercise promotes recovery after motoneuron injury via hormonal mechanisms. Neural Regen Res 15(8):1373-1376, 2020.

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

Differential mechanisms are required for phrenic long-term facilitation over the course of motor neuron loss following CTB-SAP intrapleural injections.

Borkowski LF, Nichols NL (2020) Differential mechanisms are required for phrenic long-term facilitation over the course of motor neuron loss following CTB-SAP intrapleural injections. Exp Neurol 334:113460. doi: 10.1016/j.expneurol.2020.113460

Objective: To understand the mechanism responsible for this difference in magnitude of phrenic long-term facilitation (pLTF)

Summary: pLTF in 7d CTB-SAP treated rats is elicited primarily through TrkB and PI3K/Akt-dependent mechanisms, whereas BDNF and MEK/ERK-dependent mechanisms induce pLTF in 28d CTB-SAP treated rats.

Usage: Rats received bilateral intrapleural injections of CTB-SAP; 25 μg dissolved in PBS.

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

Characterizing the neural substrate of reward with the use of specific brain lesions

Cromwell HC (2021) Characterizing the neural substrate of reward with the use of specific brain lesions. Fakhoury M (Ed.): The Brain Reward System. Neuromethods. 165. Humana, New York, NY doi: 10.1007/978-1-0716-1146-3_3

Summary: This review is focused on experimental lesions and work using the rodent model examining the neural substrates of reward processing. Saporin is listed as a neurotoxin used to target selective neuronal populations with success.

See: Pappas BA et al. Neonatal 192 IgG-saporin lesion of forebrain cholinergic neurons: focus on the life span?. Neurosci Biobehav Rev 27(4):365-376, 2003.

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

Structural and functional consequences of targeted hippocampal gaba neuron ablation by stable substance p-saporin in rats

Chun E (2020) Structural and functional consequences of targeted hippocampal gaba neuron ablation by stable substance p-saporin in rats. Morehouse School of Medicine Thesis.

See: Chun E et al. Targeted hippocampal GABA neuron ablation by Stable Substance P-saporin causes hippocampal sclerosis and chronic epilepsy in rats. Epilepsia 60(5):e52-e57, 2019.

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

Depletion of C1 neurons attenuates the salt-induced hypertension in unanesthetized rats.

Ribeiro N, Martins Sá RW, Antunes VR (2020) Depletion of C1 neurons attenuates the salt-induced hypertension in unanesthetized rats. Brain Res 1748:147107. doi: 10.1016/j.brainres.2020.147107

Objective: To determine if the ablation of C1 neurons mitigates high blood pressure induced by high-salt intake.

Summary: Data show that hypertension induced by high-salt intake is dependent on C1 neurons.

Usage: Bilateral injections of 2.4 ng/100 nl of Anti-DBH-SAP. The total number of TH+ neurons in the AS region was reduced by 37 ± 13% in the anti-DBH-SAP group when compared to control.

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

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