The effects of NBM- lesion on synaptic plasticity in rats

Hosseini, Nasrin; Alaei, Hojjatollah; Reisi, Parham; Radahmadi, Maryam

doi:10.1016/j.brainres.2016.11.013

Cited by 11 publications

(4 citation statements)

References 42 publications

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“…The major source of cortical cholinergic innervation originates in NBM in the mammalian basal forebrain. NBM‐cortical projections are responsible for cortical–cortical and cortical–subcortical theta synchrony necessary for attention control, sensory perception and integration, and movement coordination (Bloem et al, 2014; Eckenstein, Baughman, & Quinn, 1988; Hosseini, Alaei, Reisi, & Radahmadi, 2017; Karczmar, 2007; Meck, Williams, Cermak, & Blusztajn, 2008; Mesulam & Geula, 1988; Sarter & Lustig, 2020). Given the impact of early postnatal AE and behavioral intervention on cholinergic neurotransmission, we hypothesized that these factors would have an impact on the morphology of cholinergic neurons and their axons in NBM and PFC in adulthood.…”

Section: Introductionmentioning

confidence: 99%

Examination of cortically projecting cholinergic neurons following exercise and environmental intervention in a rodent model of fetal alcohol spectrum disorders

Milbocker

Klintsova

2020

Birth Defects Research

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Background Up to 1 in 5 infants in the United States are exposed to alcohol prenatally, resulting in neurodevelopmental deficits categorized as fetal alcohol spectrum disorders (FASD). Choline supplementation ameliorates some deficits, suggesting that alcohol exposure (AE) perturbs cholinergic neurotransmission and development. Behavioral interventions, which upregulate cholinergic neurotransmission, rescue cognitive deficits in rodent models of FASD. Methods We investigated the impacts of two interventions (either wheel‐running (WR) or “super intervention,” WR plus exposure to a complex environment) on cholinergic neuronal morphology in the nucleus basalis of Meynert (NBM), the source of cortical cholinergic input, and prefrontal cortex (PFC) in a rodent model of FASD. One third of the total 47 male pups received intragastric intubation of ethanol in milk substitute during postnatal days (PD) 4–9. Another third served as sham‐intubated procedural controls while the final third served as suckle controls. Rats from each group were exposed to either intervention during PD 30–72. Choline acetyltransferase (ChAT+) and acetylcholinesterase staining were used to quantify cholinergic neuron number, soma volume, and axon number. Results Our data indicate a main effect of postnatal treatment on ChAT+ neuron number in NBM in adulthood. Post hoc analysis demonstrates that ChAT+ neuron number is reduced in AE compared to suckle control rodents (p < .01). Conclusions We examined the cytoarchitectonics of cholinergic neurons in NBM and PFC in adulthood following early postnatal AE and two interventions. We show that AE reduces ChAT+ neuron number in NBM, and this is not mitigated by either intervention.

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Section: Introductionmentioning

confidence: 99%

Examination of cortically projecting cholinergic neurons following exercise and environmental intervention in a rodent model of fetal alcohol spectrum disorders

Milbocker

Klintsova

2020

Birth Defects Research

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“…The NBM sends direct cholinergic projections to the basolateral amygdaloid nuclei [ 16 ]. In addition, even though the NBM does not transfer direct cholinergic projections to the hippocampus, NBM abrasion was found to weaken the basal synaptic responsiveness, short- and long-term neural plasticity in the rats’ hippocampus [ 17 ]. The NBM-hippocampus, and NBM-amygdala circuits can hold network fluctuations for years before the AD characteristic phenotype comes into play.…”

Section: Introductionmentioning

confidence: 99%

Disruption of Cholinergic Circuits as an Area for Targeted Drug Treatment of Alzheimer’s Disease: In Vivo Assessment of Short-Term Plasticity in Rat Brain

et al. 2020

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The search for new therapeutics for the treatment of Alzheimer’s disease (AD) is still in progress. Aberrant pathways of synaptic transmission in basal forebrain cholinergic neural circuits are thought to be associated with the progression of AD. However, the effect of amyloid-beta (Aβ) on short-term plasticity (STP) of cholinergic circuits in the nucleus basalis magnocellularis (NBM) is largely unknown. STP assessment in rat brain cholinergic circuitry may indicate a new target for AD cholinergic therapeutics. Thus, we aimed to study in vivo electrophysiological patterns of synaptic activity in NBM-hippocampus and NBM-basolateral amygdala circuits associated with AD-like neurodegeneration. The extracellular single-unit recordings of responses from the hippocampal and basolateral amygdala neurons to high-frequency stimulation (HFS) of the NBM were performed after intracerebroventricular injection of Aβ 25–35. We found that after Aβ 25–35 exposure the number of hippocampal neurons exhibiting inhibitory responses to HFS of NBM is decreased. The reverse tendency was seen in the basolateral amygdala inhibitory neural populations, whereas the number of amygdala neurons with excitatory responses decreased. The low intensity of inhibitory and excitatory responses during HFS and post-stimulus period is probably due to the anomalous basal synaptic transmission and excitability of hippocampal and amygdala neurons. These functional changes were accompanied by structural alteration of hippocampal, amygdala, and NBM neurons. We have thus demonstrated that Aβ 25–35 induces STP disruption in NBM-hippocampus and NBM-basolateral amygdala circuits as manifested by unbalanced excitatory/inhibitory responses and their frequency. The results of this study may contribute to a better understanding of synaptic integrity. We believe that advancing our understanding of in vivo mechanisms of synaptic plasticity disruption in specific neural circuits could lead to effective drug searches for AD treatment.

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“…The effect of NBM lesions was also shown on the reduction of base synapse response, paired-pulse response, and LTP in the dentate gyrus. These reports indicate that although the NBM does not introduce direct cholinergic splits to the hippocampus, its lesion affects the long-term and short-term plasticity in dentate gyrus cells ( Hosseini et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

“…Also, by ibotonic acid, NBM lesion decrease basal synaptic responsiveness, paired pulse responses and long-term potentiation (LTP) in the dentate gyrus (DG) of rats. It indicates that although NBM does not send direct cholinergic projections to the hippocampus, its lesion affects both short-and long-term neural plasticities in the dentate gyrus (Hosseini, Alaei, Reisi & Radahmadi, 2017). As degeneration of cholinergic neurons in the human forebrain is one of the neuropathological features of AD, animals with lesions of NBM are considered models of AD-type amnesia (Ahmed, Hoshino, Chikuma, Yamada & Kato, 2004).…”

Section: Introductionmentioning

confidence: 99%

Effects of Memantine on the Spontaneous Firing Frequency of Hippocampal CA1 Pyramidal Neurons in Intact and Alzheimer Rat Model: An Electrophysiological Study

Zamani

Moazedi

Khaki

et al. 2022

BCN

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Introduction: Memantine (MEM) is a noncompetitive NMDAR antagonist clinically used for the treatment Alzheimer’s disease (AD) in mild to severe conditions. The present study was conducted to investigate the effects of Memantine on the spontaneous firing frequency of CA1 pyramidal neurons in rats with electrical lesion of nucleus basalis magnocellularis (NBM) as an animal model of Alzheimer's disease compared with intact adult males. Methods: In this study, adult male rats were divided into two groups. Group I (Lesion NBM, n=53) includes the following subgroups: Lesion+Saline; Sham+Saline; Lesion+MEM5mg/kg; Lesion+MEM10mg/kg; Lesion+MEM20mg/kg. And Group II (Intact, n=48) include the following subgroups: Intact+Saline; Intact+MEM3mg/kg; Intact+MEM5mg/kg; Intact+MEM10mg/kg. Extracellular single unit recording (15 min baseline+105 min after MEM or saline) was performed under urethane-anesthetized rats. Results: The results showed that the mean frequency of CA1 pyramidal neurons after saline in the Lesion+Saline (P<0.001) group significantly decreases compared with the Intact+Saline and Sham+Saline groups. In addition, after saline and memantine, the mean frequency of CA1 pyramidal neurons in the Lesion+MEM10mg/kg (P<0.01) and Lesion+MEM20mg/kg (P<0.001) groups significantly increases compared with the Lesion+Saline group. In addition the mean frequencies of CA1 pyramidal neurons in the Intact+MEM10mg/kg (P<0.001) group significantly decreases compared with the intact+saline group. Conclusion: Results showed that memantine increases the electrical activity of CA1 pyramidal neurons in rats model of Alzheimer's disease. Furthermore, in intact adult male rats, it was shown that low-dose memantine contrary to its high dose not decrease the electrical activity of CA1 pyramidal neurons.

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The effects of NBM- lesion on synaptic plasticity in rats

Cited by 11 publications

References 42 publications

Examination of cortically projecting cholinergic neurons following exercise and environmental intervention in a rodent model of fetal alcohol spectrum disorders

Examination of cortically projecting cholinergic neurons following exercise and environmental intervention in a rodent model of fetal alcohol spectrum disorders

Disruption of Cholinergic Circuits as an Area for Targeted Drug Treatment of Alzheimer’s Disease: In Vivo Assessment of Short-Term Plasticity in Rat Brain

Effects of Memantine on the Spontaneous Firing Frequency of Hippocampal CA1 Pyramidal Neurons in Intact and Alzheimer Rat Model: An Electrophysiological Study

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