An automated method to remove artifacts induced by microstimulation in local field potentials recorded from rat somatosensory cortex

Author(s):  
Mufti Mahmud ◽  
Stefano Girardi ◽  
Marta Maschietto ◽  
Stefano Vassanelli
Author(s):  
Mufti Mahmud ◽  
Davide Travalin ◽  
Alessandra Bertoldo ◽  
Stefano Girardi ◽  
Marta Maschietto ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Miguel Pais-Vieira ◽  
Carolina Kunicki ◽  
André Peres ◽  
Nuno Sousa

AbstractStress responses are associated with elevations in corticosterone levels and, as a consequence, increases in glutamate in the central nervous system which can lead to neurological impairment. Ceftriaxone promotes glutamate transport and has been used to reduce glutamate toxicity, but so far it is not known whether ceftriaxone is able to reverse the effects of corticosterone administration. Here we describe the separate and combined effects of acute ceftriaxone and acute corticosterone administration in local field potentials (LFPs) recorded from the somatosensory cortex (S1) of anesthetized mice. For this, LFPs were recorded from groups of anesthetized mice injected with saline, corticosterone, ceftriaxone, or both. Comparison of global state maps, and their displacements, as measured by ratios of different frequency bands (Ratio 1: 0.5–20 Hz/0.5–45 Hz; and Ratio 2: 0.5–4.5 Hz/0.5–9 Hz) revealed distinct and opposite effects for corticosterone and for ceftriaxone. Corticosterone specifically increased the displacement in Ratio 2, while ceftriaxone decreased it; in addition, when both corticosterone and ceftriaxone were injected, Ratio 2 displacement values were again similar to those of the control group. The present results suggest that ceftriaxone and corticosterone modulate specific frequency bands in opposite directions and reveal a potential role for ceftriaxone in counteracting the effects of corticosterone.


2021 ◽  
Vol 11 (7) ◽  
pp. 882
Author(s):  
Yeon Hee Yu ◽  
Seong-Wook Kim ◽  
Dae-Kyoon Park ◽  
Ho-Yeon Song ◽  
Duk-Soo Kim ◽  
...  

Increased prevalence of chronic kidney disease (CKD) and neurological disorders including cerebrovascular disease, cognitive impairment, peripheral neuropathy, and dysfunction of central nervous system have been reported during the natural history of CKD. Psychological distress and depression are serious concerns in patients with CKD. However, the relevance of CKD due to decline in renal function and the pathophysiology of emotional deterioration is not clear. Male Sprague Dawley rats were divided into three groups: sham control, 5/6 nephrectomy at 4 weeks, and 5/6 nephrectomy at 10 weeks. Behavior tests, local field potentials, and histology and laboratory tests were conducted and investigated. We provided direct evidence showing that CKD rat models exhibited anxiogenic behaviors and depression-like phenotypes, along with altered hippocampal neural oscillations at 1–12 Hz. We generated CKD rat models by performing 5/6 nephrectomy, and identified higher level of serum creatinine and blood urea nitrogen (BUN) in CKD rats than in wild-type, depending on time. In addition, the level of α-smooth muscle actin (α-SMA) and collagen I for renal tissue was markedly elevated, with worsening fibrosis due to renal failures. The level of anxiety and depression-like behaviors increased in the 10-week CKD rat models compared with the 4-week rat models. In the recording of local field potentials, the power of delta (1–4 Hz), theta (4–7 Hz), and alpha rhythm (7–12 Hz) was significantly increased in the hippocampus of CKD rats compared with wild-type rats. Together, our findings indicated that anxiogenic behaviors and depression can be induced by CKD, and these abnormal symptoms can be worsened as the onset of CKD was prolonged. In conclusion, our results show that the hippocampus is vulnerable to uremia.


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