The neuroprotective effects of stimulation of NMDA receptors against POX-induced neurotoxicity in hippocampal cultured neurons; a morphometric study

2020 ◽  
Vol 16 (4) ◽  
pp. 401-408
Author(s):  
Farideh Bahrami ◽  
Zahra Bahari ◽  
Reihaneh Abolghasemi ◽  
Lida Golmanesh ◽  
Gholam Hossein Meftahi
1991 ◽  
Vol 65 (1) ◽  
pp. 20-32 ◽  
Author(s):  
Y. Komatsu ◽  
S. Nakajima ◽  
K. Toyama

1. Intracellular recording was made from layer II-III cells in slice preparations of kitten (30-40 days old) visual cortex. Low-frequency (0.1 Hz) stimulation of white matter (WM) usually evoked an excitatory postsynaptic potential (EPSP) followed by an inhibitory postsynaptic potential (IPSP). The postsynaptic potentials (PSPs) showed strong dependence on stimulus frequency. Early component of EPSP and IPSP evoked by weak stimulation both decreased monotonically at frequencies greater than 0.5-1 Hz. Strong stimulation similarly depressed the early EPSP at higher frequencies (greater than 2 Hz) and replaced the IPSP with a late EPSP, which had a maximum amplitude in the stimulus frequency range of 2-5 Hz. 2. Very weak WM stimulation sometimes evoked EPSPs in isolation from IPSPs. The falling phase of the EPSP revealed voltage dependence characteristic to the responses mediated by N-methyl-D-aspartate (NMDA) receptors and was depressed by application of an NMDA antagonist DL-2-amino-5-phosphonovalerate (APV), whereas the rising phase of the EPSP was insensitive to APV. 3. The early EPSPs followed by IPSPs were insensitive to APV but were replaced with a slow depolarizing potential by application of a non-NMDA antagonist 6,7-dinitro-quinoxaline-2,3-dione (DNQX), indicating that the early EPSP is mediated by non-NMDA receptors. The slow depolarization was mediated by NMDA receptors because it was depressed by membrane hyperpolarization or addition of APV. 4. The late EPSP evoked by higher-frequency stimulation was abolished by APV, indicating that it is mediated by NMDA receptors, which are located either on the recorded cell or on presynaptic cells to the recorded cells. 5. Long-term potentiation (LTP) of EPSPs was examined in cells perfused with solutions containing 1 microM bicuculline methiodide (BIM), a gamma-aminobutyric acid (GABA) antagonist. WM was stimulated at 2 Hz for 15 min as a conditioning stimulus to induce LTP, and the resultant changes were tested by low-frequency (0.1 Hz) stimulation of WM. 6. LTP of early EPSPs occurred in more than one-half of the cells (8/13) after strong conditioning stimulation. The rising slope of the EPSP was increased 1.6 times on average. 7. To test involvement of NMDA receptors in the induction of LTP in the early EPSP, the effect of conditioning stimulation was studied in a solution containing 100 microM APV, which was sufficient to block completely synaptic transmission mediated by NMDA receptors. LTP occurred in the same frequency and magnitude as in control solution.


2013 ◽  
Vol 386 (1-2) ◽  
pp. 251-258 ◽  
Author(s):  
Le Yang ◽  
Zhi-ming Yang ◽  
Nan Zhang ◽  
Zhen Tian ◽  
Shui-bing Liu ◽  
...  

1994 ◽  
Vol 76 (3) ◽  
pp. 1293-1301 ◽  
Author(s):  
D. R. Karius ◽  
L. Ling ◽  
D. F. Speck

This study tested the hypothesis that excitatory amino acid (EAA) neurotransmission at non-N-methyl-D-aspartate (non-NMDA), but not NMDA, receptors within medial regions of the nucleus tractus solitarius (NTS) is required in the inspiratory termination elicited by vagal or intercostal nerve (ICN) stimulation. Adult cats were anesthetized, decerebrated, vagotomized, and ventilated. After control responses to stimulation of the superior laryngeal nerve (SLN), vagus, and ICN were obtained, EAA receptor antagonists were injected into the medial aspects of the NTS. Injections of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) or 6,7-dinitro-quinoxaline-2,3-dione (DNQX), EAA receptor antagonists; (+/-)-2-amino-5-phosphonopentanoic acid (AP5), an NMDA antagonist; or 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline (NBQX), a non-NMDA antagonist, ipsilateral to the vagus abolished the termination response. The SLN-elicited response persisted after AP5 injection but was abolished by NBQX injections. The ICN-elicited response persisted after bilateral injections of CNQX/DNQX or procaine. We conclude that the inspiratory termination elicited by ICN stimulation is independent of the regions medial to the NTS. Inspiratory termination elicited by vagal or SLN stimulation requires non-NMDA-mediated EAA neurotransmission within medial aspects of the NTS, but the vagally elicited response also requires NMDA receptors.


2021 ◽  
pp. JN-RM-1968-21
Author(s):  
Yuying Huang (黄玉莹) ◽  
Shao-Rui Chen (陈少瑞) ◽  
Hong Chen (陈红) ◽  
Jing-Jing Zhou (周京京) ◽  
Daozhong Jin (金道忠) ◽  
...  

1993 ◽  
Vol 70 (5) ◽  
pp. 1759-1766 ◽  
Author(s):  
Y. I. Kim ◽  
W. J. Peacock ◽  
F. E. Dudek

1. Bicuculline-induced epileptiform bursts in slices of neocortical tissue resected from children (3 mo to 14 yr) undergoing neurosurgical treatment for intractable epilepsy were studied with conventional intracellular recording techniques. The purposes of this study were to characterize the bursts evoked in immature human neocortical slices, to gain further insight to how N-methyl-D-aspartate (NMDA) and non-NMDA receptors contribute to the genesis of the bursts, and to determine whether the characteristics of the bursts were related to patient age or clinically defined abnormality of the tissue. 2. Epileptiform bursts evoked by focal stimulation of the underlying white or gray matter in bicuculline (10 microM) were all-or-none events. Once evoked, the bursts in a given neuron appeared very similar to one another, regardless of stimulus intensity. Stronger stimuli only decreased the onset latency of the bursts. The bursts evoked with relatively weak stimuli (< 2-3 times the threshold), particularly those from stimulation of a distant site (4-5 mm), were variable in onset latency. The bursts from stimulation of a close site (0.5-2 mm) with stronger stimuli (> 3 times the threshold) were invariable in onset latency. 3. Across different cells, particularly across the cells in different slices, the bursts were quite variable in terms of their morphology and duration. When measured at one-half of the amplitude of the underlying depolarization (approximately 20-50 mV), the duration of the bursts ranged from 20 to 775 ms (n = 80 cells). In 23% of the cases (18 of 80 cells), afterdischarges lasting for tens of milliseconds to a few seconds followed the bursts.(ABSTRACT TRUNCATED AT 250 WORDS)


2004 ◽  
Vol 286 (3) ◽  
pp. R451-R464 ◽  
Author(s):  
Hakan S. Orer ◽  
Gerard L. Gebber ◽  
Shaun W. Phillips ◽  
Susan M. Barman

We tested the hypothesis that blockade of N-methyl-d-aspartate (NMDA) and non-NMDA receptors on medullary lateral tegmental field (LTF) neurons would reduce the sympathoexcitatory responses elicited by electrical stimulation of vagal, trigeminal, and sciatic afferents, posterior hypothalamus, and midbrain periaqueductal gray as well as by activation of arterial chemoreceptors with intravenous NaCN. Bilateral microinjection of a non-NMDA receptor antagonist into LTF of urethane-anesthetized cats significantly decreased vagal afferent-evoked excitatory responses in inferior cardiac and vertebral nerves to 29 ± 8 and 24 ± 6% of control ( n = 7), respectively. Likewise, blockade of non-NMDA receptors significantly reduced chemoreceptor reflex-induced increases in inferior cardiac (from 210 ± 22 to 129 ± 13% of control; n = 4) and vertebral nerves (from 253 ± 41 to 154 ± 20% of control; n = 7) and mean arterial pressure (from 39 ± 7 to 21 ± 5 mmHg; n = 8). Microinjection of muscimol, but not an NMDA receptor antagonist, caused similar attenuation of these excitatory responses. Sympathoexcitatory responses to the other stimuli were not attenuated by microinjection of a non-NMDA receptor antagonist or muscimol into LTF. In fact, excitatory responses elicited by stimulation of trigeminal, and in some cases sciatic, afferents were enhanced. These data reveal two new roles for the LTF in control of sympathetic nerve activity in cats. One, LTF neurons are involved in mediating sympathoexcitation elicited by activation of vagal afferents and arterial chemoreceptors, primarily via activation of non-NMDA receptors. Two, non-NMDA receptor-mediated activation of other LTF neurons tonically suppresses transmission in trigeminal-sympathetic and sciatic-sympathetic reflex pathways.


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