Aim: To study the effect of glutamate on the intracellular calcium signal of pure cultured rat astrocytes and the role of N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors in the procedure.
Methods: The fluorescence of calcium was measured by Fura-2/AM (F(345)/F(380)).
Results: L-Glutamate induced [Ca(2+)](i) increase in most of the cells in concentration- and time-dependent manner. NMDA 50 mmol/L induced the fluorescence increase by almost three to four times, while the effect of AMPA 50 mmol/L was just half of that of D-(-)-2-amino-5-phosphonopentanoic acid (D-AP-5; a selective antagonist of the NMDA receptor). 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX, a selective antagonist of the AMPA receptor) abolished the effects of NMDA and AMPA, respectively. D-AP-5 and CNQX simultaneously or respectively attenuated the effect of L-glutamate at different degrees, but could not abolish it entirely.
Conclusion: Glutamate modulated intracellular Ca(2+) of pure cultured rat astrocytes through different pathways. The activation of NMDA and AMPA receptors took part in the complex mechanisms.
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Alzheimers Dement
December 2024
Buck Institute for Research on Aging, Novato, CA, USA.
Background: Synapses can modify their strength in response to activity, and the unique properties of synapses that regulate their plasticity are essential for memory. Long-term potentiation (LTP) is considered the physiological basis for how neurons encode new memories. A complex series of postsynaptic signaling events in LTP is associated with memory deficits in tauopathy models, but the mechanism by which pathogenic tau inhibits plasticity at synapses is unknown.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Centre for Brain Research, Indian Institute of Science, Bangalore, Karnataka, India.
Background: F-actin plays crucial roles in establishment and maintenance of synapses including post synaptic density organization, facilitation of vesicle trafficking, anchoring of postsynaptic receptors, and involvement in translational machinery. Proteomic analysis of actin-interacting proteins revealed the interaction of PSD-95 with actin in synaptosomes from brain cortex of APP/PS1 mice. PSD-95 functions as a critical scaffold for the assembly of neurotransmitter receptors at the synapse, playing a pivotal role in regulating synaptic strength and plasticity.
View Article and Find Full Text PDFCurr Top Behav Neurosci
January 2025
Department of Experimental Psychology, University of Oxford, Oxford, UK.
A decline in hippocampal function has long been associated with the progression of cognitive impairments in patients with Alzheimer's disease (AD). The disruption of hippocampal synaptic plasticity [primarily the reduction of long-term potentiation LTP] by excess production of soluble beta-amyloid (Aβ) has long been accepted as the mechanism by which AD pathology impairs memory, at least during the early stages of AD pathogenesis. However, the premise that hippocampal LTP underpins the formation of associative, long-term memories has been challenged.
View Article and Find Full Text PDFNeuropharmacology
December 2024
Department of Experimental Physiology and Pathophysiology, Medical University of Białystok, Ul. Mickiewicza 2A, 15-222, Białystok, Poland.
Although angiotensin 1-7 (Ang 1-7) and its role as a part of the "protective" axis of the renin-angiotensin system are well described in the literature, the mechanisms of its angiotensin II-like pressor and tachycardic effects following its acute central administration are not fully understood. It was the aim of the present study to examine which receptors contribute to the aforementioned cardiovascular effects. Ang 1-7 and antagonists for glutamate, GABA, vasopressin, thromboxane A (TP), α-adrenergic, and P2X purinoceptors or modulators of oxidative stress were injected into the paraventricular nucleus of the hypothalamus (PVN) of urethane-anesthetized male Wistar rats.
View Article and Find Full Text PDFPsychopharmacology (Berl)
December 2024
Bowles Center for Alcohol Studies, Department of Psychiatry, School of Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA.
Rationale: The positive reinforcing effects of alcohol (ethanol) drive repetitive use and contribute to alcohol use disorder (AUD). Ethanol alters the expression of glutamate AMPA receptor (AMPAR) subunits in reward-related brain regions, but the extent to which this effect regulates ethanol's reinforcing properties is unclear.
Objective: This study investigates whether ethanol self-administration changes AMPAR subunit expression and synaptic activity in the nucleus accumbens core (AcbC) to regulate ethanol's reinforcing effects in male C57BL/6 J mice.
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