Demonstration of Postsynaptic Receptor Plasticity in an Amphibian Neuroendocrine Interface

2002 ◽  
Vol 14 (11) ◽  
pp. 843-845 ◽  
Author(s):  
B. G. Jenks ◽  
D. T. W. M. Ouwens ◽  
M. W. Coolen ◽  
E. W. Roubos ◽  
G. J. M. Martens
2013 ◽  
pp. 32-36
Author(s):  
David Papke ◽  
Claudio Grosman

2009 ◽  
Vol 10 (S1) ◽  
Author(s):  
Ronald AJ van Elburb ◽  
Laurens WJ Bosman ◽  
Margreet C Ridder ◽  
Arjen B Brussaard ◽  
Arjen van Ooyen

1996 ◽  
Vol 76 (1) ◽  
pp. 448-460 ◽  
Author(s):  
C. A. Lewis ◽  
D. S. Faber

1. To identify the type(s) and properties of inhibitory postsynaptic receptor(s) involved in synaptic transmission in cultured rat embryonic spinal cord and medullary neurons, we have used whole cell patch-clamp techniques to record miniature inhibitory postsynaptic currents (mIPSCs) in the presence of tetrodotoxin, DL-2-amino-5-phosphonovaleric acid, and 6-cyano-7-nitroquinoxaline-2,3-dione. 2. The mIPSCs recorded from both spinal cord and medullary neurons had skewed amplitude distributions. 3. The glycinergic antagonist strychnine and the GABAergic antagonist bicuculline each decreased both the frequency and mean peak amplitudes of mIPSCs. We conclude that both glycine and gamma-aminobutyric acid (GABA) are neurotransmitters at inhibitory synapses in our cultured cells. 4. Most (approximately 96-97%) mIPSCs decay with single-exponential time constants, and decay time distributions were consistently best fitted by the sum of four Gaussians with decay constants as follows: D1 = 5.8 +/- 0.1 (SE) ms (n = 63), D2 = 12.2 +/- 0.2 ms (n = 61), D3 = 23.2 +/- 0.4 ms (n = 54), and D4 = 44.7 +/- 1.0 ms (n = 57). We conclude that the four classes of decay times represent kinetically different inhibitory postsynaptic receptor populations. 5. Strychnine and bicuculline usually had one of two different effects on the mIPSC decay time constant distributions; either selective decreases in the frequency of mIPSCs with decay times in certain classes (i.e., the D1 class was reduced by bicuculline, the D2 class by strychnine, and the D3 and D4 classes by both antagonists) or a nonselective depression in the frequency of mIPSCs with decay times in all four classes. The particular effect observed in a given neuron was correlated with the presence or absence of ATP and guanosine 5'-triphosphate (GTP) in the patch pipette. Namely, in 71% of the antagonist applications where the pipette contained ATP and GTP, the result was a nonselective decrease in mIPSCs in all decay time constant classes. Conversely, in 54% of the antagonist applications in their absence, the result was a selective decrease in the frequency of mIPSCs in specific decay time constant classes. 6. In some experiments, mIPSCs reappeared in antagonist solution after an essentially complete block. Recovery from block in the continued presence of antagonist was never observed in the absence of ATP and GTP (8 neurons), and, at the same time, 5 of 9 neurons patched with ATP and GTP in the pipette did show recovery (56%).


2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Kyle Michael Stang ◽  
Keith B Hengen ◽  
Nathan R Nelson ◽  
Steve M Johnson ◽  
Mary Behan

2022 ◽  
Author(s):  
Alma Rodenas-Ruano ◽  
Kaoutsar Nasrallah ◽  
Stefano Lutzu ◽  
Maryann Castillo ◽  
Pablo E. Castillo

The dentate gyrus is a key relay station that controls information transfer from the entorhinal cortex to the hippocampus proper. This process heavily relies on dendritic integration by dentate granule cells (GCs) of excitatory synaptic inputs from medial and lateral entorhinal cortex via medial and lateral perforant paths (MPP and LPP, respectively). N-methyl-D-aspartate receptors (NMDARs) can contribute significantly to the integrative properties of neurons. While early studies reported that excitatory inputs from entorhinal cortex onto GCs can undergo activity-dependent long-term plasticity of NMDAR-mediated transmission, the input-specificity of this plasticity along the dendritic axis remains unknown. Here, we examined the NMDAR plasticity rules at MPP-GC and LPP-GC synapses using physiologically relevant patterns of stimulation in acute rat hippocampal slices. We found that MPP-GC, but not LPP-GC synapses, expressed homosynaptic NMDAR-LTP. In addition, induction of NMDAR-LTP at MPP-GC synapses heterosynaptically potentiated distal LPP-GC NMDAR plasticity. The same stimulation protocol induced homosynaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)-LTP at MPP-GC but heterosynaptic AMPAR-LTD at distal LPP synapses, demonstrating that NMDAR and AMPAR are governed by different plasticity rules. Remarkably, heterosynaptic but not homosynaptic NMDAR-LTP required Ca2+ release from intracellular, ryanodine-dependent Ca2+ stores. Lastly, the induction and maintenance of both homo- and heterosynaptic NMDAR-LTP were blocked by GluN2D antagonism, suggesting the recruitment of GluN2D-containing receptors to the synapse. Our findings uncover a mechanism by which distinct inputs to the dentate gyrus may interact functionally and contribute to hippocampal-dependent memory formation.


2013 ◽  
Vol 1 (1) ◽  
pp. 9-15
Author(s):  
Fuzhou Wang

Events in cerebral vessel have long been considered as a leading cause of disability in postmenopausal women with the physiological changes in expression and secretion of sex hormones. Hormone replacement therapy (HRT) emerged as a supplementary therapeutic strategy for them with the potential risk of cerebrovascular accidents. Epidemiological and genetic data showed that an interrelationship exists between hormone replacement and cerebrovascular disorders. Many animal experiments and clinical observations produced different results: these varied from positive to negative. Furthermore, recent studies could not identify the particular hormone, estrogen or progesterone that is more beneficial than the other. Here we summarize the two hormones’ effects on cerebrovascular diseases; associated epidemiological and genetic evidences; and the real status of the benefits and risks of HRT as well. We further hypothesize that whatever effects of HRT on brain vessel, hormone receptor expression, density, sensitivity and function may undergo alteration to varying extents, i.e. receptor plasticity gives rise to the receptor remodeling in postmenopausal older women, this may terminally produce the unwelcome effects.


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