scholarly journals NMDA Receptor in Vasopressin 1b Neurons Is Not Required for Short-Term Social Memory, Object Memory or Aggression

2019 ◽  
Vol 13 ◽  
Author(s):  
Sarah K. Williams Avram ◽  
Heon-Jin Lee ◽  
Jarrett Fastman ◽  
Adi Cymerblit-Sabba ◽  
Adam Smith ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Social Memory ◽  
Short Term ◽  
Object Memory ◽  
Memory Object

scholarly journals NMDA receptor in vasopressin 1b neurons is not required for short-term social memory, object memory or aggression

2019 ◽  
Author(s):  
Sarah K. Williams Avram ◽  
Jarrett Fastman ◽  
Adi Cymerblit-Sabba ◽  
Adam Smith ◽  
Matthew Vincent ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Social Learning ◽  
Learning And Memory ◽  
Transgenic Mouse ◽  
Social Recognition ◽  
Receptor Expression ◽  
Short Term ◽  
Direct Role ◽  
Object Memory ◽  
Transgenic Mouse Line

AbstractThe vasopressin 1b receptor (Avpr1b) plays an important role in social behaviors including aggression, social learning and memory. Genetic removal of Avpr1b from mouse models results in deficits in aggression and short-term social recognition in adults. Avpr1b gene expression is highly enriched in the pyramidal neurons of the hippocampal cornu ammonis 2 (CA2) region. Activity of the hippocampal CA2 has been shown to be required for normal short-term social recognition and aggressive behaviors. Vasopressin acts to enhance synaptic responses of CA2 neurons through a NMDA-receptor dependent mechanism. Genetic removal of the obligatory subunit of the NMDA receptor (Grin1) within distinct hippocampal regions impairs non-social learning and memory. However, the question of a direct role for NMDA receptor activity in Avpr1b neurons to modulate social behavior remains unclear. To answer this question, we first created a novel transgenic mouse line with Cre recombinase knocked into the Avpr1b coding region to genetically target Avpr1b neurons. We confirmed this line has dense Cre expression throughout the dorsal and ventral CA2 regions of the hippocampus, along with scattered expression within the caudate-putamen and olfactory bulb. Conditional removal of the NMDA receptor was achieved by crossing our line to an available floxed Grin1 line. The resulting mice were measured on a battery of social and memory behavioral tests. Surprisingly, we did not observe any differences between Avpr1b-Grin1 knockout mice and their wildtype siblings. We conclude that mice without typical NMDA receptor function in Avpr1b neurons can develop normal aggression as well as short-term social and object memory performance.Significance StatementActivity of neurons that express vasopressin 1b receptor are essential for aggressive and social recognition behaviors. We created a novel transgenic mouse to allow selective targeting of vasopressin 1b neurons. Our studies indicate that NMDA receptor expression in vasopressin 1b neurons (including most CA2 neurons) are not required for development of the typical expression of aggression or recognition memory. Thus, CA2 neurons may have a unique way of incorporating novel stimuli into memory that deserves further investigation.

No effect of acute tryptophan depletion on phosphodiesterase inhibition-related improvements of short-term object memory in male Wistar rats

2013 ◽  
Vol 128 (2) ◽  
pp. 107-113 ◽  
Author(s):  
E. L. van Donkelaar ◽  
J. Prickaerts ◽  
S. Akkerman ◽  
K. Rutten ◽  
H. W. M. Steinbusch ◽  
...  
Keyword(s):  
Wistar Rats ◽  
Acute Tryptophan Depletion ◽  
Tryptophan Depletion ◽  
Phosphodiesterase Inhibition ◽  
Short Term ◽  
Object Memory ◽  
Male Wistar Rats

scholarly journals Anti-Ma2, anti-NMDA-receptor and anti-GluR^|^epsilon;2 limbic encephalitis with testicular seminoma: short-term memory disturbance

2012 ◽  
Vol 52 (9) ◽  
pp. 666-671 ◽  
Author(s):  
Akihiro Kubota ◽  
Takashi Tajima ◽  
Shinya Narukawa ◽  
Masamizu Yamazato ◽  
Hikoaki Fukaura ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Short Term Memory ◽  
Limbic Encephalitis ◽  
Short Term ◽  
Testicular Seminoma ◽  
Term Memory ◽  
Memory Disturbance

scholarly journals NMDA Receptor-Dependent Afterdepolarizations Are Curtailed by Carbonic Anhydrase 14: Regulation of a Short-Term Postsynaptic Potentiation

2012 ◽  
Vol 32 (47) ◽  
pp. 16754-16762 ◽  
Author(s):  
S. Makani ◽  
H.-Y. Chen ◽  
S. Esquenazi ◽  
G. N. Shah ◽  
A. Waheed ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Carbonic Anhydrase ◽  
Short Term ◽  
Postsynaptic Potentiation

scholarly journals Phosphorylation-State-Dependent Regulation of NMDA Receptor Short-Term Plasticity Modifies Hippocampal Dendritic Ca2+ Transients

2010 ◽  
Vol 104 (4) ◽  
pp. 2203-2213 ◽  
Author(s):  
Debika Chatterjea ◽  
Edaeni Hamid ◽  
John P. Leonard ◽  
Simon Alford
Keyword(s):  
Nmda Receptor ◽  
Pyramidal Neurons ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Short Term ◽  
Short Term Plasticity ◽  
State Dependent ◽  
Term Potentiation ◽  
Protocol Enhancement

N-methyl-d-aspartate (NMDA) receptor-mediated currents are enhanced by phosphorylation. We have investigated effects of phosphorylation-dependent short-term plasticity of NMDA receptor-mediated excitatory postsynaptic currents (EPSCs) on the induction of long-term depression (LTD). We confirmed in whole cell clamped CA1 pyramidal neurons that LTD is induced by pairing stimulus protocols. However, after serine-threonine phosphorylation was modified by postsynaptic introduction of a protein phosphatase-1 (PP1) inhibitor, the same pairing protocol evoked long-term potentiation (LTP). We determined effects of modification of phosphatase activity on evoked NMDA EPSCs during LTD induction protocols. During LTD induction, using a protocol pairing depolarization to –40 mV and 0.5 Hz stimulation, NMDA receptor-mediated EPSCs undergo a short-term enhancement at the start of the protocol. In neurons in which PP1 activity was inhibited, this short-term enhancement was markedly amplified. We then investigated the effect of this enhancement on Ca2+ entry during the start of the LTD induction protocol. Enhancement of NMDA receptor-mediated responses was accompanied by an amplification of induction protocol-evoked Ca2+ transients. Furthermore, this amplification required synaptic activation during the protocol, consistent with an enhancement of Ca2+ entry mediated by NMDA receptor activation. The sign of NMDA receptor-mediated long-term plasticity, whether potentiation or depression depends on the amplitude of the synaptic Ca2+ transient during induction. We conclude that short-term phosphorylation-dependent plasticity of the NMDA receptor-mediated EPSCs contributes significantly to the effect of phosphatase inhibition on the subsequent induction of LTD or LTP.

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