scholarly journals NMDA receptors promote hippocampal sharp‐wave ripples and the associated coactivity of CA1 pyramidal cells

Hippocampus ◽  
2020 ◽  
Vol 30 (12) ◽  
pp. 1356-1370
Author(s):  
Timothy Howe ◽  
Anthony J. Blockeel ◽  
Hannah Taylor ◽  
Matthew W. Jones ◽  
Maxim Bazhenov ◽  
...  
Keyword(s):  
Nmda Receptors ◽  
Pyramidal Cells ◽  
Ca1 Pyramidal Cells ◽  
Sharp Wave

Blocking GABAA Inhibition Reveals AMPA- and NMDA-Receptor-Mediated Polysynaptic Responses in the CA1 Region of the Rat Hippocampus

1997 ◽  
Vol 77 (4) ◽  
pp. 2071-2082 ◽  
Author(s):  
V. Crépel ◽  
R. Khazipov ◽  
Y. Ben-Ari
Keyword(s):  
Nmda Receptor ◽  
Nmda Receptors ◽  
Pyramidal Cell ◽  
Pyramidal Cells ◽  
Stratum Radiatum ◽  
External Concentration ◽  
Physiological Concentration ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Region ◽  
Stimulation Of

Crépel, V., R. Khazipov, and Y. Ben-Ari. Blocking GABAA inhibition reveals AMPA- and NMDA-receptor-mediated polysynaptic responses in the CA1 region of the rat hippocampus. J. Neurophysiol. 77: 2071–2082, 1997. We have investigated the conditions required to evoke polysynaptic responses in the isolated CA1 region of hippocampal slices from Wistar adult rats. Experiments were performed with extracellular and whole cell recording techniques. In the presence of bicuculline (10 μM), 6-cyano-7-nitroquinoxaline-2-3-dione (10 μM), glycine (10 μM), and a low external concentration of Mg2+ (0.3 mM), electrical stimulation of the Schaffer collaterals/commissural pathway evoked graded N-methyl-d-aspartate (NMDA)-receptor-mediated late field potentials in the stratum radiatum of the CA1 region. These responses were generated via polysynaptic connections because their latency varied strongly and inversely with the stimulation intensity and they were abolished by a high concentration of divalent cations (7 mM Ca2+). These responses likely were driven by local collateral branches of CA1 pyramidal cell axons because focal application of tetrodotoxin (30 μM) in the stratum oriens strongly reduced the late synaptic component and antidromic stimulation of CA1 pyramidal cells could evoke the polysynaptic response. Current-source density analysis suggested that the polysynaptic response was generated along the proximal part of the apical dendrites of CA1 pyramidal cells (50–150 μm below the pyramidal cell layer in the stratum radiatum). In physiological concentration of Mg2+ (1.3 mM), the pharmacologically isolated NMDA-receptor-mediated polysynaptic response was abolished. In control artificial cerebrospinal fluid (with physiological concentration of Mg2+), bicuculline (10 μM) generated a graded polysynaptic response. Under these conditions, this response was mediated both by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/NMDA receptors. In the presence of d-2-amino-5-phosphonovalerate (50 μM), the polysynaptic response could be mediated by AMPA receptors, although less efficiently. In conclusion, suppression of γ-aminobutyric acid-A inhibition reveals glutamate receptor-mediated network-driven events in the isolated CA1 region. These polysynaptic responses are mediated by AMPA and/or NMDA receptors depending on the pharmacological conditions and the external concentration of Mg2+ used. We suggest that these responses are driven by local recurrent collaterals of CA1 pyramidal cells.

scholarly journals Most hippocampal CA1 pyramidal cells in rabbits increase firing during awake sharp-wave ripples and some do so in response to external stimulation and theta

2020 ◽  
Vol 123 (5) ◽  
pp. 1671-1681
Author(s):  
Miriam S. Nokia ◽  
Tomi Waselius ◽  
Joonas Sahramäki ◽  
Markku Penttonen
Keyword(s):  
Eyeblink Conditioning ◽  
Cell Activity ◽  
Pyramidal Cells ◽  
External Stimulation ◽  
Ca1 Pyramidal Cells ◽  
Sharp Wave ◽  
Hippocampal Ca1 ◽  
Trace Eyeblink Conditioning ◽  
Do So

We studied hippocampal sharp-wave ripples and theta and CA1 pyramidal cell activity during trace eyeblink conditioning in rabbits. Conditioning trials suppressed ripples while increasing theta for a period of several seconds. A quarter of the cells increased firing in response to the conditioned stimulus and fired extensively during endogenous theta as well as ripples. The role of endogenous theta epochs in off-line memory consolidation should be studied further.

scholarly journals Prenatal alcohol exposure disrupts hippocampal sharp‐wave ripple‐associated spike dynamics

2021 ◽  
Author(s):  
Ryan E Harvey ◽  
Laura E Berkowitz ◽  
Daniel D Savage ◽  
Benjamin J Clark
Keyword(s):  
Prenatal Alcohol Exposure ◽  
Pyramidal Cells ◽  
Population Level ◽  
Alcohol Exposure ◽  
Intrinsic Structure ◽  
Ca1 Pyramidal Cells ◽  
Sharp Wave ◽  
Activation Rate ◽  
Prenatal Alcohol ◽  
Spike Dynamics

Prenatal alcohol exposure (PAE) is among the most common developmental insults to the nervous system and is characterized by memory disruption. There is a pressing need to identify physiological alterations that help explain this memory impairment. Hippocampal sharp-wave ripples (SPW-Rs) are a compelling candidate for this purpose as they are the electrophysiological signatures of memory consolidation. We report that rats exposed to moderate prenatal alcohol display abnormalities restricted to SPW-R episodes that manifest as decreased recruitment of CA1 pyramidal cells and interneurons to SPW-R events, altered excitation during SPW-Rs, and decreased cell assembly activation rate. These differences observed at the single neuron and the population level may limit the ability of memory trace reactivation during SPW-Rs through the disruption of the intrinsic structure of cell sequences. Together, our results suggest that alterations in hippocampal SPW-R spike dynamics may underlie alcohol exposure-related memory deficits.

scholarly journals Disruption of perineuronal nets increases the frequency of sharp wave ripples

2017 ◽  
Author(s):  
ZhiYong Sun ◽  
P. Lorenzo Bozzelli ◽  
Adam Caccavano ◽  
Megan Allen ◽  
Jason Balmuth ◽  
...  
Keyword(s):  
Slow Wave Sleep ◽  
Neuronal Cell ◽  
Pyramidal Cells ◽  
Neuronal Population ◽  
Stratum Radiatum ◽  
Perineuronal Nets ◽  
Ca1 Pyramidal Cells ◽  
Sharp Wave ◽  
Initial Excitation ◽  
Ca3 Pyramidal Cells

AbstractHippocampal sharp wave ripples (SWRs) represent irregularly occurring synchronous neuronal population events that are observed during phases of rest and slow wave sleep. SWR activity that follows learning involves sequential replay of training-associated neuronal assemblies and is critical for systems level memory consolidation. SWRs are initiated by CA2 or CA3 pyramidal cells and require initial excitation of CA1 pyramidal cells as well as subsequent participation of parvalbumin (PV) expressing fast spiking (FS) inhibitory interneurons. These interneurons are relatively unique in that they represent the major neuronal cell type known to be surrounded by perineuronal nets (PNNs), lattice like structures composed of a hyaluronin backbone that surround the cell soma and proximal dendrites. Though the function of the PNN is not completely understood, previous studies suggest it may serve to localize glutamatergic input to synaptic contacts and thus influence the activity of ensheathed cells. Noting that FS PV interneurons impact the activity of pyramidal cells thought to initiate SWRs, and that their activity is critical to ripple expression, we examine the effects of PNN integrity on SWR activity in the hippocampus. Extracellular recordings from the stratum radiatum of 490 micron horizontal murine hippocampal hemisections demonstrate SWRs that occur spontaneously in CA1. As compared to vehicle, pretreatment (120 min) of paired hemislices with hyaluronidase, which cleaves the hyaluronin backbone of the PNN, decreases PNN integrity and increases SWR frequency. Pretreatment with chondroitinase, which cleaves PNN side chains, also increases SWR frequency. Together, these data contribute to an emerging appreciation of extracellular matrix as a regulator of neuronal plasticity and suggest that one function of mature perineuronal nets could be to modulate the frequency of SWR events.

scholarly journals Early postnatal switch in magnesium sensitivity of NMDA receptors in rat CA1 pyramidal cells

1999 ◽  
Vol 521 (1) ◽  
pp. 99-111 ◽  
Author(s):  
Eilon D. Kirson ◽  
Claudia Schirra ◽  
Arthur Konnerth ◽  
Yoel Yaari
Keyword(s):  
Nmda Receptors ◽  
Pyramidal Cells ◽  
Ca1 Pyramidal Cells

scholarly journals Excitatory Amino Acid Binding Sites in the Rat Hippocampus after Transient Forebrain Ischemia

1989 ◽  
Vol 9 (5) ◽  
pp. 623-628 ◽  
Author(s):  
Hiroshi Onodera ◽  
Tsutomu Araki ◽  
Kyuya Kogure
Keyword(s):  
Dentate Gyrus ◽  
Nmda Receptors ◽  
Binding Sites ◽  
Nmda Antagonist ◽  
Pyramidal Cells ◽  
Receptor Density ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Ca1 Pyramidal Cells ◽  
Antagonist Binding

The influence of transient forebrain ischemia on the temporal alteration of glutamate receptors in the hippocampal formation was analyzed by means of in vitro quantitative receptor autoradiography. We compared the binding of N-methyl-d-aspartate (NMDA) receptors using [3H]3-((±)2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), noncompetitive NMDA antagonist binding sites using [3H]N-(1-(2-thienyl)-cyclohexyl)-3,4-piperidine (TCP), and kainate (KA) receptors. In the CA1 subfield of the hippocampus, the number of NMDA receptors and noncompetitive NMDA antagonist binding sites remained constant during the early stage of recirculation when the CA1 pyramidal cells remained histologically intact. A significant reduction of these receptor densities was observed 7 days following ischemia, when NMDA receptors and noncompetitive NMDA antagonist binding sites lost 64 and 29% of their binding sites in the stratum radiatum of the CA1, respectively. The KA receptor density in the CA1 subfield decreased by 44% 7 days after ischemia. Marked loss of the above-mentioned receptors in the CA1 after selective depletion of the CA1 pyramidal cells indicated that NMDA receptors, noncompetitive NMDA antagonist binding sites, and KA receptors in the CA1 are predominantly localized on the CA1 pyramidal cells. NMDA receptor density in the CA3 gradually decreased during the recirculation period. The stratum moleculare of the dentate gyrus, whose structure was histologically intact after ischemic insult, also showed a reduction of NMDA receptors 7 days following ischemia. [3H]KA receptor density in the stratum lucidum of the CA3 and in the hilus also decreased during recirculation. These results indicate that postischemic change of neuronal activity was not restricted to the ischemic-lesioned CA1 but that the histologically intact CA3 and dentate gyrus had also modulated neuronal transmission after ischemia.

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