Muscarinic ( M 1 ) cholinergic receptor activation within the dorsal hippocampus promotes destabilization of strongly encoded object location memories

Hippocampus ◽  
2021 ◽  
Author(s):  
Andrew E. Huff ◽  
Shelby D. McGraw ◽  
Boyer D. Winters
Keyword(s):  
Dorsal Hippocampus ◽  
Cholinergic Receptor ◽  
Receptor Activation ◽  
Object Location

Cholinergic modulation of synaptic inhibition in the guinea pig hippocampus in vitro: excitation of GABAergic interneurons and inhibition of GABA-release

1993 ◽  
Vol 69 (2) ◽  
pp. 626-629 ◽  
Author(s):  
J. C. Behrends ◽  
G. ten Bruggencate
Keyword(s):  
Guinea Pig ◽  
Synaptic Transmission ◽  
Pyramidal Neurons ◽  
Gaba Release ◽  
Cholinergic Receptor ◽  
Receptor Activation ◽  
Release Mechanism ◽  
Gabaergic Interneurons ◽  
Gamma Aminobutyric Acid

1. The effect of cholinergic receptor activation on gamma-aminobutyric acid (GABA)-mediated inhibitory synaptic transmission was investigated in voltage-clamped CA1 pyramidal neurons (HPNs) in the guinea pig hippocampal slice preparation. 2. The cholinergic agonist carbachol (1-10 microM) induced a prominent and sustained increase in the frequency and amplitudes of spontaneous inhibitory postsynaptic currents (IPSCs) in Cl(-)-loaded HPNs. The potentiation of spontaneous IPSCs was not dependent on excitatory synaptic transmission but was blocked by atropine (1 microM). 3. Monosynaptically evoked IPSCs were reversibly depressed by carbachol (10 microM). 4. The frequency of miniature IPSCs recorded in the presence of tetrodotoxin (0.6 or 1.2 microM) was reduced by carbachol (10 or 20 microM) in an atropine-sensitive manner. 5. We conclude that, while cholinergic receptor activation directly excites hippocampal GABAergic interneurons, it has, in addition, a suppressant effect on the synaptic release mechanism at GABAergic terminals. This dual modulatory pattern could explain the suppression of evoked IPSCs despite enhanced spontaneous transmission.

Domoic acid, the alleged "mussel toxin," might produce its neurotoxic effect through kainate receptor activation: an electrophysiological study in the rat dorsal hippocampus

1989 ◽  
Vol 67 (1) ◽  
pp. 29-33 ◽  
Author(s):  
Guy Debonnel ◽  
Luc Beauchesne ◽  
Claude de Montigny
Keyword(s):  
Amino Acid ◽  
Domoic Acid ◽  
Pyramidal Neurons ◽  
Excitatory Amino Acid ◽  
Dorsal Hippocampus ◽  
Electrophysiological Study ◽  
Receptor Activation ◽  
Kainate Receptor ◽  
Neurotoxic Effect ◽  
Excitatory Effect

Domoic acid, an excitatory amino acid structurally related to kainate, was recently identified as being presumably responsible for the recent severe intoxication presented by more than 100 people having eaten mussels grown in Prince Edward Island (Canada). The amino acid kainate has been shown to be highly neurotoxic to the hippocampus, which is the most sensitive structure in the central nervous system. The present in vivo electrophysiological studies were undertaken to determine if domoic acid exerts its neurotoxic effect via kainate receptor activation. Unitary extracellular recordings were obtained from pyramidal neurons of the CA1 and the CA3 regions of the rat dorsal hippocampus. The excitatory effect of domoic acid applied by microiontophoresis was compared with that of agonists of the three subtypes of glutamatergic receptors: kainate, quisqualate, and N-methyl-D-aspartate. In CA1, the activation induced by domoic acid was about threefold greater than that induced by kainate; identical concentrations and similar currents were used. In CA3, domoic acid was also three times more potent than kainate. However, the most striking finding was that domoic acid, similar to kainate, was more than 20-fold more potent in the CA3 than in the CA1 region, whereas no such regional difference could be detected with quisqualate and N-methyl-D-aspartate. As the differential regional response of CA1 and CA3 pyramidal neurons to kainate is attributable to the extremely high density of kainate receptors in the CA3 region, these results provide the first electrophysiological evidence that domoic acid may produce its neurotoxic effects through kainate receptor activation.Key words: domoate, kainate, excitotoxin, hippocampus, N-methyl-D-aspartate.

scholarly journals Acetylcholine disinhibits hippocampal circuits to enable rapid formation of overlapping memory ensembles

2017 ◽  
Author(s):  
Luke Y. Prince ◽  
Krasimira Tsaneva-Atanasova ◽  
Claudia Clopath ◽  
Jack R. Mellor
Keyword(s):  
Granule Cells ◽  
Mossy Fiber ◽  
Pyramidal Cells ◽  
Cholinergic Receptor ◽  
Receptor Activation ◽  
Cellular Excitability ◽  
Rapid Formation ◽  
Ca3 Pyramidal Cells ◽  
Episodic Memories ◽  
Spiking Neural Network Model

AbstractIn the hippocampus, episodic memories are thought to be encoded by the formation of ensembles of synaptically coupled CA3 pyramidal cells driven by sparse but powerful mossy fiber inputs from dentate gyrus granule cells. Acetylcholine is proposed as the salient signal that determines which memories are encoded but its actions on mossy fiber transmission are largely unknown. Here, we show experimentally that cholinergic receptor activation suppresses feedforward inhibition and enhances excitatory-inhibitory ratio. In reconstructions of CA3 pyramidal cells, this disinhibition enables postsynaptic dendritic depolarization required for synaptic plasticity at CA3-CA3 recurrent synapses. We further show in a spiking neural network model of CA3 how a combination of disinhibited mossy fiber activity, enhanced cellular excitability and reduced recurrent synapse strength can drive rapid overlapping ensemble formation. Thus, we propose a coordinated set of mechanisms by which acetylcholine release enables the selective encoding of salient high-density episodic memories in the hippocampus.

scholarly journals Striatal cholinergic receptor activation causes a rapid, selective, & state-dependent rise in corticostriatal β activity

2017 ◽  
Author(s):  
Benjamin R. Pittman-Polletta ◽  
Allison Quach ◽  
Ali I. Mohammed ◽  
Michael Romano ◽  
Krishnakanth Kondabolou ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Cholinergic Receptor ◽  
Receptor Activation ◽  
Reverse Direction ◽  
Experimental Paradigm ◽  
Partial Directed Coherence ◽  
State Dependent ◽  
Cholinergic Tone ◽  
Movement Disability ◽  
Phase Amplitude

Cortico-basal ganglia-thalamic (CBT) β oscillations (15–30 Hz) are elevated in Parkinson’s disease and correlated with movement disability. To date, no experimental paradigm outside of loss of dopamine has been able to specifically elevate β oscillations in the CBT loop. Here, we show that activation of striatal cholinergic receptors selectively increased β oscillations in mouse striatum and motor cortex. In individuals showing simultaneous β increases in both striatum and M1, β partial directed coherence (PDC) increased from striatum to M1 (but not in the reverse direction). In individuals that did not show simultaneous β increases, β PDC increased from M1 to striatum (but not in the reverse direction), and M1 was characterized by persistent β-HFO phase-amplitude coupling. Finally, the direction of β PDC distinguished between β subbands. This suggests: (1) striatal cholinergic tone exerts state-dependent and frequency-selective control over CBT β power and coordination; (2) ongoing rhythmic dynamics can determine whether elevated β oscillations are expressed in striatum and M1; (3) altered striatal cholinergic tone differentially modulates distinct β subbands.

scholarly journals Injection of galanin into the dorsal hippocampus impairs emotional memory independent of 5-HT1A receptor activation

2021 ◽  
Vol 405 ◽  
pp. 113178
Author(s):  
Oliver Stiedl ◽  
Eugenia Kuteeva ◽  
Tomas Hökfelt ◽  
Sven Ove Ögren
Keyword(s):  
Dorsal Hippocampus ◽  
Emotional Memory ◽  
Receptor Activation
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