Stimulation of Metabotropic Glutamate (mGlu) 2 Receptor and Blockade of mGlu1 Receptor Improve Social Memory Impairment Elicited by MK-801 in Rats

AbstractIntrinsic interneurons within the dorsal lateral geniculate nucleus (dLGN) provide a feed-forward inhibitory pathway for afferent visual information originating from the retina. These interneurons are unique because in addition to traditional axodendritic output onto thalamocortical neurons, these interneurons have presynaptic dendrites that form dendrodendritic synapses onto thalamocortical neurons as well. These presynaptic dendrites, termed F2 terminals, are tightly coupled to the retinogeniculate afferents that synapse onto thalamocortical relay neurons. Retinogeniculate stimulation of F2 terminals can occur through the activation of ionotropic and/or metabotropic glutamate receptors. The stimulation of ionotropic glutamate receptors can occur with single stimuli and produces a short-lasting inhibition of the thalamocortical neuron. By contrast, activation of metabotropic glutamate receptors requires tetanic activation and results in longer-lasting inhibition in the thalamocortical neuron. The F2 terminals are predominantly localized to the distal dendrites of interneurons, and the excitation and output of F2 terminals can occur independent of somatic activity within the interneuron thereby allowing these F2 terminals to serve as independent processors, giving rise to focal inhibition. By contrast, strong transient depolarizations at the soma can initiate a backpropagating calcium-mediated potential that invades the dendritic arbor activating F2 terminals and leading to a global form of inhibition. These distinct types of output, focal versus global, could play an important role in the temporal and spatial roles of inhibition that in turn impacts thalamocortical information processing.

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The novel and systemically active metabotropic glutamate 1 (mGlu1) receptor antagonist 3-MATIDA reduces post-ischemic neuronal death

Neuropharmacology ◽

10.1016/s0028-3908(02)00033-3 ◽

2002 ◽

Vol 42 (6) ◽

pp. 741-751 ◽

Cited By ~ 44

Author(s):

Flavio Moroni ◽

Sabina Attucci ◽

Andrea Cozzi ◽

Elena Meli ◽

Roberta Picca ◽

...

Keyword(s):

Receptor Antagonist ◽

Neuronal Death ◽

The Novel ◽

Metabotropic Glutamate ◽

Mglu1 Receptor

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Intrastriatal and intrasubthalamic stimulation of metabotropic glutamate receptors: A behavioral and Fos immunohistochemical study

Neuroscience ◽

10.1016/0306-4522(94)00568-p ◽

1995 ◽

Vol 66 (1) ◽

pp. 55-65 ◽

Cited By ~ 49

Author(s):

K.W. Kaatz ◽

R.L. Albin

Keyword(s):

Glutamate Receptors ◽

Metabotropic Glutamate Receptors ◽

Immunohistochemical Study ◽

Metabotropic Glutamate ◽

Stimulation Of

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Characterization of [3H] desmethylimipramine binding in bovine adrenal medulla: interactions with σ- and (or) phencyclidine-receptor ligands

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y92-214 ◽

1992 ◽

Vol 70 (11) ◽

pp. 1508-1514 ◽

Cited By ~ 7

Author(s):

Cheryl Rogers ◽

Simon Lemaire

Keyword(s):

Adrenal Medulla ◽

Binding Sites ◽

Scatchard Analysis ◽

Noradrenaline Uptake ◽

Receptor Ligands ◽

Mk 801 ◽

Bovine Adrenal Medulla ◽

Sodium Dependent ◽

Stimulation Of

High-affinity binding sites (apparent KD 2.87 nM) for [3H]desmethylimipramine ([3H]DMI), have been demonstrated and characterized in membrane preparations of bovine adrenal medulla. The binding of [3H]DMI improved upon pretreatment of the membrane with KCl and was saturable, sodium dependent, and potently inhibited by nisoxetine and imipramine. [3H]DMI binding was also inhibited by various phencyclidine (PCP)- and (or) σ-receptor ligands, with the following order of potency: haloperidol > rimcazole > (−)-butaclamol > dextromethorphan > MK-801 > (+)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine((+)-3-PPP) > PCP > N-(2-thienyl)cyclohexyl-3,4-piperidine (TCP) > (+)-SKF-10047 > (−)-SKF-10047. The inhibition produced by σ ligands was not attributed to stimulation of either σ1- or σ2-receptors, owing to inactivity of the selective σ-receptor ligands (+)-pentazocine and 1,3-di(2-tolyl)guanidine (DTG). The inhibition of [3H]DMI binding by σ- and PCP-receptor ligands was not attributed to PCP1- or PCP2-receptor stimulation, owing to the decreased potency (100-fold) of these ligands in [3H]DMI assays compared with the affinity for brain PCP1 sites, and the ineffectiveness of the PCP2-ligand N-(1-(2-benzo(b)thiophenyl)cyclohexyl)piperidine (BTCP). Scatchard analysis of the inhibition by the σ-ligands haloperidol and (+)-3-PPP, as well as the PCP1 receptor ligand MK-801, demonstrated noncompetitive interaction with the site bound by [3H]DMI. These studies indicate that bovine adrenomedullary membranes possess a specific receptor for the noradrenaline uptake inhibitor [3H]DMI, which is sensitive to allosteric modulation produced by PCP and σ-ligands.Key words: desmethylimipramine, σ-receptor, phencyclidine, noradrenaline uptake, adrenal medulla.

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Pontine-evoked inspiratory inhibitions after antagonism of NMDA, GABAA, or glycine receptor

Journal of Applied Physiology ◽

10.1152/jappl.1993.74.3.1265 ◽

1993 ◽

Vol 74 (3) ◽

pp. 1265-1273 ◽

Cited By ~ 12

Author(s):

L. Ling ◽

D. R. Karius ◽

D. F. Speck

Keyword(s):

Electrical Stimulation ◽

Glycine Receptor ◽

Inhibitory Response ◽

Glycine Receptors ◽

Onset Latency ◽

Nerve Activity ◽

Systemic Injection ◽

Mk 801 ◽

Inspiratory Motor ◽

Stimulation Of

Single-shock stimulation of the pontine respiratory group (PRG) produces a transient short-latency inhibition of inspiratory motor activity. Stimulus trains delivered to the PRG can elicit a premature termination of inspiration. This study examined the involvement of N-methyl-D-aspartate (NMDA), gamma-aminobutyrateA (GABAA), or glycine receptors in these inhibitory responses. Experiments were conducted in decerebrate, paralyzed, and ventilated cats. Control responses to PRG stimulation were obtained from recordings of the left phrenic nerve activity. After systemic injection of MK-801, bicuculline, or strychnine (antagonists to NMDA, GABAA, or glycine receptors, respectively), responses to stimulation were again recorded. Inspiratory termination elicited by the PRG stimulation persisted after antagonism of NMDA, GABAA, or glycine receptors. The onset latency and duration of the transient inhibition were not changed after administration of bicuculline, but MK-801 administration did significantly prolong the duration of the transient inhibition. Strychnine significantly prolonged both the onset latency and the duration. These data suggest that none of the three receptor types is required in the inspiratory termination response elicited by electrical stimulation of the PRG region and that NMDA, GABAA, or glycine receptor-mediated neurotransmission is not solely responsible for the transient inhibitory response. However, the prolonged onset and duration of the transient inhibition after strychnine administration suggest that glycine does normally participate in this response.

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