Excitation of interneurons in piriform cortex by 5-hydroxytryptamine: Blockade by MDL 100,907, a highly selective 5-HT2A receptor antagonist

1994 ◽  
Vol 259 (2) ◽  
pp. 137-141 ◽  
Author(s):  
Gerard J. Marek ◽  
George K. Aghajanian
2006 ◽  
Vol 96 (6) ◽  
pp. 3006-3015 ◽  
Author(s):  
Douglas A. Caruana ◽  
Robert E. Sorge ◽  
Jane Stewart ◽  
C. Andrew Chapman

Dopaminergic modulation of neuronal function has been extensively studied in the prefrontal cortex, but much less is known about its effects on glutamate-mediated synaptic transmission in the entorhinal cortex. The mesocortical dopamine system innervates the superficial layers of the lateral entorhinal cortex and may therefore modulate sensory inputs to this area. In awake rats, systemic administration of the dopamine reuptake inhibitor GBR12909 (10 mg/kg, ip) enhanced extracellular dopamine levels in the entorhinal cortex and significantly facilitated field excitatory postsynaptic potentials (fEPSPs) in layer II evoked by piriform cortex stimulation. An analysis of the receptor subtypes involved in the facilitation of evoked fEPSPs was conducted using horizontal slices of lateral entorhinal cortex in vitro. The effects of 15-min bath application of dopamine on synaptic responses were bidirectional and concentration dependent. Synaptic responses were enhanced by 10 μM dopamine and suppressed by concentrations of 50 and 100 μM. The D1-receptor antagonist SCH23390 (50 μM) blocked the significant facilitation of synaptic responses induced by 10 μM dopamine and the D2-receptor antagonist sulpiride (50 μM) prevented the suppression of fEPSPs observed with higher concentrations of dopamine. We propose here that dopamine release in the lateral entorhinal cortex, acting through D1 receptors, can lead to an enhancement of the salience of sensory representations carried to this region from adjacent sensory cortices.


1998 ◽  
Vol 44 (6) ◽  
pp. 508-515 ◽  
Author(s):  
Marie-Louise G Wadenberg ◽  
Paul B Hicks ◽  
J.Travis Richter ◽  
Keith A Young

2020 ◽  
Vol 45 (3) ◽  
pp. 195-202
Author(s):  
Can Wang ◽  
Le Xin ◽  
Chen-Chen Cai ◽  
Chao-Yu Cong ◽  
Jun-Fan Xie ◽  
...  

Abstract Neuropeptide S (NPS) is an endogenous peptide recently recognized to be presented in the brainstem and believed to play an important role in maintaining memory. The deletion of NPS or NPS receptor (NPSR) in mice shows a deficit in memory formation. Our recent studies have demonstrated that central administration of NPS facilitates olfactory function and ameliorates olfactory spatial memory impairment induced by muscarinic cholinergic receptor antagonist and N-methyl-D-aspartate receptor antagonist. However, it remains to be determined if endogenous NPS is an indispensable neuromodulator in the control of the olfactory spatial memory. In this study, we examined the effects of NPSR peptidergic antagonist [D-Val5]NPS (10 and 20 nmol, intracerebroventricular) and nonpeptidergic antagonist SHA 68 (10 and 50 mg/kg, intraperitoneal) on the olfactory spatial memory using computer-assisted 4-hole-board olfactory spatial memory test in mice. Furthermore, immunofluorescence was employed to identify the distributions of c-Fos and NPSR immunoreactive (-ir) neurons in olfactory system and hippocampal formation known to closely relate to the olfactory spatial memory. [D-Val5]NPS dosing at 20 nmol and SHA 68 dosing at 50 mg/kg significantly decreased the number of visits to the 2 odorants interchanged spatially, switched odorants, in recall trial, and simultaneously reduced the percentage of Fos-ir in NPSR-ir neurons, which were densely distributed in the anterior olfactory nucleus, piriform cortex, subiculum, presubiculum, and parasubiculum. These findings suggest that endogenous NPS is a key neuromodulator in olfactory spatial memory.


2002 ◽  
Vol 927 (2) ◽  
pp. 111-121 ◽  
Author(s):  
Juan Nacher ◽  
Gregori Alonso-Llosa ◽  
Daniel Rosell ◽  
Bruce McEwen

2010 ◽  
Vol 103 (5) ◽  
pp. 2728-2736 ◽  
Author(s):  
Giovanni Carriero ◽  
Laura Uva ◽  
Vadym Gnatkovsky ◽  
Massimo Avoli ◽  
Marco de Curtis

In vitro studies performed on brain slices demonstrate that the potassium channel blocker 4-aminopyridine (4AP, 50 μM) discloses electrographic seizure activity and interictal discharges. These epileptiform patterns have been further analyzed here in a isolated whole guinea pig brain in vitro by using field potential recordings in olfactory and limbic structures. In 8 of 13 experiments runs of fast oscillatory activity ( fast runs, FRs) in the piriform cortex (PC) propagated to the lateral entorhinal cortex (EC), hippocampus and occasionally to the medial EC. Early and late FRs were asynchronous in the hemispheres showed different duration [1.78 ± 0.51 and 27.95 ± 4.55 (SD) s, respectively], frequency of occurrence (1.82 ± 0.49 and 34.16 ± 6.03 s) and frequency content (20–40 vs. 40–60 Hz). Preictal spikes independent from the FRs appeared in the hippocampus/EC and developed into ictal-like discharges that did not propagate to the PC. Ictal-like activity consisted of fast activity with onset either in the hippocampus ( n = 6) or in the mEC ( n = 2), followed by irregular spiking and sequences of diffusely synchronous bursts. Perfusion of the N-methyl-d-aspartate receptor antagonist 2-amino-5-phosphonopentanoic acid (100 μM) did not prevent FRs, increased the duration of limbic ictal-like discharges and favored their propagation to olfactory structures. The AMPA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (50 μM) blocked ictal-like events and reduced FRs. In conclusion, 4AP-induced epileptiform activities are asynchronous and independent in olfactory and hippocampal-entorhinal regions. Epileptiform discharges in the isolated guinea pig brain show different pharmacological properties compared with rodent in vitro slices.


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