Actions of kynurenic acid and quinolinic acid in the rat hippocampus in vivo

The excitatory effects of microiontophoretically applied quisqualic (QUIS), N-methyl-D-aspartic (NMDA), and quinolinic (QUIN) acids were investigated using intracellular recording from CA1 pyramidal neurones in slices of rat hippocampus. QUIS evoked only simple action potentials superimposed upon a depolarization which attained a clear plateau. When this level had been reached, increased ejecting currents did not produce further depolarization. By contrast, with low currents NMD A and QUIN elicited small membrane depolarizations which triggered bursts of action potentials superimposed upon rhythmically occurring depolarizing shifts. Larger currents caused depolarization which if sufficiently large completely blocked spike activity. Tetrodotoxin (TTX) prevented the spikes evoked by QUIS and the bursts of action potentials seen with NMDA and QUIN, and the rhythmic depolarizing shifts then appeared as broad spikes of up to 50 mV in amplitude. These and the underlying membrane depolarization were blocked by Co2+, by the NMDA antagonist D(−)-2-amino-5-phosphonovaleric acid (DAPV), and by kynurenic acid (KYNU). It thus appears that the depolarization and burst firing of rat CA1 pyramidal neurones elicited by NMDA and QUIN are Ca2+ dependent while the actions of QUIS are not.

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Kynurenic Acid Accelerates Healing of Corneal Epithelium In Vitro and In Vivo

Pharmaceuticals ◽

10.3390/ph14080753 ◽

2021 ◽

Vol 14 (8) ◽

pp. 753

Author(s):

Anna Matysik-Woźniak ◽

Waldemar A. Turski ◽

Monika Turska ◽

Roman Paduch ◽

Mirosław Łańcut ◽

...

Keyword(s):

Epithelial Cell ◽

Corneal Epithelium ◽

Kynurenic Acid ◽

Pharmaceutical Products ◽

Corneal Epithelial Cell ◽

Eye Drops ◽

Conjunctival Epithelium ◽

Corneal Erosion

Kynurenic acid (KYNA) is an endogenous compound with a multidirectional effect. It possesses antiapoptotic, anti-inflammatory, and antioxidative properties that may be beneficial in the treatment of corneal injuries. Moreover, KYNA has been used successfully to improve the healing outcome of skin wounds. The aim of the present study is to evaluate the effects of KYNA on corneal and conjunctival cells in vitro and the re-epithelization of corneal erosion in rabbits in vivo. Normal human corneal epithelial cell (10.014 pRSV-T) and conjunctival epithelial cell (HC0597) lines were used. Cellular metabolism, cell viability, transwell migration, and the secretion of IL-1β, IL-6, and IL-10 were determined. In rabbits, after corneal de-epithelization, eye drops containing 0.002% and 1% KYNA were applied five times a day until full recovery. KYNA decreased metabolism but did not affect the proliferation of the corneal epithelium. It decreased both the metabolism and proliferation of conjunctival epithelium. KYNA enhanced the migration of corneal but not conjunctival epithelial cells. KYNA reduced the secretion of IL-1β and IL-6 from the corneal epithelium, leaving IL-10 secretion unaffected. The release of all studied cytokines from the conjunctival epithelium exposed to KYNA was unchanged. KYNA at higher concentration accelerated the healing of the corneal epithelium. These favorable properties of KYNA suggest that KYNA containing topical pharmaceutical products can be used in the treatment of ocular surface diseases.

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Sodium salicylate enhances neural excitation via reducing GABAergic transmission in the dentate gyrus area of rat hippocampus in vivo

Hippocampus ◽

10.1002/hipo.23312 ◽

2021 ◽

Author(s):

Hui‐Ping Tang ◽

Hua‐Rui Gong ◽

Xu‐Lai Zhang ◽

Yi‐Na Huang ◽

Chuan‐Yun Wu ◽

...

Keyword(s):

Dentate Gyrus ◽

Sodium Salicylate ◽

Rat Hippocampus ◽

Gabaergic Transmission ◽

Neural Excitation

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N-cholinergic facilitation of glutamate release from an individual retinotectal fiber in frog

Visual Neuroscience ◽

10.1017/s0952523801184051 ◽

2001 ◽

Vol 18 (4) ◽

pp. 549-558 ◽

Cited By ~ 16

Author(s):

A. KURAS ◽

N. GUTMANIENĖ

Keyword(s):

Nicotinic Acetylcholine Receptors ◽

Action Potentials ◽

Acetylcholine Receptors ◽

Kynurenic Acid ◽

Glutamate Release ◽

Synaptic Potentials ◽

Lower Vertebrates ◽

Optic Fibers ◽

Retinotectal Transmission

Nicotinic acetylcholine receptors are localized on retinotectal axons' terminals in lower vertebrates. The effects of activation of these receptors by endogenous acetylcholine were observed under stimulation of mass optic fibers. This study was designed to determine whether endogenous acetylcholine facilitates frog retinotectal transmission, provided only the synapses of an individual optic axon are activated, and to evaluate the feasible extent of nicotinic facilitation in these synapses by applied agonist. To this end, the effects of cholinergic drugs on the extracellular action and synaptic potentials recorded from the terminal arborization of a separate retinotectal fiber (in layer F of the tectum) were investigated in vivo. Glutamatergic nature of retinotectal synapses was reexamined by treatment with kynurenic acid. Both kynurenic acid (0.25–1 mM) and d-tubocurarine chloride (10–15 μM) significantly depressed the synaptic potentials. Carbamylcholine chloride (50–150 μM) evoked a large augmentation of the synaptic potentials and a slight but statistically significant decrease of the action potentials. D-tubocurarine reduced the effect of carbamylcholine. Pilocarpine hydrochloride (50 μM) had only a weak effect. The paired-pulse facilitation of the synaptic potentials changed significantly under the action of carbamylcholine and d-tubocurarine. The obtained results suggest that the glutamate release from activated synapses of individual retinotectal axons is facilitated by endogenous acetylcholine via presynaptic nicotinic receptors. Under used stimulation conditions, this modulation mechanism was employed only partially since its activation by applied carbamylcholine could enhance synaptic transmission up to 2.8 times.

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