Articles
Publication Date: 2024
Physiology And Pharmacology (24765236)28(4)pp. 419-429
Introduction: It is known that glial cells are crucial for memory formation. Glial cells and neurons interconnect via gap junction channels made of connexin (Cx) proteins. Glial connexins were shown to be involved in memory formation. However, the expression profile of different glial connexins was not measured during memory consolidation. Cx43 and Cx30 are expressed in astrocytes, whereas Cx32 is expressed in oligodendrocytes. We quantified the messenger RNA (mRNA) levels of the hippocampal Cx30, Cx32, and Cx43 throughout the consolidation stage of fear or spatial memory. Methods: Male Wistar rats were distributed into eight groups of four each. To assess the spatial or fear memory consolidation, the Morris water maze and passive avoidance task were utilized. At different time intervals (one, three, and twenty-four hours) following the training sessions, rats were sacrificed and the hippocampi were isolated and frozen instantly in liquid nitrogen. A quantitative real-time polymerase chain reaction (PCR) was employed to measure mRNA levels of the target genes. Results: The results revealed that Cx43 and Cx32 downregulated significantly, one or three hours after training in the inhibitory avoidance model. In the Morris water maze, Cx43 expression was upregulated three hours after training. The expression of Cx30 did not exhibit significant alterations in either of the experimental assays. Conclusion: The results indicate the crucial, but differential role of the hippocampal Cx32 and Cx43 during fear or spatial memory consolidation. The exact outcomes of these potential changes need to be clarified. © 2024, Iranian Society of Physiology and Pharmacology. All rights reserved.
Beheshti, S.,
Ershadi, S.,
Zamani, F.,
Azimzadeh, M.,
Wesal, M.W. Publication Date: 2023
Epilepsy Research (09201211)197
Ghrelin is a peptide, which has been shown to affect seizures. However, there is not a consensus about its real impact on the control of seizure severity. We assessed the influence of intra-amygdala injections of a ghrelin receptor (GHSR) antagonist, as well as a GHSR inverse agonist on the electrical kindling-induced seizures. Two unipolar electrodes and a tripolar electrode twisted with a guide cannula were implanted in the skull surface or the basolateral amygdala of adult male rats, respectively. A rapid electrical kindling protocol was applied for kindling epileptogenesis. The stimulations were applied until rats showed three consecutive stage five seizures. Each rat was considered as its control. D-Lys-3-GHRP-6 (1, 12.5, and 25 μg/rat) or [D-Arg, D-phe, D-Trp, heu] substance P (D-SP) (50, 500 and 5000 ng/rat) as the GHSR antagonist or inverse agonist were injected into the basolateral amygdala. Seizure parameters including after-discharge duration (ADD), stage five duration (S5D), and seizure stage (SS) were documented thirty minutes following administration of the drugs or saline. Antagonism of the GHSR in the amygdala, significantly increased seizure induction in the kindled rats, in a dose-dependent manner, and induced spontaneous seizures leading to status epilepticus. Conversely, D-SP had a dose-dependent anticonvulsant activity, indicated by decreased ADD and S5D. The results show that GHSR inverse agonism suppressed seizure severity in the rat amygdala kindling model, whereas GHSR antagonism made seizures more severe. Therefore, when considering the ghrelin system to modulate seizures, it is crucial to note the differential impact of various GHSR ligands. © 2023 Elsevier B.V.
