Effect of carbamazepine on cholinergic parameters in rat brain areas

Consolo, S.; Bianchi, S.; Ladinsky, H.

doi:10.1016/0028-3908(76)90031-9

Cited by 33 publications

(12 citation statements)

References 18 publications

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“…The role of cholinergic function in memory and related cognitive processes is well known. Deterioration of cholinergic neurons in the medial septal nucleus that project to the hippocampus, amygdale, and cortex (e.g., critical memory areas) was demonstrated in rat models of epilepsy [172]. In support, acetylcholine esterase inhibitors are shown to improve memory functioning in diverse neurological conditions [173].…”

Section: Cognitive States With Antiepileptic Medicationsmentioning

confidence: 99%

The Aspects and Mechanisms of Cognitive Alterations in Epilepsy: The Role of Antiepileptic Medications

Hamed

2009

CNS Neuroscience & Therapeutics

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Epilepsy is a major health problem. Several studies suggest a significant influence of epilepsy and its treatment on dynamic and functional properties of brain activity. Epilepsy can adversely affect mental development, cognition, and behavior. Epileptic patients may experience reduced intelligence, attention, and problems in memory, language, and frontal executive functions. Neuropsychological, functional, and quantitative neuroimaging studies revealed that epilepsy affect the brain as a whole. Mechanisms of epilepsy-related cognitive dysfunction are poorly delineated. Cognitive deficits with epilepsy may be transient, persistent, or progressive. Transient disruption of cognitive encoding processes may occur with paroxysmal focal or generalized epileptic discharges, whereas epileptogenesis-related neuronal plasticity, reorganization, sprouting, and impairment of cellular metabolism are fundamental determinants for progressive cognitive deterioration. Also antiepileptic drugs (AEDs) have differential, reversible, and sometimes cumulative cognitive adverse consequences. AEDs not only reduce neuronal irritability but also may impair neuronal excitability, neurotransmitter release, enzymes, and factors critical for information processing and memory. The present article serves as an overview of recent studies in adult and childhood epilepsy literatures present in PubMed that highlighted cognitive evaluation in epilepsy field (publications till 2008 were checked). We also checked the reference lists of the retrieved studies for additional reports of relevant studies, in addition to our experience in this field. Our search revealed that although the aspects of cognitive dysfunction, risk factors, and consequences have been explored in many studies; however, the mechanisms of contribution of epilepsy-related variables, including AEDs, to patients' cognition are largely unexplored. In this review, we discussed the differential effect of AEDs in mature and immature brains and the known mechanisms underlying epilepsy and AEDs adverse effects on cognition. The nature, timing, course, and mechanisms of cognitive alteration with epilepsy and its medications are of considerable clinical and research implications.

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Section: Cognitive States With Antiepileptic Medicationsmentioning

confidence: 99%

The Aspects and Mechanisms of Cognitive Alterations in Epilepsy: The Role of Antiepileptic Medications

Hamed

2009

CNS Neuroscience & Therapeutics

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“…Further studies revealed that either acute or chronic carbamazepine at low and relatively therapeutic doses could increase basal acetylcholine levels in the rat frontal cortex, hippocampus as well as whole brain slices (Mizuno, 1997;Mizuno et al, 2000;Zhu et al, 2002). However, higher doses of carbamazepine had no effect or even decreased the basal acetylcholine level in various brain regions (Consolo et al, 1976;Mizuno, 1997;Mizuno et al, 2000;Zhu et al, 2002). This bimodal action of carbamazepine may be explained by the fact that therapeutic dose of carbamazepine (e.g.…”

Section: Effect On Seizure Threshold Referencesmentioning

confidence: 89%

“…Chronic treatment with relatively low dose carbamazepine (25 mg/kg, i.p., twice daily for 6 days) also increased the striatal acetylcholine level (Consolo et al, 1976). Further studies revealed that either acute or chronic carbamazepine at low and relatively therapeutic doses could increase basal acetylcholine levels in the rat frontal cortex, hippocampus as well as whole brain slices (Mizuno, 1997;Mizuno et al, 2000;Zhu et al, 2002).…”

Section: Effect On Seizure Threshold Referencesmentioning

confidence: 94%

“…As summarized in Table 5, the results are controversial which is likely due to the different methods, brain regions, and duration and concentrations of carbamazepine used in these studies. An initial study by Consolo et al (1976) (Aceto et al, 1969) α-Conotoxin ImI Blocks homomeric α 7 nAChR with the highest apparent affinity and homomeric α 9 nAChR with 8-fold lower affinity Intracranial injection in young mice (6-10 g weight) Induces complex generalized seizures (McIntosh et al, 1994) Decamethonium bromide nAChR partial agonist; neuromuscular blocking agent Nicotine (i.c.v.) extensor convulsions in mice Nicotine extensor convulsions and lethality in mice ↑ ↑ (Aceto et al, 1969) (Aceto et al, 1969) Penicillin-induced seizure in dogs ↑ (Tsoucaris-Kupfer et al,…”

Section: Carbamazepinementioning

confidence: 98%

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Pathologic role of neuronal nicotinic acetylcholine receptors in epileptic disorders: implication for pharmacological interventions

Ghasemi¹,

Hadipour-Niktarash

2015

Reviews in the Neurosciences

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AbstractAccumulating evidence suggests that neuronal nicotinic acetylcholine receptors (nAChRs) may play a key role in the pathophysiology of some neurological diseases such as epilepsy. Based on genetic studies in patients with epileptic disorders worldwide and animal models of seizure, it has been demonstrated that nAChR activity is altered in some specific types of epilepsy, including autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) and juvenile myoclonic epilepsy (JME). Neuronal nAChR antagonists also have antiepileptic effects in pre-clinical studies. There is some evidence that conventional antiepileptic drugs may affect neuronal nAChR function. In this review, we re-examine the evidence for the involvement of nAChRs in the pathophysiology of some epileptic disorders, especially ADNFLE and JME, and provide an overview of nAChR antagonists that have been evaluated in animal models of seizure.

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“…Thus, carbamazepine increases acetylcholine in the striatum (Consolo et aL, 1976), decreases CSF H V A and other indices of dopamine turnover (Post et aL, 1986c), decreases CSF NE and inhibits NE release , and decreases adenylate cyclase and guanylate cyclase activity (Post et aL, 1982), as reviewed above. Thus, carbamazepine increases acetylcholine in the striatum (Consolo et aL, 1976), decreases CSF H V A and other indices of dopamine turnover (Post et aL, 1986c), decreases CSF NE and inhibits NE release , and decreases adenylate cyclase and guanylate cyclase activity (Post et aL, 1982), as reviewed above.…”

Section: Psychotropic Effectsmentioning

confidence: 99%