পৃষ্ঠা 1 থেকে 460 ফলাফল
Pharmacological and neurochemical evidence indicates that brain noradrenergic systems play an important role in the determination of audiogenic seizure severity in genetically epilepsy-prone rats (GEPRs). In earlier studies, intracerebroventricular (ICV) injections of norepinephrine suppressed
We recently reported that systemic administration of the anticholinesterase, soman, caused rapid depletion of forebrain norepinephrine (NE) in convulsive but not in nonconvulsive rats. As neurons in nucleus locus coeruleus (LC) provide the bulk of NE innervation to most of the forebrain and the sole
Epilepsy is a disease of neuronal hyperexcitability, and pharmacological and genetic studies have identified norepinephrine (NE) and neuropeptide Y (NPY) as important endogenous regulators of neuronal excitability. Both transmitters signal through G-protein-coupled receptors, are expressed either
It has been known for many years that norepinephrine (NE) is a potent endogenous anticonvulsant, yet there is confusion as to which receptor(s) mediate this effect. This is probably due to multiple factors, including the importance of distinct signaling pathways for different seizure paradigms, a
Ketogenic diets (KD) have been known to be effective against epilepsy for more than 80 years, yet the mechanism(s) responsible for this action remain unknown. Norepinephrine (NE) has been shown to have anti-ictal effects against a wide variety of pro-convulsants and in animal models of epilepsy.
Norepinephrine (NE) has been reported to modulate neuronal excitability and act as endogenous anticonvulsant. In the present study we used NE transporter knock-out mice (NET-KO), which are characterized by high levels of extracellular NE, to investigate the role of endogenous NE in seizure
Epilepsy and depression are comorbid disorders, but the mechanisms underlying their relationship have not been identified. Traditionally, many antidepressants have been thought to increase seizure incidence, although this remains controversial, and it is unclear which medications should be used to
We investigated in rats whether alterations in noradrenergic function caused by 6-hydroxydopamine or alpha- and beta-adrenoceptor agonists and antagonists would modify the susceptibility of the brain to electroencephalographic seizures induced by intrahippocampal infusion of quinolinic acid.
Infusions of an excitant amino acid, N-methyl-D-aspartate (NMDA) into the inferior colliculus (IC) render normal rats susceptible to audiogenic seizures (AGS) and/or spontaneous audiogenic-like seizures without tonic components. The excess excitant amino acid in the IC and the anticonvulsant effects
The time course effects of the benzoquinolizine Ro 4-1284 on spinal cord norepinephrine (NE) and 5-hydroxytryptamine (5-HT) levels were compared to the effects of this same drug on electrically-induced spinal cord seizures. The data show that a significant decrease in spinal cord NE levels and a
Audiogenic seizures (AGS) in genetically epilepsy-prone rats (GEPR) of the moderate-seizure substrain (GEPR-3s) were investigated to determine whether norepinephrine (NE) depletion induced by 6-hydroxydopamine (6-OHDA) microinfusion into the locus coeruleus (LC) could alter the efficacy of
The genetically epilepsy-prone rat (GEPR) seizure model is characterized by extensive abnormalities in brain noradrenergic function. Earlier studies had suggested that GEPRs might not regulate adrenoceptors in a normal fashion. The purpose of the present study was to determine if GEPR-9s are capable
Seizure predisposition in the Genetically Epilepsy-Prone Rat (GEPR) is at least partially dependent on central nervous system noradrenergic deficits. We have previously shown that moderate seizure GEPRs (GEPR-3) experience an increase in seizure severity after receiving Ro 4-1284, a monoamine
Alterations of norepinephrine transporter (NET) function by chronic inhibition of NET in relation to sensitization to seizures induce by cocaine and local anesthetics were studied in mice. Daily administration of desipramine, an inhibitor of the NET, for 5 days decreased [(3)H]norepinephrine uptake
The effects of central norepinephrine depletion produced by DSP-4 on drug-induced catalepsy and pot-decapitation convulsions were examined in the rat. Haloperidol-induced catalepsy was potentiated in DSP-4 treated rats, while arecoline-induced catalepsy was attenuated. Furthermore, post-decapitation