Guide Cannula (guide + cannula)

Distribution by Scientific Domains

Selected Abstracts

High-frequency Oscillations after Status Epilepticus: Epileptogenesis and Seizure Genesis

EPILEPSIA, Issue 9 2004
Anatol Bragin
Summary:,Purpose: To investigate the temporal relation between high-frequency oscillations (HFOs) in the dentate gyrus and recurrent spontaneous seizures after intrahippocampal kainite-induced status epilepticus. Methods: Recording microelectrodes were implanted bilaterally in different regions of hippocampus and entorhinal cortex. A guide cannula for microinjection of kainic acid (KA) was implanted above the right posterior CA3 area of hippocampus. After recording baseline electrical activity, KA (0.4 ,g/0.2 ,l) was injected. Beginning on the next day, electrographic activity was recorded with video monitoring for seizures every day for 8 h/day for ,30 days. Results: Of the 26 rats studied, 19 revealed the appearance of sharp-wave activity and HFOs in the frequency range of 80 to 500 Hz in the dentate gyrus ipsilateral to the KA injection. In the remaining seven rats, no appreciable activity was noted in this frequency range. In some rats with recurrent seizures, HFOs were in the ripple frequency range (100,200 Hz); in others, HFOs were in the fast ripple frequency range (200,500 Hz), or a mixture of both oscillation frequencies was found. The time of detection of the first HFOs after status epilepticus varied between 1 and 30 days, with a mean of 6.3 ± 2.0 (SEM). Of the 19 rats in which HFO activity appeared, all later developed recurrent spontaneous seizures, whereas none of the rats without HFOs developed seizures. The sooner HFO activity was detected after status epilepticus, the sooner the first spontaneous seizure occurred. A significant inverse relation was found between the time to the first HFO detection and the subsequent rate of spontaneous seizures. Conclusions: A strong correlation was found between a decreased time to detection of HFOs and an increased rate of spontaneous seizures, as well as with a decrease in the duration of the latent period between KA injection and the detection of spontaneous seizures. Two types of HFOs were found after KA injection, one in the frequency range of 100 to 200 Hz, and the other, in the frequency range of 200 to 500 Hz, and both should be considered pathological, suggesting that both are epileptogenic. [source]

Cardiovascular Regulation through Hypothalamic GABAA Receptors in a Genetic Absence Epilepsy Model in Rat

EPILEPSIA, Issue 2 2002
Rezzan Gülhan Aker
Summary: ,Purpose: ,-Aminobutyric acid (GABA) plays a vital role in both central cardiovascular homeostasis and pathogenesis of epilepsy. Epilepsy affects autonomic nervous system functions. In this study, we aimed to clarify the role of GABAA receptors in hypothalamic cardiovascular regulation in a genetically determined animal model of absence epilepsy. Methods: Nonepileptic Wistar rats and genetic absence epilepsy rats from Strasbourg (GAERS) were instrumented with a guide cannula for drug injection and extradural electrodes for EEG recording. After a recovery period, iliac arterial catheters were inserted for direct measurement of mean arterial pressure and heart rate. Bicuculline, a GABAA -receptor antagonist, was injected into the dorsomedial (DMH) or posterior (PH) hypothalamic nuclei of nonepileptic control rats or GAERS. Blood pressure, heart rate, and EEG recordings were performed in conscious unrestrained animals. Results: Bicuculline injections into the hypothalamus produced increases in blood pressure and heart rate of both control rats and GAERS. The DMH group of GAERS showed a twofold increase in the blood pressure and the heart rate compared with those of control rats. Pressor responses to bicuculline, when microinjected into the PH, were similar in the nonepileptic animals and GAERS. Conversely, the amplitude of tachycardic responses to the administration of bicuculline into the PH was significantly higher in GAERS compared with those of control rats. Conclusions: The bicuculline-induced increases in blood pressure and heart rate were more prominent when given in the DMH of GAERS. These results indicate an increased GABAA receptor,mediated cardiovascular response through the DMH in conscious rats with absence epilepsy. [source]

Antisense oligodeoxynucleotide-induced suppression of basal forebrain NMDA-NR1 subunits selectively impairs visual attentional performance in rats

Janita Turchi
Abstract It is generally agreed that basal forebrain neuronal circuits contribute to the mediation of the ability to detect, select and discriminate signals, to suppress the processing of irrelevant information, and to allocate processing resources to competing tasks. Rats were trained in a task designed to assess sustained attention, or in a cued discrimination task that did not tax attentional processes. Animals were equipped with guide cannula to infuse bilaterally antisense oligodeoxynucleotides (ODNs) against the N -methyl- d -aspartate (NMDA) NR1 subunits, or missense ODNs, into the substantia innominata of the basal forebrain. Infusions of antisense or missense ODNs did not affect cued visual discrimination performance. Infusions of antisense ODNs dose-dependently impaired sustained attention performance by selectively decreasing the animals' ability to detect signals while their ability to reject nonsignal trials remained unchanged. The detrimental attentional effects of antisense infusions were maximal 24 h after the third and final infusion, and performance returned to baseline 24 h later. Missense infusions did not affect attentional performance. Separate experiments demonstrated extensive suppression of NR1 subunit immunoreactivity in the substantia innominata. Furthermore, infusions of antisense did not produce neurotoxic effects in that region as demonstrated by the Fluoro-Jade method. The present data support the hypothesis that NMDA receptor (NMDAR) stimulation in the basal forebrain, largely via glutamatergic inputs originating in the prefrontal cortex, represents a necessary mechanism to activate the basal forebrain corticopetal system for mediation of attentional performance. [source]

The Dopamine Response in the Nucleus Accumbens Core,Shell Border Differs From That in the Core and Shell During Operant Ethanol Self-Administration

ALCOHOLISM, Issue 8 2009
Elaina C. Howard
Background:, Ethanol self-administration has been shown to increase dopamine in the nucleus accumbens; however, dopamine levels in the accumbal subregions (core, shell, and core,shell border) have not yet been measured separately in this paradigm. This study was designed to determine if dopamine responses during operant ethanol self-administration are similar in the core, core,shell border, and shell, particularly during transfer from the home cage to the operant chamber and during consumption of the drinking solution. Methods:, Six groups of male Long,Evans rats were trained to lever-press for either 10% sucrose (10S) or 10% sucrose + 10% ethanol (10S10E) (with a guide cannula above the core, core,shell border, or shell of the accumbens). On experiment day, 5-minute microdialysis samples were collected from the core, core,shell border, or shell before, during, and after drinking. Dopamine and ethanol concentrations were analyzed in these samples. Results:, A significant increase in dopamine occurred during transfer of the rats from the home cage into the operant chamber in all 6 groups, with those trained to drink 10S10E exhibiting a significantly higher increase than those trained to drink 10S in the core and shell. No significant increases were observed during drinking of either solution in the core or shell. A significant increase in dopamine was observed during consumption of ethanol in the core,shell border. Conclusions:, We conclude that dopamine responses to operant ethanol self-administration are subregion specific. After operant training, accumbal dopamine responses in the core and shell occur when cues that predict ethanol availability are presented and not when the reinforcer is consumed. However, core,shell border dopamine responses occur at the time of the cue and consumption of the reinforcer. [source]

Behavioral Interaction Between Nicotine and Ethanol: Possible Modulation by Mouse Cerebellar Glutamate

ALCOHOLISM, Issue 7 2006
Salim Al-Rejaie
Background: Epidemiological studies show that people who drink alcoholic beverages also smoke cigarettes and vice versa. Furthermore, animal studies provide circumstantial evidence for ethanol and nicotine interaction. Previously, we demonstrated that intracerebellar nicotine attenuates ethanol ataxia. This study investigated the possible role of glutamate in modulating the interaction of nicotine and ethanol. Methods: Glutamate drugs N -methyl- d -aspartate (NMDA) and (+)- , -amino-3-hydroxy-5-methylisoxazole-4-propionic acid hydrate (AMPA) as well as their antagonists were directly microinfused into the cerebellum of CD-1 male mice to evaluate their effect on ethanol (2 g/kg i.p.) ataxia. Drug microinfusions were made via stereotaxically implanted stainless-steel guide cannulas. Rotorod was used to evaluate the ataxic response of ethanol. Results: Microinfusion of nicotine (0.3125, 1.25, 5 ng) significantly attenuated ethanol ataxia dose-dependently, confirming the functional interaction between nicotine and ethanol as reported earlier. Intracerebellar pretreatment with hexamethonium, a nicotinic receptor (nAChR) antagonist, significantly blocked nicotine-induced attenuation of ethanol ataxia suggesting participation of nAChRs. When ethanol was injected before nicotine microinfusion, nicotine failed to attenuate ethanol ataxia, indicating the critical importance of initial activation of nAChRs by nicotine. Intracerebellar microinfusion of NMDA (30, 60, 125 ng) and its antagonist, (+)-MK-801 (50, 100, 200 ng), significantly increased and decreased, respectively, the nicotine-induced attenuation of ethanol ataxia in a dose-related manner, suggesting participation of the NMDA receptor. Similarly, intracerebellar microinfusion of AMPA (7.5, 15, 30 ng) and its antagonist, nitro -2, 3-dioxobenzoquinoxaline-sulfonamide (NBQX; 25, 50, 100 ng), significantly increased and decreased, respectively, the nicotine-induced attenuation of ethanol ataxia in a dose-dependent manner. This suggests participation of the AMPA receptor and further supports involvement of the glutamate system in the ethanol,nicotine interaction. Intracerebellar nicotine failed to attenuate sodium-pentobarbital (25 mg/kg i.p.) ataxia, suggesting the relative specificity of the nicotine,ethanol interaction. Conclusions: The results suggested that glutamate modulates the functional interaction between nicotine and ethanol because NMDA and AMPA enhanced the nicotine-induced attenuation of ethanol ataxia, whereas (+)-MK-801 and NBQX reduced the attenuation. [source]