Regional neural activity within the substantia nigra during peri-ictal flurothyl generalized seizure stages

Velı́šková, Jana; Miller, Alexandra; Nunes, Magda L.; Brown, Lucy L.

doi:10.1016/j.nbd.2005.05.007

Cited by 33 publications

(18 citation statements)

References 55 publications

(83 reference statements)

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“…Increased deoxyglucose uptake in SNR posterior subregion just before onset of seizure has been reported, and SNR posterior was considered to be a gateway for the spread of seizure activity [24]. We did not detect any difference between basal values of GABA at nerve terminals in GAERS and Wistar control groups.…”

Section: Discussioncontrasting

confidence: 56%

Evaluation of GAD67 immunoreactivity in the substantia nigra pars reticulata region of the genetic absence epilepsy rats for the resistance to development of convulsive epilepsy seizure

Gulcebi

Akman

Çarçak

et al. 2016

North Clin Istanbul

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OBJECTIVE:Nonconvulsive absence epilepsy and convulsive epilepsy seizures are rarely seen in the same patient. It has been demonstrated that there is a resistance to development of convulsive seizures in genetic absence epilepsy models. The present study investigated glutamic acid decarboxylase (GAD) immunoreactivity in the brain region related to the interaction of these two seizure types, namely substantia nigra pars reticulata (SNR) subregions, SNRanterior and SNRposterior.METHODS:Nonepileptic adult male Wistar rats and Genetic Absence Epilepsy Rats from Strasbourg (GAERS) were used. Experimental groups of Wistar and GAERS were electrically stimulated for kindling model to induce convulsive epileptic seizures. An electrical stimulation cannula was stereotaxically implanted to the basolateral amygdala and recording electrodes were placed on the cortex. Sagittal sections of SNR were used to evaluate immunohistochemical reaction. Sections were incubated with anti-GAD67 antibody. Densitometric analysis of GAD67 immunoreactive neurons was performed using photographs of stained sections. One-way analysis of variance and post hoc Bonferroni test were used for statistical analysis of the data.RESULTS:There was no difference in GAD67 immunoreactivity of SNR subregions of control Wistar and control GAERS. An increase in GAD67 immunoreactivity was detected in SNRposterior subregion of stimulated Wistar rats, whereas there was a decrease in GAD67 immunoreactivity in SNRposterior of stimulated GAERS. The difference in GAD67 immunoreactivity between these two groups was statistically significant.CONCLUSION:Level of synthetized gamma-aminobutyric acid in SNRposterior subregion plays an important role in the interaction of nonconvulsive absence epilepsy seizures and convulsive epilepsy seizures.

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Section: Discussioncontrasting

confidence: 56%

Evaluation of GAD67 immunoreactivity in the substantia nigra pars reticulata region of the genetic absence epilepsy rats for the resistance to development of convulsive epilepsy seizure

Gulcebi

Akman

Çarçak

et al. 2016

North Clin Istanbul

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“…The rostral and caudal SNr mediate distinct facilitatory and inhibitory effects on seizures (Moshe and Albala, 1984; Veliskova et al, 1996; Fan et al, 1997; Thompson et al, 2000; Veliskova and Moshe, 2001). Caudal SNr is active during the pre-clonic period and may facilitate seizure initiation/propagation, while rostral SNr becomes involved after a motor seizure occurs (Collins et al, 1986; Veliskova et al, 2005). Thus, regionally-specific receptor expression and/or intrinsic properties of SNr neurons may influence site-specific effects on withdrawal.…”

Section: Discussionmentioning

confidence: 99%

Involvement of the Limbic Basal Ganglia in Ethanol Withdrawal Convulsivity in Mice Is Influenced by a Chromosome 4 Locus

Chen¹,

Kozell²,

Hitzemann³

et al. 2008

J. Neurosci.

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Physiological dependence and associated withdrawal episodes are thought to constitute a motivational force that sustains ethanol (alcohol) use/abuse and may contribute to relapse in alcoholics. Although no animal model duplicates alcoholism, models for specific factors, like the withdrawal syndrome, are useful for identifying potential genetic and neural determinants of liability in humans. We generated congenic mice that confirm a quantitative trait locus (QTL) on chromosome 4 with a large effect on predisposition to alcohol withdrawal. Using c-Fos expression as a high-resolution marker of neuronal activation, congenic mice demonstrated significantly less neuronal activity associated with ethanol withdrawal than background strain mice in the substantia nigra pars reticulata (SNr), subthalamic nucleus (STN), rostromedial lateral globus pallidus, and ventral pallidum. Notably, neuronal activation in subregions of the basal ganglia associated with limbic function was more intense than in subregions associated with sensorimotor function. Bilateral lesions of caudolateral SNr attenuated withdrawal severity following acute and repeated ethanol exposures, whereas rostrolateral SNr and STN lesions did not reduce ethanol withdrawal severity. Caudolateral SNr lesions did not affect pentylenetetrazol-enhanced convulsions. Our results suggest that this QTL impacts ethanol withdrawal via basal ganglia circuitry associated with limbic function, and that the caudolateral SNr plays a critical role. These are the first analyses to elucidate circuitry by which a confirmed addiction-relevant QTL influences behavior. This mouse QTL is syntenic with human chromosome 9p. Given the growing body of evidence that a gene(s) on chromosome 9p influences alcoholism, our results can facilitate human research on alcohol dependence and withdrawal.

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“…The caudal SNr displays greater expression of NMDA and metabotropic glutamate receptor densities (Hedberg, Velísková, Sperber, Nunes, & Moshé, 2003) and 5-HT 2C receptor mRNA (Eberle-Wang, Mikeladze, Uryu, & Chesselet, 1997) than the rostral SNr. The rostral and caudal SNr mediate distinct facilitatory and inhibitory effects on seizures (Fan et al, 1997; Velísková & Moshé, 2001), with the caudal SNr active during the pre-clonic period and thought to facilitate seizure initiation/propagation, while the rostral SNr becomes involved after a motor seizure occurs (Velísková, Miller, Nunes, & Brown, 2005). Thus, regionally specific receptor expression and/or intrinsic properties of SNr neurons may influence site-specific effects on withdrawal.…”

Section: Discussionmentioning

confidence: 99%

Limbic circuitry activation in ethanol withdrawal is regulated by a chromosome 1 locus

Buck

Chen

Kozell

2017

Alcohol

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Physiological dependence and associated withdrawal episodes are thought to constitute a motivational force sustaining alcohol use/abuse and contributing to relapse in alcoholics. Although no animal model exactly duplicates alcoholism, models for specific factors, including the withdrawal syndrome, are useful for identifying potential genetic and neural determinants of liability in humans. We previously identified highly significant quantitative trait loci (QTLs) with large effects on predisposition to withdrawal after chronic and acute alcohol exposure in mice and mapped these loci to the same region of chromosome 1 (Alcdp1 and Alcw1, respectively). The present studies utilize a novel Alcdp1/Alcw1 congenic model (in which an interval spanning Alcdp1 and Alcw1 from the C57BL/6J donor strain [build GRCm38 150.3–174.6 Mb] has been introgressed onto a uniform inbred DBA/2J genetic background) known to demonstrate significantly less severe chronic and acute withdrawal compared to appropriate background strain animals. Here, using c-Fos induction as a high-resolution marker of neuronal activation, we report that male Alcdp1/Alcw1 congenic animals demonstrate significantly less alcohol withdrawal-associated neural activation compared to appropriate background strain animals in the prelimbic and cingulate cortices of the prefrontal cortex as well as discrete regions of the extended amygdala (i.e., basolateral) and extended basal ganglia (i.e., dorsolateral striatum, and caudal substantia nigra pars reticulata). These studies are the first to begin to elucidate circuitry by which this confirmed addiction-relevant QTL could influence behavior. This circuitry overlaps limbic circuitry involved in stress, providing additional mechanistic information. Alcdp1/Alcw1 maps to a region syntenic with human chromosome 1q, where multiple studies find significant associations with risk for alcoholism.

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Regional neural activity within the substantia nigra during peri-ictal flurothyl generalized seizure stages

Cited by 33 publications

References 55 publications

Evaluation of GAD67 immunoreactivity in the substantia nigra pars reticulata region of the genetic absence epilepsy rats for the resistance to development of convulsive epilepsy seizure

Evaluation of GAD67 immunoreactivity in the substantia nigra pars reticulata region of the genetic absence epilepsy rats for the resistance to development of convulsive epilepsy seizure

Involvement of the Limbic Basal Ganglia in Ethanol Withdrawal Convulsivity in Mice Is Influenced by a Chromosome 4 Locus

Limbic circuitry activation in ethanol withdrawal is regulated by a chromosome 1 locus

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