Investigation of the role of 5-hydroxytryptophan (5-HT), which functions as a modulator in the central nervous system, across behavioral contexts suggests that a general principle of transmitter function may be derived that is independent of specific behaviors and specific neural loci. A functional principle of 5-HT action in neural information processing in the central nervous system is proposed. Extremes deviations in 5-HT activity result in biases in information processing that may have direct effects on behavior. Such biases may predispose to pathological conditions such as violent suicide and aggression.

Modulatory role of serotonin in neural information processing: implications for human psychopathology.

Modulatory Role of Serotonin in Neural Information Processing

Neurobiology of seizure predisposition in the genetically epilepsy-prone rat.

A significant proportion of the childhood epilepsies have a genetic component. Therefore, animal models that can be bred for seizure expression may provide important information regarding the mechanisms by which molecular defects result in the neuronal hyperexcitability states collectively termed "epilepsy." Because of the rate and ease of breeding, rodent models are the most commonly used. The genetically epilepsy-prone rat has motor seizures in response to auditory stimuli. It is likely that the seizures are generated in the inferior colliculus because of an abnormality in the noradrenergic system. The seizure predisposition is inherited as an autosomal dominant trait. The genetic absence epilepsy rat has age-related spontaneous seizures characterized by motor arrest and head drops that are correlated with generalized spike-wave on the electroencephalogram (EEG). The seizure generating mechanism appears to be located in the lateral thalamic nuclei. The epileptic mongolian gerbil demonstrates behavioral arrest followed by myoclonic, tonic, and tonic-clonic seizures in response to unfamiliar environments. The underlying neuroanatomy involves hippocampal-cortical interactions indicative of a partial epilepsy. The tottering mouse has absence and myoclonic seizures, a 6- to 7-Hz ictal spike-wave EEG, and noradrenergic hyperinnervation that are linked to a mutation on chromosome 8. Hippocampal network hyperexcitability has been found with normal neuronal intrinsic properties. Stargazer is a mouse mutant with almost identical clinical and electrographic features as found in tottering. However, the genetic defect is located on chromosome 15 and no abnormalities of norepinephrine have been discovered. The El mouse demonstrates ictal automatisms in response to vestibular stimulation. Metabolic and structural abnormalities have been found in the hippocampus. Linkage to chromosomes 9 and 2 have been reported recently. The dilute brown agouiti mouse demonstrates motor seizures in response to auditory stimuli. Chromosomes 4 and 17 are linked to seizure expression. Thus, a variety of models exist to study the genetic, biochemical, structural and electrophysiological mechanisms that underlie the predisposition and expression of the inherited epilepsies.

Animal models of inherited epilepsy.

https://escholarship.org/content/qt5g7637wv/qt5g7637wv.pdf?t=q0ni1u

Increased numbers of GABAergic neurons occur in the inferior colliculus of an audiogenic model of genetic epilepsy.

Summary: Norepinephrine, dopamine, and 5-hydroxytryptamine concentrations were determined in the central nervous systems of genetically epilepsy-prone rats (GEPR) and in control rats. Norepinephrine concentrations were abnormal in all major areas of the central nervous system of the GEPR, with decrements existing in the telencephalon, hypothalamus-thalamus, midbrain, pons-medulla and spinal cord. An increment in the concentration of this neurotransmitter existed in the cerebellum. Dopamine concentrations were normal in all areas of the GEPR brain. Abnormalities in 5-hydroxytryptamine concentrations were also present in the GEPR. They were exclusively decrements and occurred in the telencephalon, hypothalamus-thalamus, midbrain, and pons medulla. Concentrations of this neurotransmitter were normal in the cerebellum and spinal cord. Coupled with our earlier pharmacologic data, these observations support our concept that noradrenergic and/or 5-hydroxytryptaminergic decrements are etiologically important in seizure susceptibility in the GEPR. The lack of abnormalities in brain dopamine concentrations strengthens our hypothesis that dopaminergic transmission does not regulate seizure susceptibility in this model.



RESUME

Les concentrations de norepinephrine, dopamine et 5-hydroxytryptamine ont ete determinees dans le systeme nerveux central de rats genetiquement predisposes a l'epilepsie (GEPR) et de rats de controle. Les concentrations de norepinephrine etaient anormales dans toutes les regions majeures du systeme nerveux central des GEPR, diminuees dans le telencephale, le thalamus-hypothalamus, le mesencephale, la region pontobulbaire et la moelle epiniere, augmentees dans le cervelet. Les concentrations de dopamine etaient normales dans toutes les zones cerebrales des GEPR. Des anomalies dans les concentrations de la 5-hydroxytryptamine ont eteegalement constatees. C'etaient exclusivement des diminutions et elles se voyaient dans le telencephale, le thalamus-hypothalamus, le mesencephale et la region pontobulbaire. Les concentrations de ce neurotransmetteur etaient normales dans le cervelet et la moelle epiniere. Associees a nos donnees pharmacologiques precedentes, ces observations soutiennent notre conception que les diminutions noradrenergiques et/ou 5-hydroxy-tryptaminergiques ont une importance etiologique dans la susceptibilite aux crises des GEPR. L'absence d'anomalie dans les concentrations cerebrales de dopamine renforce notre hypothese que la transmission dopaminergique n'intervient pas dans la regulation de la susceptibilite aux crises dans ce modele.



RESUMEN

Se han determinado las concentraciones de nore-pinefrina, dopamina y 5-hidroxitriptamina en el SNC de ratas geneticamente predispuestas a padecer epilepsia (GEPR) y en ratas control. Las concentraciones de norepinefrinafueron anormales en todas las regiones importantes del SNC de las GEPR, con disminucion en el telencefalo, hipotalamo-talamo, mesencefalo, protuberancia-bulbo y medula. En el cerebelo, este neurotransmisor se encuentra incrernentado. Las concentraciones de dopamina fueron normales en todas las areas del cerebro de las GEPR. Tambien se en-contraron exclusivamente reducciones de las concentraciones de la 5-hidroxitriptamina en el cerebro de las GEPR en el telencefalo, hipotalamo-talamo, mesencefalo y protuberancia-medula. Las concentraciones de este neurotransimor fueron normales en el cerebelo y en la medula. Unidas a nuestras observaciones farmacologicas previas, esta informacion apoya nuestro concepto de que las reducciones noradrenergicas o 5-hidroxitriptaminergicas son etiologicamente importantes en la susceptibilidad para ataques de las GEPR. La ausencia de anormalidades en las concentraciones cerebrales de dopamina fortalecen nuestra hipotesis de que la transmision dopamineergica no regula la susceptibilidad para ataques de este modelo.

Abnormalities in Monoamine Levels in the Central Nervous System of the Genetically Epilepsy‐Prone Rat

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Abnormalities in Monoamine Levels in the Central Nervous System of the Genetically Epilepsy‐Prone Rat