Bicuculline induced seizures in infant rats: ontogeny of behavioral and electrocortical phenomena

Baram, Tallie Z.; Snead, O. Carter

doi:10.1016/0165-3806(90)90055-4

Cited by 52 publications

(31 citation statements)

References 20 publications

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“…The inhibitory action of GABA at the network level is probably due to the shunting mechanisms amplified by the activation of the voltage-gated potassium channels and inactivation of sodium channels (73,219,244,401). These results are in general agreement with the findings that administration of GABA A antagonists induces hypersynchronous seizurelike activity in the neocortex in vivo by P3 (34) and in vitro by P2 (659).…”

Section: For Review)supporting

confidence: 82%

GABA: A Pioneer Transmitter That Excites Immature Neurons and Generates Primitive Oscillations

Ben-Ari

Gaı̈arsa

Tyzio

et al. 2007

Physiological Reviews

1,143

1,123

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Developing networks follow common rules to shift from silent cells to coactive networks that operate via thousands of synapses. This review deals with some of these rules and in particular those concerning the crucial role of the neurotransmitter γ-aminobuytric acid (GABA), which operates primarily via chloride-permeable GABAAreceptor channels. In all developing animal species and brain structures investigated, neurons have a higher intracellular chloride concentration at an early stage leading to an efflux of chloride and excitatory actions of GABA in immature neurons. This triggers sodium spikes, activates voltage-gated calcium channels, and acts in synergy with NMDA channels by removing the voltage-dependent magnesium block. GABA signaling is also established before glutamatergic transmission, suggesting that GABA is the principal excitatory transmitter during early development. In fact, even before synapse formation, GABA signaling can modulate the cell cycle and migration. The consequence of these rules is that developing networks generate primitive patterns of network activity, notably the giant depolarizing potentials (GDPs), largely through the excitatory actions of GABA and its synergistic interactions with glutamate signaling. These early types of network activity are likely required for neurons to fire together and thus to “wire together” so that functional units within cortical networks are formed. In addition, depolarizing GABA has a strong impact on synaptic plasticity and pathological insults, notably seizures of the immature brain. In conclusion, it is suggested that an evolutionary preserved role for excitatory GABA in immature cells provides an important mechanism in the formation of synapses and activity in neuronal networks.

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Section: For Review)supporting

confidence: 82%

GABA: A Pioneer Transmitter That Excites Immature Neurons and Generates Primitive Oscillations

Ben-Ari

Gaı̈arsa

Tyzio

et al. 2007

Physiological Reviews

1,143

1,123

View full text Add to dashboard Cite

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“…Neuronal death has been described following status epilepticus in hypermetabolic brain areas, mostly neocortex and hippocampus (25,37,39,41). In young experimental animals, repeated seizures had long-lasting debilitating effects on brain development, learning abilities, and behavioral milestones (3,35,37,41).…”

Section: Discussionmentioning

confidence: 99%

Epileptic seizures cause extended postictal cerebral vascular dysfunction that is prevented by HO-1 overexpression

Parfenova

Carratù

Tcheranova

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

131

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The extended postictal state is characterized by neurological problems in patients. Inadequate blood supply to the brain and impaired cerebral autoregulation may contribute to seizure-induced neuronal damage. Recent evidence in newborn pigs indicates that activation of the antioxidative enzyme heme oxygenase (HO) at the onset of seizures is necessary for increased cerebral blood flow during the ictal episode and for normal cerebral vascular functioning during the immediate postictal period. We hypothesized that seizures cause prolonged postictal cerebral vascular dysfunction that can be accentuated by HO inhibition and rescued by HO overexpression. Cerebral vascular responses to endothelium-dependent (hypercapnia, bradykinin) and -independent (isoproterenol, sodium nitroprusside) stimuli were assessed 48 h after bicuculline-induced seizures in: 1) saline-control newborn piglets, 2) HO-inhibited animals (HO was inhibited by tin protoporphyrin, SnPP, 3 mg/kg iv), and 3) HO-overexpressing piglets (HO-1 was upregulated by cobalt protoporphyrin, CoPP, 50 mg/kg ip). Extended alterations of HO expression in cerebral microvessels were confirmed by measuring CO production and inducible HO (HO-1) and constitutive HO (HO-2) proteins. Our data provide evidence that seizures cause a severe, sustained, postictal cerebral vascular dysfunction as reflected by impaired vascular reactivity to physiologically relevant dilators. During the delayed postictal state, vascular reactivity to all dilator stimuli was reduced in saline control and, to a greater extent, in HO-inhibited animals. In CoPP-treated piglets, no reduction in postictal cerebral vascular reactivity was observed. These findings may indicate that CoPP prevents postictal cerebral vascular dysfunction by upregulating HO-1, a finding that might have implications for preventing postictal neurological complications. cerebral circulation; epilepsy; postictal state; heme oxygenase; cobalt protoporphyrin THE POSTICTAL STATE as a consequence of epileptic seizures is associated with serious neurological problems and contributes to morbidity in patients. Debilitating effects of seizures are often extended to several days or even weeks of the postictal period (18). The multifactorial mechanisms of the postictal state are poorly understood. Human status epilepticus is consistently associated with cognitive problems and with widespread neuronal necrosis in the brain. Inadequate blood supply to the brain may contribute to seizure-induced neuronal damage and to the overall postictal state. During seizures, blood flow to the brain increases in patients (7, 9) and in animal models (11,34). In newborn piglets, neuronal activation at the onset of bicuculline-induced seizures is accompanied by the immediate increase in diameter of pial arterioles, major resistance vessels of the brain that determine the cerebral blood flow (30). The increase in the cerebral blood flow is required to match increased metabolic demands of activated neurons during the ictal episode and to prevent subsequent n...

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“…Electrodes were implanted under halothane anesthesia, using an infant rat stereotaxic apparatus as previously described [10,13]. Two or four cortical stainless-steel electrodes were placed over the frontal and posteroparietal cortex.…”

Section: Surgical Proceduresmentioning

confidence: 99%

Corticotropin‐releasing hormone–induced seizures in infant rats originate in the amygdala

Baram

Hirsch

Snead

et al. 1992

Annals of Neurology

Self Cite

113

156

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The neuroanatomical substrate of seizures induced by picomolar amounts of corticotropinreleasing hormone in infant rats was investigated. Electrographic and behavioral phenomena were monitored in 42 rat pups aged 5 to 22 days. Rat pups carried bipolar electrodes implanted in subcortical limbic structures, as well as cortical electrodes and intracerebroventricular cannulae. The administration of corticotropin-releasing hormone produced age-specific seizures within minutes, which correlated with rhythmic amygdala discharges. Paroxysmal hippocampal and cortical discharges developed subsequently in some rats. Corticotropin-releasing hormone-induced electrographic and behavioral seizures originate in the amygdala.Corticotropin-releasing hormone (CRH) is a 41-amino acid neuropeptide, isolated originally from the mammalian hypothalamus [1], It has since been shown to be distributed nonrandomly in the central nervous system, and to perform roles other than the control of secretion of ACTH and endorphins from the anterior pituitary [2]. Specifically, central transduction of stress, anxiety, depression, and anorexia have been demonstrated [2,3].CRH activates neurons both in vivo and in vitro [4][5][6][7][8][9]. The peptide increases both spontaneous and evoked spike discharge from locus ceruleus neurons in vivo [4], CRH induces neuronal depolarization in CA1 and CA3 hippocampal pyramidal cells in the slice preparation in vitro [5]. CRH administered into the cerebral ventricles of adult rats causes epileptiform discharges in the amygdala after a 1-to 3-hour delay, which spread to the dorsal hippocampus [6]. These discharges progress over 3 to 7 hours to behavioral and electrographic seizures. The doses needed for frank seizure generation in adult rats axe 1-5 to 3-75 × 10 −9 mol (0.75-1.88 × 10 −9 mol/gm of brain weight) [6][7][8].We have previously shown that CRH is a far more rapid and potent convulsant in the neonatal rat [10]. Seizures occur with a latency of as little as 2 minutes and with CRH doses as low as 7.5 × 10 −12 mo! or 0.05 × 10 −9 mol/gm of brain weight [10]. The present study was designed to define the neurobiological matrix of the behavioral and electrographic effects of the neuropeptide. We used infant rats, starting on postnatal day 5. Materials and Methods AnimalsTimed-pregnancy Sprague-Dawley-derived rats were obtained from Zivic-Miller (Zelionplc, PA). They were housed under a 12-hour light/dark cycle and fed ad libitum. Copyright © 1992 Delivery times were monitored and were accurate to within 12 hours. The day of birth was considered day zero. The pups were kept with the mothers, and litters were culled to 12 pups. Infant rats were subjected to surgery 24 hours before recording and returned to their mothers. CRH was always administered between 9 and 10:30 AM, to minimize diurnal variations in seizure susceptibility [11] and in endogenous CRH levels [12]. Surgical ProcedureElectrodes were implanted under halothane anesthesia, using an infant rat stereotaxic apparatus as previously describe...

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Bicuculline induced seizures in infant rats: ontogeny of behavioral and electrocortical phenomena

Cited by 52 publications

References 20 publications

GABA: A Pioneer Transmitter That Excites Immature Neurons and Generates Primitive Oscillations

GABA: A Pioneer Transmitter That Excites Immature Neurons and Generates Primitive Oscillations

Epileptic seizures cause extended postictal cerebral vascular dysfunction that is prevented by HO-1 overexpression

Corticotropin‐releasing hormone–induced seizures in infant rats originate in the amygdala

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