Development of rat brain uptake and calcium-dependent release of GABA

Redburn, Dianna A.; Broome, David T.; Ferkany, J.W.; Enna, S.J.

doi:10.1016/0006-8993(78)91106-x

Cited by 61 publications

(14 citation statements)

References 15 publications

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“…Calcium-dependent release may develop either concurrently with, or after maturation of high-affinity uptake systems. REDBURN, BROOME, FER.KARY & ENNA (1978) found a more gradual development of Ca-dependent release in rat brain than we are reporting for chick brain. These authors suggest that the ontogenesis of release mechanisms correlates more closely with synaptogenesis than does high-affinity uptake.…”

Section: Lrifluence Of Temperature and Of Developmental Agecontrasting

confidence: 41%

Calcium-dependent release of putative neurotransmitters in the chick visual system

Bondy¹,

Harrington

1979

Neuroscience

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Section: Lrifluence Of Temperature and Of Developmental Agecontrasting

confidence: 41%

Calcium-dependent release of putative neurotransmitters in the chick visual system

Bondy¹,

Harrington

1979

Neuroscience

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“…In addition, morphological and biochemical markers for GABAergic activity, including high-affinity GABA uptake, glutamic acid decarboxylase (GAD) activity, and Ca'+-dependent GABA release are present at birth in rat cortex and hippocampus but increase markedly in postnatal weeks 2 and 3 (64)(65)(66)(67)(68)(69)(70). Uptake of GABA is near adult levels by birth, peaking considerably above that of the adult between postnatal weeks 1 and 2 and then decreasing toward adult activity by postnatal week 4 (69).…”

Section: Development Of Inhibitionmentioning

confidence: 99%

Epilepsy in the Developing Brain: Lessons from the Laboratory and Clinic

1997

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Summary:Children with epilepsy present unique challenges to the clinician. In addition to having differences in clinical and EEG phenomena, children differ from adults in regard to etiological factors, response to antiepileptic drugs (AEDs), and outcome. It is now recognized that the immature brain also differs from the mature brain in the basic mechanisms of epileptogenesis and propagation of seizures. The immature brain is more prone to seizures due to an imbalance between excitation and inhibition. y-Aminobutyric acid (GABA), the major CNS inhibitory neurotransmitter in the mature brain, can lead to depolarization in the hippocampal CA3 region in very young rats. There are also age-related differences in response to GABA agonists and antagonists in the substantia nigra, a structure important in the propagation of seizures. These age-related Epilepsy is a common disorder, leading to staggering costs, both in regard to human suffering and to economics. Because epilepsy frequently begins during childhood and has a higher incidence during the first decade of life than at any other time (l), issues of morbidity and mortality represent a major concern in pediatrics.Clinicians caring for children with epilepsy and developmental neuroscientists have long been aware that the immature brain differs considerably from the mature brain in the development and propagation of seizures, the behavioral and EEG features of the seizures, and their consequences. It is becoming increasingly clear that lessons learned about the mature brain in regard to the pathophysiology and treatment of seizures can not always be applied to the developing brain. An understanding of the unique features of epileptogenesis during development is essential before progress can be made in improving treatment. Despite the significance of the health care problem, it is surprising that relatively little differences in response to GABAergic agents provide further evidence that the pathophysiology of seizures in the immature brain differs from that in the mature brain. Although prolonged seizures can cause brain damage at any age, the extent of brain damage after prolonged seizures is highly age dependent. Far less histological damage and fewer disturbances in cognition result from prolonged seizures in the immature brain than from seizures of similar duration and intensity in mature animals. However, detrimental effects of AEDs may be greater in the immature brain, than in the mature brain. These lessons from the animal laboratory raise questions about the appropriateness of current therapeutic approaches to childhood seizure disorders. Key Words: Epilepsy-Developing brain-Electroencephalography-Epileptogenesis-Pathophysiology . attention has been directed toward developing treatment strategies that specifically address these age-related factors.In this article, features of epileptogenesis during brain development are reviewed and age-related differences in response to seizures and antiepileptic drugs (AEDs) are discussed. Table 1 shows some of the major p...

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“…Some studies have been made of develop mental changes in GABA transport, but the results appear to be hopelessly discrepant. For example, GABA uptake by rat brai n syn aptosomes has been reported to decrease [27] or to increase [29] during development or first to increase to a maximum on the Age. days 14th-15th postnatal day and then to decrease [5.…”

Section: Introductionmentioning

confidence: 99%

GABA, Hypotaurine and Taurine Transport in Brain Slices from Developing Mouse

Oja¹,

Kontro²

1983

Dev Neurosci

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The kinetics and sodium-dependence of γ-aminobutyric acid (GABA), hypotaurine and taurine uptake were analyzed in cerebral slices prepared from mice of different postnatal ages. The maximal velocities of transport (V) and the K_m constants for the high-affinity uptake all decreased with age, whereas the developmental changes in the low-affinity uptake were exactly opposite. Both high- and low-affinity uptakes were sodium-dependent in all age groups. The general patterns of developmental changes were similar with all three amino acids, in keeping with the assumption of a common transport system for all of them.

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Development of rat brain uptake and calcium-dependent release of GABA

Cited by 61 publications

References 15 publications

Calcium-dependent release of putative neurotransmitters in the chick visual system

Calcium-dependent release of putative neurotransmitters in the chick visual system

Epilepsy in the Developing Brain: Lessons from the Laboratory and Clinic

GABA, Hypotaurine and Taurine Transport in Brain Slices from Developing Mouse

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