Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During a restricted period of early postnatal development, rat neocortical neurons receive a powerful N-methyl-D-aspartate (NMDA) receptor-mediated synaptic input of variable onset latency and duration. These large-amplitude excitatory postsynaptic potentials are especially pronounced in supragranular layers and are generated by activities in polysynaptic circuits. Their occurrence in cortical slices from juvenile (postnatal (P) days 11-20), but not neonatal (P5-10) or adult (greater than or equal to P28) animals, appears to be in part a consequence of the relative immaturity of gamma-aminobutyric acid (GABA)-mediated inhibition, at a time when the requisite functional excitatory circuitry has been established. The transient manifestation of strong NMDA receptor-mediated potentials coincides temporally with a 'developmental window' within which there is enhanced sensitivity for epileptogenesis and for induction of long-term synaptic modifications in rat cortex.
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PMID:Transient expression of polysynaptic NMDA receptor-mediated activity during neocortical development. 197 Aug 56

The purpose of this study was to investigate the developmental differences in seizure susceptibility in mice and the roles of the histaminergic neuron system in inhibition of convulsions in development. First, we studied developmental differences in electrically-induced seizures. Since the 14-day-old mice showed a different seizure pattern from that of older mice, we evaluated the seizure susceptibility of mice older than 21 days. The durations of all the convulsive phases were significantly increased in 21- and 30-day-old mice, compared with older mice. Second, pyrilamine (or mepyramine), ketotifen, and d-chlorpheniramine, centrally-acting H1-antagonists, increased the durations of all the convulsive phases in the 21- and 30-day-old mice, but did not increase duration in 42-day-old mice. Terfenadine and astemizole, H1-antagonists that hardly enter the brain, did not affect the durations of all the convulsive phases in 21-, 30- and 42-day-old mice. The proconvulsant effect of centrally-acting H1-antagonists in 21- and 30-day-old mice were considered to be mediated via the central H1-receptors. Thus, the histaminergic neuron system may have an important physiological role in inhibition of seizures in 21- and 30-day-old mice which have higher seizure susceptibility. This would compensate for the immaturity of the other protective neuron systems such as NMDA receptor complexes and GABA receptors. In conclusion, the present findings support the view that the central histaminergic system plays a role in inhibition of convulsions.
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PMID:Proconvulsive effects of histamine H1-antagonists on electrically-induced seizure in developing mice. 787 Oct 20

We determined the conditions (immaturity, species, anesthesia, receptor blockade selectivity) under which glutamate receptor blockade produces respiratory depression in mammals. In unrestrained 0- to 2-day-old neonate and adult mice and cats, ventilation was measured by the barometric method, before and after separate or sequential administration of a non-NMDA receptor antagonist, NBQX (2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(F)quinoxaline, 2-200 mg kg(-1) in mice, 10-40 mg kg(-1) in cats), and a NMDA receptor antagonist, dizocilpine (3 mg kg(-1) in mice, 0.15-1.0 mg kg(-1) in cats). NBQX or dizocilpine alone did not decrease ventilation in awake adults, but NBQX strongly depressed ventilation in neonate awake mice and in adult anesthetized animals. Given together, dizocilpine and NBQX always profoundly depressed ventilation by producing a lethal apnea in neonate mice, and an apneustic pattern of breathing in adults of both species and in neonate cats. We conclude that blockade of either NMDA or non-NMDA receptors is innocuous in awake adults. The factors which may potentiate respiratory depression are (1) anesthesia, (2) immaturity, and (3) combined blockade of both receptors types. The mechanism of depression is species-dependent and age-dependent.
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PMID:Respiratory effects of glutamate receptor antagonists in neonate and adult mammals. 965 39

Nitric oxide (NO) is a diffusible chemical messenger functionally linked to N-methyl-D-aspartate (NMDA) receptor activity and has been shown to be involved in modulating numerous pathways in the central nervous system. In order to investigate the role of the neuronal NO synthase type I (nNOS)/NO system in the postnatal development of dorsal horn nociceptive pathways in rats, the specific nNOS inhibitor 7-nitroindazole sodium salt (7-NI) and the non-specific NOS inhibitor nitro-L-arginine methyl ester (L-NAME) were applied spinally at postnatal days (P) 14, 21, 28 and >56 (adult) and their effects on neuronal responses were compared. In response to a train of 16 noxious electrical stimuli, the wide dynamic range neurones in the deep dorsal horn showed a dose-dependent inhibition of C-fibre-evoked response, post-discharge and windup to both 7-NI and L-NAME. No difference between any age group was observed with either agent on these responses. However, the effect of both 7-NI and L-NAME on the primary evoked response, a measure of the events occurring pre-synaptic and intrinsic to the neurone recorded, was significantly different between the P14 and older age groups. nNOS is known to be expressed later in postnatal development than the NMDA receptor and from the results presented here, it is fully mature and functional from P14 onwards. The subtle differences in attenuation of the primary evoked response at P14 compared with older ages may reflect the immaturity of the dorsal horn and in particular the incomplete development of intrinsic and descending inhibitory controls.
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PMID:Neuronal nitric oxide synthase modulation of dorsal horn neuronal responses in the rat: a developmental study. 1461 56