Synaptic GABAA activation induces Ca2+ rise in pyramidal cells and interneurons from rat neonatal hippocampal slices.

Abstract

1. Changes in intracellular Ca2+ concentration ([Ca2+]1) induced by activation of GABAA receptors (synaptic stimulation or application of the GABAA agonist isoguvacine) were studied on pyramidal cells and interneurons from hippocampal slices of rats from two age groups (postnatal days (P) 2-5 and P12-13) using the fluorescent dye fluo-3 and a confocal laser scanning microscope. Cells were loaded with the dye either intracellularly, using patch pipettes containing fluo-3 in the internal solution, or extracellularly, using pressure pulses applied to an extracellular pipette containing the permeant dye fluo-3 AM. 2. Interneurons and pyramidal cells from P2-5 slices loaded with fluo-3 AM responded by an increase in [Ca2+]i to isoguvacine and to glutamate, in contrast to cells from P12-13 slices which responded to glutamate but not to isoguvacine. In the mammalian adult central nervous system, GABA postsynaptically localized GABAB receptors activate (y-aminobutyric acid) is the main inhibitory neuro-potassium conductances or decrease calcium currents transmitter, acting on two main classes of

Response to neonatal anesthesia: Effect of sex on anatomical and behavioral outcome

“…While surgical procedures cannot be avoided, care needs to be taken with the choice of anesthesia. As stated previously, activation of the GABA A receptor in the immature mammalian hippocampus results in membrane depolarization and cellular excitation (Leinekugel et al, 1995;Nuñez et al, 2005). This is the opposite of what occurs in the adult.…”

“…In the neonatal mammalian hippocampus, activation of the GABA A receptor leads to chloride efflux and membrane depolarization sufficient to open voltage sensitive calcium channels (Leinekugel et al, 1995;LoTurco et al, 1995;Obrietan and van den Pol, 1995). This cellular excitation is in stark contrast to chloride influx and membrane hyperpolarization (cellular inhibition) that occurs following GABA A receptor activation in the hippocampus in adulthood (Duggan, 1978).…”

“…Many commonly used anesthetics act on the GABA A receptor, the predominant inhibitory neurotransmitter system in the adult CNS . However, GABA A receptor activation in the developing brain, including the hippocampus, cerebral cortex and hypothalamus, leads to chloride efflux and membrane depolarization sufficient to open voltage sensitive calcium channels (Leinekugel et al, 1995;LoTurco et al, 1995;Obrietan and van den Pol, 1995). GABA mediated excitation persists through the first postnatal week in the rodent hippocampus (Nuñez et al, 2005;Nuñez and McCarthy, 2007).…”

Biphasic Effect of GABA on Rat Sperm Acrosome Reaction: Involvement of GABA A and GABA B Receptors

“…Hence, within the CNS, GABA regulates neuronal activity by interacting with both GABA A receptors and the G protein-coupled GABA B receptors. In the mature nervous system, both receptor subtypes tend to reduce neural excitability; whereas in most neurons during development, activation of the GABA A receptors tends to increase neural excitability by raising cytosolic Ca 2 ‡ levels [6,19]; GABA B receptors play an inhibitory role in modulating the rise in Ca 2 ‡ elicited by the activation of GABA A receptors [24]. There may exist other mechanisms by which the biphasic e ect of GABA in triggering mammalian sperm AR is operational.…”

GABA and neuroligin signaling: linking synaptic activity and adhesion in inhibitory synapse development

“…The trophic effects of GABA on neuronal migration and neurite growth during the embryonic and perinatal period are largely explained by its depolarizing action in immature neurons, which triggers calcium influx and signaling [23,24,25]. In fact, GABA signaling in the neonatal brain represents an early form of neural communication, which precedes and promotes the formation of glutamatergic synapses [26][27][28].…”