Maturation of excitatory synaptic transmission of the rat nucleus accumbens from juvenile to adult.
Precise control of synaptic strength is critical for maintaining accurate network activity and normal brain functions. Several major brain diseases are related to synaptic alterations in the adult brain. Detailed descriptions of the normal physiological properties of adult synapses are scarce, mainly because of the difficulties in performing whole cell patch-clamp recording in brain slices from adult animals. Here we present the portrait of excitatory synapses and intrinsic properties of medium spiny neurons (MSNs) of the nucleus accumbens (NAc), a central structure of the mesocorticolimbic system, from youth (P14) to adulthood (P120). We found that intrinsic neuronal excitability decreased over development, mainly due to an enhancement of potassium conductance and the consequent reduction in membrane resistance. The ratio between paired-pulse synaptic responses was similar in juvenile, adolescent, and adult MSNs, suggesting that the probability of neurotransmitter release was unaltered. alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)-mediated excitatory postsynaptic currents (EPSCs) decayed more slowly in adult MSN. In contrast, the kinetic properties and the subunit composition of N-methyl-d-aspartate receptor (NMDAR)-mediated EPSC in the NAc were conserved from youth to adulthood. Changes in synaptic strength were estimated from the ratio of AMPAR to NMDAR evoked and spontaneous EPSCs (AMPAR/NMDAR ratio). Although both AMPAR and NMDAR EPSCs decreased over development, there was an increase of the AMPAR/NMDAR ratio that was linked to changes in NMDAR EPSC. Furthermore, distribution of the AMPAR/NMDAR ratio was more heterogeneous in MSNs from adults, suggesting that synaptic strength is continuously refined during life.
Kasanetz
Fernando
F
Institut National de la Santé et de la Recherche Médicale U862, Neurocentre Magendie, Pathophysiology of Synaptic Transmission and Plasticity Laboratory, Bordeaux, F-33000, France.
Manzoni
Olivier J
OJ
D000367:Age Factors; D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D001703:Biophysics; D002122:Calcium Chloride / Q000494:pharmacology; D004558:Electric Stimulation / Q000379:methods; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D009714:Nucleus Accumbens / Q000166:cytology* / Q000254:growth & development*; D018408:Patch-Clamp Techniques / Q000379:methods; D010880:Piperidines / Q000494:pharmacology; D011810:Quinoxalines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018091:Receptors, AMPA / Q000037:antagonists & inhibitors / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology*
D018691:Excitatory Amino Acid Antagonists; D010880:Piperidines; D011810:Quinoxalines; D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate; C056723:FG 9041; D002122:Calcium Chloride; C010739:ifenprodil