Disparity for disinhibitory and excitatory effects during cortical reorganization.
Inhibitory and excitatory transmission have been shown to be two dominant forces in the process of injury-induced cortical reorganization. However, the contributions of each individual neurotransmitter system have been difficult to characterize, mainly because they often affect overlapping domains of the reorganizing cell's receptive field (RF). The present work differentiates the effects of either neurotransmitter system by studying reorganizing neurons where pharmacological intervention directed at glutamatergic or GABAergic networks affected spatially non-overlapping subfields within a cell's RF. Microiontophoresis was used to apply glutamate and bicuculline, a selective GABA-A receptor antagonist, to cells in the deafferented cortex at various post-amputation times, that ranged from 2 to 37 weeks. It was found that at all post-amputation times studied, glutamate increased the neural activity that could be evoked from mechanical stimulation over the wound area, in addition to decreasing the threshold for activation. Disinhibition with bicuculline application often lowered the response threshold for subfields within the reorganized RF, usually located on the digits, and could also expand RF area. Interestingly, the effects of GABAergic transmission to the process of reorganization appeared later than those mediated through glutamatergic networks. These findings suggest that recruitment of inhibition in reorganizing cells relies on activity-dependent mechanisms, with reinstatement of GABAergic transmission being secondary to the formation of novel glutamatergic drives.
Tremere
Liisa A
LA
CROET, OHSU, Portland, Oregon 97201, USA. liisa.tremere@gmail.com
Pinaud
Raphael
R
D000671:Amputation, Surgical / Q000379:methods; D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000166:cytology*; D018756:GABA Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000494:pharmacology; D007478:Iontophoresis / Q000379:methods; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009434:Neural Pathways / Q000187:drug effects; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D011821:Raccoons; D013997:Time Factors
D018756:GABA Antagonists; D018698:Glutamic Acid; D001640:Bicuculline