Cholinergic and noradrenergic afferents influence the functional properties of the postnatal visual cortex in rats.
Based on previous evidence that acetylcholine (ACh) and noradrenaline (NA) play a permissive role in developmental plasticity in the kitten visual cortex, we reinvestigated this topic in the postnatal visual cortex of rats with normal vision. In rats, the functional properties of visual cortical cells develop gradually between the second and the sixth postnatal week (Fagiolini et al., 1994). Cortical cholinergic depletion, by basal forebrain (BF) lesions at postnatal day (PD) 15 (eye opening), leads to a transient disturbance in the distribution of ocular dominance (Siciliano et al., 1997). In the present study, we investigated the development of visual cortical response properties following cytotoxic lesions of the locus coeruleus (LC) alone or in combination with lesions of cholinergic BF. The main result is that early NA depletion impairs the orientation selectivity of cortical neurons, causes a slight increase of their receptive-field size, and reduces the signal-to-noise ratio of cell responses. Similar effects are obtained following NA depletion in adult animals, although the effects of adult noradrenergic deafferentation are significantly more severe than those obtained after early NA depletion. Additional cholinergic depletion causes an additional transient change in ocular-dominance distribution similarly to that obtained after cholinergic deafferentation alone. Comparisons between depletion of NA on the one hand and depletion of both NA and ACh on the other suggest that the effects of combined deafferentation on the functional properties studied result from simple linear addition of the effects of depleting each afferent system alone.
Siciliano
R
R
Department of Physiology and Biochemistry G. Moruzzi, University of Pisa, Italy.
Fornai
F
F
Bonaccorsi
I
I
Domenici
L
L
Bagnoli
P
P
D000109:Acetylcholine / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D004292:Dominance, Cerebral / Q000502:physiology; D004594:Electrophysiology; D007124:Immunoenzyme Techniques; D008125:Locus Coeruleus / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D009475:Neurons, Afferent / Q000502:physiology*; D009638:Norepinephrine / Q000502:physiology*; D016627:Oxidopamine / Q000633:toxicity; D016548:Prosencephalon / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D016318:Quisqualic Acid / Q000633:toxicity; D051381:Rats; D020318:Rats, Long-Evans; D012701:Serotonin / Q000378:metabolism; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism; D014793:Visual Cortex / Q000254:growth & development / Q000502:physiology*
D012701:Serotonin; D016627:Oxidopamine; D016318:Quisqualic Acid; D014446:Tyrosine 3-Monooxygenase; D002795:Choline O-Acetyltransferase; D000109:Acetylcholine; D009638:Norepinephrine