Blockade of cholinergic receptors in rat barrel cortex prevents long-term changes in the evoked potential during sensory preconditioning

Maalouf, M.; Miasnikov, A.A.; Dykes, R.W.

Авторы: Maalouf M., Miasnikov A.A., Dykes R.W.
Журнал: Journal of Neurophysiology
Том: 80
Номер: 2
Год издания: 1998
Издательство: American Physiological Society
Местоположение издательства: United States
Первая страница: 529
Последняя страница: 545
Аннотация: We offer evidence that acetyl- tensive cell loss. choline (ACh) is involved in the emergence of functional neuronal The NBM is the major source of cortical acetylcholine plasticity induced by whisker pairing. Evoked potentials were re- corded within the barrel cortex of awake, adult rats before, during, (ACh) (Johnston et al. 1981; Mesulam 1989) . Several lines and after one of five paradigms. In the pairing procedure, each of of evidence support an important role for ACh in learning 50 deflections of a whisker (S1) was followed 150 ms later by the and, more generally, in neuronal plasticity: the levels of ACh deflection of a second whisker (S2). The explicitly unpaired con- increase in various regions of the cerebral cortex (CCx) trol procedure differed by the lack of contiguity and contingency during learning (Butt et al. 1997) ; ACh can modulate neubetween the stimulation of S1 and S2. In the three remaining ronal excitability and enhance the responsiveness of cortical groups, pairing was performed 30 min after an intraperitoneal injec- neurons to afferent stimuli for periods of time that outlast tion of either 0.5 ml of saline (150 mM NaCl), 100 mg/kg of its presence (Kotlyar and Ovcharenko 1978; Metherate et atropine methyl nitrate (0.5 ml of AMN in saline), or 100 mg/kg al. 1987, 1988a,b) ; changes in the firing of suspected NBM of atropine sulfate (0.5 ml of ATS in saline). Changes in respon- cholinergic neurons has been reported during learning (Pirch siveness to S1 were compared with, and adjusted by, changes in responsiveness to stimulation of S2. Changes in potentials evoked et al. 1991; Richardson and DeLong 1991; Wilson and Rolls by S1 were interpreted as a change in neuronal excitability oc- 1990a,b) ; cholinergic antagonists or lesions of the NBM curring when the first innocuous stimulus systematically predicted prevent or, at least, delay the acquisition of various learned the appearance of the second innocuous stimulus. When whisker tasks (Butt and Hodge 1995; Jacobs and Juliano 1995) ; pairing was performed alone or in the presence of either saline or these deficits are reduced by the administration of choliner- AMN (a blocker of muscarinic cholinoreceptors that does not cross gic agonists or acetylcholinesterase (AChE) inhibitors the blood-brain barrier, BBB), responses to S1 increased, whereas, (Muff et al. 1993; Myers et al. 1996) ; and the severity of in the presence of ATS (blocker of muscarinic cholinoreceptors memory impairment in AD has been correlated with the that does cross the BBB) or following the explicitly unpaired con- extent of NBM degeneration (Albert 1996; Levey 1996; trol, they decreased. The effects of saline, AMN, and ATS on the Poirier et al. 1995) . evoked potential without vibrissae pairing were opposite to those More recently, however, the significance of cholinergic observed when these substances were injected and pairing oc- curred. Analysis of the behavioral state of the animal showed that systems for learning and memory and the effects of their the changes observed in the evoked potential could not be attributed disruption in AD has been questioned. Although there is now to changes in behavioral state. The changes in responsiveness to general agreement that ACh is not necessary for retention, its S1 induced by whisker pairing were independent of neuronal excit- role in acquisition of memories is the subject of considerable ability, did not occur in the absence of contingency and contiguity controversy in view of several findings: the decreased learnbetween S1 and S2, were blocked by the muscarinic receptor antag- ing performance induced by NBM lesions or cholinergic onist ATS, but not by blockade of muscarinic modulation of normal antagonists could be explained by the lack of specificity of synaptic transmission. Thus activation of muscarinic cholinorecep- such procedures and the possible side effects on processes tors within the CNS were a necessary condition for this form of more directly related to attention rather than to memory neuronal plasticity.
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Blockade of cholinergic receptors in rat barrel cortex prevents long-term changes in the evoked potential during sensory preconditioningстатья

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