Electrophysiological and pharmacological properties of nucleus basalis magnocellularis neurons in rats
Abstract
AIM:
To investigate the primary electrophysiological and pharmacological properties of the nucleus basalis magnocellularis (nbM) neurons.
METHODS:
Single unit extracellular recordings from the nbM neurons were obtained with glass micropipettes in urethane-anesthetized rats.
RESULTS:
Most nbM neurons responded to noxious but not innocuous mechanical, thermal, chemical, and electrical stimuli. The receptive fields were usually very large and bilateral. Electrical stimulation applied to the frontal cortex (FCX) either activated orthodromically or antidromically the nbM neurons. The FCX stimulation-induced excitatory response in the nbM neurons could be partly blocked by intracerebroventricular (icv) injection of atropine 2.5 mmol/L or tubocurarine 0.1 mmol/L. Icv injection of ach (1, 10, and 100 mmol/L) dose-dependently increased the spontaneous firing rate in most of the nbM neurons. Atropine (2.5, 25, and 250 mmol/L) or tubocurarine (0.1, 1, and 10 mmol/L) not only antagonized the ACh-induced excitation, but also inhibited the spontaneous firing of the nbM neurons.
CONCLUSION:
The nbM might be involved in nociception, although it was considered to play a critical role in cognitive function. Also, the nbM appears to be rich in cholinergic autoreceptors.
Keywords:
To investigate the primary electrophysiological and pharmacological properties of the nucleus basalis magnocellularis (nbM) neurons.
METHODS:
Single unit extracellular recordings from the nbM neurons were obtained with glass micropipettes in urethane-anesthetized rats.
RESULTS:
Most nbM neurons responded to noxious but not innocuous mechanical, thermal, chemical, and electrical stimuli. The receptive fields were usually very large and bilateral. Electrical stimulation applied to the frontal cortex (FCX) either activated orthodromically or antidromically the nbM neurons. The FCX stimulation-induced excitatory response in the nbM neurons could be partly blocked by intracerebroventricular (icv) injection of atropine 2.5 mmol/L or tubocurarine 0.1 mmol/L. Icv injection of ach (1, 10, and 100 mmol/L) dose-dependently increased the spontaneous firing rate in most of the nbM neurons. Atropine (2.5, 25, and 250 mmol/L) or tubocurarine (0.1, 1, and 10 mmol/L) not only antagonized the ACh-induced excitation, but also inhibited the spontaneous firing of the nbM neurons.
CONCLUSION:
The nbM might be involved in nociception, although it was considered to play a critical role in cognitive function. Also, the nbM appears to be rich in cholinergic autoreceptors.