TY - JOUR
T1 - Lesions of the basal forebrain alter stimulus‐evoked metabolic activity in mouse somatosensory cortex
AU - Ma, Wu
AU - Höhmann, Christine F.
AU - Coyle, Joseph T.
AU - Juliano, Sharon L.
PY - 1989/10/15
Y1 - 1989/10/15
N2 - The role that acetylcholine plays in processing sensory stimuli is beginning to be characterized; however, morphological correlates of cholinergic effects on activity patterns in sensory cortex are not available. To study this problem, unilateral neurotoxic lesions that depleted the neocortex of acetylcholine were made in the basal forebrains of mice. The aim of these experiments was to study the effect of cholinergic depletion on stimulus‐evoked activity in the barrel field of the mouse somatosensory cortex. One month following the lesion, 2‐deoxyglucose (2DG) experiments were conducted on the lesioned and on normal mice while the animal received bilateral stimulation to the C3 whisker. The tissue was processed for acetylcholinesterase and cytochrome oxidase histochemistry and 2DG autoradiography. Evaluation of the column‐like 2DG label evoked in the somatosensory cortex revealed that the activity on the lesioned side was significantly reduced in dimension and intensity from that in the normal hemisphere. On the normal side, the activated barrels averaged 641 μm in tangential width, were 76.5% above background in density, and extended from lamina I‐V. On the lesioned side, the activated barrels were 485 μm in tangential width, 65.4% above background in density, and extended from lamina II–V. In other cortical regions, outside the stimulus‐evoked barrel field, 2DG activity values were similar on the normal and lesioned side. Additionally, both the pattern and intensity of the cytochrome oxidase staining within the barrel field displayed no differences in either hemisphere. These studies suggest that acetylcholine plays a significant role in the processing of somatosensory information. Neurotoxic lesions that diminish cortical cholinergic innervation cause a reduction of stimulus‐evoked activity levels, while underlying metabolic activity is either not affected or recovers over time.
AB - The role that acetylcholine plays in processing sensory stimuli is beginning to be characterized; however, morphological correlates of cholinergic effects on activity patterns in sensory cortex are not available. To study this problem, unilateral neurotoxic lesions that depleted the neocortex of acetylcholine were made in the basal forebrains of mice. The aim of these experiments was to study the effect of cholinergic depletion on stimulus‐evoked activity in the barrel field of the mouse somatosensory cortex. One month following the lesion, 2‐deoxyglucose (2DG) experiments were conducted on the lesioned and on normal mice while the animal received bilateral stimulation to the C3 whisker. The tissue was processed for acetylcholinesterase and cytochrome oxidase histochemistry and 2DG autoradiography. Evaluation of the column‐like 2DG label evoked in the somatosensory cortex revealed that the activity on the lesioned side was significantly reduced in dimension and intensity from that in the normal hemisphere. On the normal side, the activated barrels averaged 641 μm in tangential width, were 76.5% above background in density, and extended from lamina I‐V. On the lesioned side, the activated barrels were 485 μm in tangential width, 65.4% above background in density, and extended from lamina II–V. In other cortical regions, outside the stimulus‐evoked barrel field, 2DG activity values were similar on the normal and lesioned side. Additionally, both the pattern and intensity of the cytochrome oxidase staining within the barrel field displayed no differences in either hemisphere. These studies suggest that acetylcholine plays a significant role in the processing of somatosensory information. Neurotoxic lesions that diminish cortical cholinergic innervation cause a reduction of stimulus‐evoked activity levels, while underlying metabolic activity is either not affected or recovers over time.
KW - 2‐deoxyglucose
KW - acetylcholine
KW - barrel field
KW - cytochrome oxidase
KW - neuronal plasticity
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U2 - 10.1002/cne.902880305
DO - 10.1002/cne.902880305
M3 - Article
C2 - 2551936
AN - SCOPUS:0024431516
SN - 0021-9967
VL - 288
SP - 414
EP - 427
JO - Journal of Comparative Neurology
JF - Journal of Comparative Neurology
IS - 3
ER -