The effect of thiamine deficiency on the structure and physiology of the rat forebrain

Abstract

Dietary thiamine deficiency, enhanced by pyrithiamine administration in adult rats, produces overt lesions in the brain that are especially prominent in the thalamus. The present study was undertaken to determine whether the thalamic lesions could be correlated with alterations in the physiological properties of neurons in the thalamus and somatosensory cortex. The regimen for experimentally inducing thiamine deficiency produced large lesions in the thalamus of every case; the lesions included most, if not all, of the neurons in the intralaminar thalamic nuclei. The extent of the lesion in the intralaminar thalamus was highly correlated with the loss of bilaterally synchronous spontaneous activity in the cerebral cortex. This correlation was seen in animals analyzed as early as 1-18 hr after the appearance of opisthotonus, the crisis state of thiamine deficiency, and as late as 2-9 weeks of recovery following thiamine replacement therapy. The loss of bilateral synchronous bursting neuronal activity following intralaminar thalamic lesions is consistent with the proposed role of the intralaminar thalamus as a pacemaker for rhythmic cortical activity (Armstrong-James et al., Exp. Brain Res., 1985; Fox and Armstrong-James, Exp. Brain Res. 63: 505-518, 1986). The location and size of the central lesions within the thalamus suggest that the observed neuronal loss could result from a nonhemorrhagic infarction in the ventromedial branches of the superior cerebellar arteries. Experimental thiamine deficiency also produced alterations in the receptive field properties of the somatosensory cortex neurons in all animals examined. Changes in cortical receptive field properties were correlated with the destruction of sensory relay neurons in the thalamic ventrobasal complex. The loss of the central lateral thalamic input to the cortex and the loss of somatosensory relay neurons in the ventrobasal thalamus in experimental thiamine deficiency produce alterations in cortical function which may contribute to deficits in memory and cognition analogous to those which characterize Korsakoff's psychosis in humans.