Functional Changes in Thalamic Relay Neurons after Focal Cerebral Infarct: A Study of Unit Recordings from VPL Neurons after MCA Occlusion in Rats

Abstract

Summary:We evaluated neuronal and histological changes of thalamic neurons 1, 4, 7, and 14 days after middle cerebral artery (MCA) occlusion in rats. After the somatosensory evoked potentials (SEPs) were measured from the cerebral cortex, the thalamic relay neuronal ac tivities were recorded with a glass microelectrode follow ing repetitive electrical stimulation of the contralateral forepaw at frequencies ranging from 1 to 50 Hz. In -95% of the occluded rats, the ipsilateral somatosensory cortex and/or the subcortical somatosensory pathway developed infarct, resulting in SEP loss. We evaluated unit data from rats with abolished SEPs. The average firing rate of the nucleus ventralis posterolateralis (VPL) neurons in response to 25 stimulations at 30 Hz was significantly reduced to 0.1 spike/stimulus 1 day after MCA occlusion.After the occurrence of a localized brain lesion, neuronal structures remote from the primary lesion develop functional and/or histological changes through the neuronal pathway. The thalamocortical and the corticothalamic pathway closely connects the cerebral cortex and the ipsilateral thalamus. Cortical infarct results in progressive degeneration in the ipsilateral thalamus in humans and rats

Disruption of the Serotonergic System after Neonatal Hypoxia-Ischemia in a Rodent Model

“…The thalamus, substantia nigra, hippocampus, and amygdala have substantial neural connections with primary injury sites (e.g., the cerebral cortex) and can undergo prolonged periods of apoptosis and degeneration in the neonatal brain after HI [25–27, 146]. It has been shown that after ischemic conditions, disrupted somatosensory transmission in the thalamus is associated with increased numbers of thalamic neurons degenerating in the secondary phase [26, 147, 148]. Progressive loss of serotonergic neural connections with damaged areas could lead to the disruption and loss of raphé serotonergic neurons in the brainstem.…”

Early detection of secondary damage in ipsilateral thalamus after acute infarction at unilateral corona radiata by diffusion tensor imaging and magnetic resonance spectroscopy

“…Secondary damage in the ipsilateral thalamus separate from the primary infarcted area has been demonstrated by a number of studies [1-9]. In rats with distal middle cerebral artery occlusion (MCAO), secondary neuronal degeneration and gliosis in non-ischemic ipsilateral thalamus were observed at 1 week after ischemic injury of the thalamocortical pathway [5].…”

Differential Effects of NMDA and AMPA Glutamate Receptors on Functional Magnetic Resonance Imaging Signals and Evoked Neuronal Activity during Forepaw Stimulation of the Rat

“…The first positive component P1 (mean latencies of 14 ms) is supposed to reflect mainly the activity of the thalamocortical pathway (Tokuno et al, 1992), whereas the other components N1 (24 ms) and P2 (50 ms) are probably generated later in the cortex (Peterson et al, 1995). NMDA-Rs are involved in both fast (10 ms) and slow (until 100 ms) transmissions to layers I-IV so that their contribution should be observed in all three components, including P1.…”