Experimental neurology
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Experimental neurology · Jul 1998
Chronic effects of traumatic brain injury on hippocampal vesicular acetylcholine transporter and M2 muscarinic receptor protein in rats.
Experimental traumatic brain injury (TBI) produces cholinergic neurotransmission deficits that may contribute to chronic spatial memory deficits. Cholinergic neurotransmission deficits may be due to presynaptic alterations in the storage and release of acetylcholine (ACh) or from changes in the receptors for ACh. The vesicular ACh transporter (VAChT) mediates accumulation of ACh into secretory vesicles, and M2 receptors can modulate cholinergic neurotransmission via a presynaptic inhibitory feedback mechanism. ⋯ At 2 and 4 weeks postinjury, an increase in hippocampal VAChT protein and a corresponding loss of hippocampal M2 protein was observed compared to sham controls. Consistent with these results, Western blot analyses at 4 weeks postinjury demonstrated a 40-50% increase in VAChT and a 25-30% decrease in M2. These changes may represent a compensatory response of cholinergic neurons to increase the efficiency of ACh neurotransmission chronically after TBI, by upregulating the storage capacity and subsequent release of ACh and downregulating presynaptic inhibitory receptors.
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Experimental neurology · Jul 1998
Motoneuron survival after neonatal peroneal nerve injury in the rat-evidence for the sparing effect of reciprocal inhibition.
Sciatic nerve crush at birth results in the death of most of the motoneurons in the sciatic motor pool. It has been proposed that these cells die through excessive activation which can be explained partly by an increased susceptibility to NMDA. However, it is also possible that decreased inhibitory mechanisms resulting from nerve injury may contribute to overactivation of the motoneurons. ⋯ A control experiment excluded the possible involvement of increased stretch of the muscles as a result of common peroneal nerve crush alone as an explanation for the improvement. We therefore suggest that the increased survival of motoneurons after peroneal nerve crush was due to the preservation of their reciprocal inhibitory input. However, since even with this improvement the majority of motoneurons still died, loss of reciprocal inhibition probably does not play a major role in the death of motoneurons induced by overactivation.