Neo-Timm staining in the thalamus of chronically epileptic rats

Abstract

The thalamus is an important modulator of seizures and is severely affected in cholinergic models of epilepsy. In the present study, chronically epileptic rats had their brains processed for neo-Timm and acetylcholinesterase two months after the induction of status epilepticus with pilocarpine. Both controls and pilocarpine-treated animals presented neo-Timm staining in the anterodorsal nucleus, laterodorsal nucleus, reticular nucleus, most intralaminar nuclei, nucleus reuniens, and rhomboid nucleus of the thalamus, as well as in the zona incerta. The intensity of neo-Timm staining was similar in control and pilocarpine-treated rats, except for the nucleus reuniens and the rhomboid nucleus, which had a lower intensity of staining in the epileptic group. In animal models of temporal lobe epilepsy, zinc seems to modulate glutamate release and to decrease seizure activity. In this context, a reduction of neo-Timm-stained terminals in the midline thalamus could ultimately result in an increased excitatory activity, not only within its related nuclei, but also in anatomical structures that receive their efferent connections. This might contribute to the pathological substrate observed in chronic pilocarpine-treated epileptic animals. Correspondence

Long-term monotherapy treatment with vitamin E reduces oxidative stress, but not seizure frequency in rats submitted to the pilocarpine model of epilepsy

“…This is a modification of the traditional Timm's method [16,17], which intensifies the specific staining of zinc, producing a better visualization of the mossy fibers. The rats of each subgroup were deeply anesthetized with sodium pentobarbital and perfused transcardially with 25 ml of Millonig's buffer (MB), followed by 50 ml of 0.1% solution of sodium sulfide (Na 2 S solution) dissolved in MB (pH 7.4), and then perfused with fixative solution (100 ml of 3% solution of glutaraldehyde in 0.1 M phosphate buffer and 200 ml of 0.1% solution of sodium sulfide diluted in MB; pH 7.4).…”

Chemogenetic silencing of the midline and intralaminar thalamus blocks amygdala-kindled seizures

“…In patients with, and animal models of TLE, midline and intralaminar nuclei of the thalamus display volumetric alterations, as well as changes in glucose uptake and synaptic function (Bertram et al, 1998; Cassidy and Gale, 1998; Hamani et al, 2005; Handforth and Treiman, 1995a, 1995b; Rajasekaran et al, 2009; Sierra et al, 2011; Szabó et al, 2006). The midline/intralaminar thalamus is a diverse collection of nuclei located between the third ventricle and lateral thalamic nuclei.…”

Different patterns of neuronal activation and neurodegeneration in the thalamus and cortex of epilepsy‐resistant Proechimys rats versus Wistar rats after pilocarpine‐induced protracted seizures

“…SE‐induced neurodegenerative phenomena have also been reported in several brain structures outside the hippocampus. In particular, in the pilocarpine model of epilepsy, neurodegeneration has been repeatedly described in the medial thalamus and other thalamic regions (Turski et al., 1983, 1986; Fujikawa, 1996; Dubé et al., 1998; Bertram & Scott, 2000; Covolan & Mello, 2000; Hamani et al., 2005; Niessen et al., 2005), as well as in the cerebral cortex (Sanabria et al., 2002; Silva et al., 2002). On this basis, we used Fluoro‐Jade B (FJB) histochemistry (Schmued & Hopkins, 2000) to investigate the occurrence of degenerating neurons in the thalamus and cortex in the postacute phase of pilocarpine‐induced seizures.…”