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Perirhinal cortex and temporal lobe epilepsy.

Biagini G, D'Antuono M, Benini R, de Guzman P, Longo D, Avoli M - Front Cell Neurosci (2013)

Bottom Line: The perirhinal cortex-which is interconnected with several limbic structures and is intimately involved in learning and memory-plays major roles in pathological processes such as the kindling phenomenon of epileptogenesis and the spread of limbic seizures.However, we have recently identified in pilocarpine-treated epileptic rats the presence of selective losses of interneuron subtypes along with increased synaptic excitability.Overall, these data indicate that perirhinal cortex networks are hyperexcitable in an animal model of temporal lobe epilepsy, and that this condition is associated with a selective cellular damage that is characterized by an age-dependent sensitivity of interneurons to precipitating injuries, such as status epilepticus.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Experimental Epileptology, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia Modena, Italy.

ABSTRACT
The perirhinal cortex-which is interconnected with several limbic structures and is intimately involved in learning and memory-plays major roles in pathological processes such as the kindling phenomenon of epileptogenesis and the spread of limbic seizures. Both features may be relevant to the pathophysiology of mesial temporal lobe epilepsy that represents the most refractory adult form of epilepsy with up to 30% of patients not achieving adequate seizure control. Compared to other limbic structures such as the hippocampus or the entorhinal cortex, the perirhinal area remains understudied and, in particular, detailed information on its dysfunctional characteristics remains scarce; this lack of information may be due to the fact that the perirhinal cortex is not grossly damaged in mesial temporal lobe epilepsy and in models mimicking this epileptic disorder. However, we have recently identified in pilocarpine-treated epileptic rats the presence of selective losses of interneuron subtypes along with increased synaptic excitability. In this review we: (i) highlight the fundamental electrophysiological properties of perirhinal cortex neurons; (ii) briefly stress the mechanisms underlying epileptiform synchronization in perirhinal cortex networks following epileptogenic pharmacological manipulations; and (iii) focus on the changes in neuronal excitability and cytoarchitecture of the perirhinal cortex occurring in the pilocarpine model of mesial temporal lobe epilepsy. Overall, these data indicate that perirhinal cortex networks are hyperexcitable in an animal model of temporal lobe epilepsy, and that this condition is associated with a selective cellular damage that is characterized by an age-dependent sensitivity of interneurons to precipitating injuries, such as status epilepticus.

No MeSH data available.


Related in: MedlinePlus

Parvalbumin (PV)-immunopositive interneurons in the rat perirhinal cortex. Photomicrographs showing interneurons stained with an antibody against PV in the perirhinal cortex of 3-week-old rats (A–C). Specifically, PV immunostaining is shown in a control, non-epileptic rat (A), and in pilocarpine-treated rats 7 (B) and 14 days (C) after pilocarpine treatment. (D) Normalized (respect to control) quantification of PV immunostained neurons in 3 and 8-week-old rats following pilocarpine treatment. Note in the 3-week-old animals (n = 3–6 for each time interval) that PV immunostained neurons decrease significantly 3 days as well as 7 and 14 days later. Note that similar findings were observed in 8-week-old rats (n = 4–5 for each time interval). **p < 0.01, analysis of variance followed by Tukey's test for multiple comparisons. Scale bar: 100 μm. Animal treatment is described in Biagini et al. (2008). Details of the immunostaining procedure and cell counts are in de Guzman et al. (2006, 2008); Bortel et al. (2010) and Benini et al. (2011).
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Figure 6: Parvalbumin (PV)-immunopositive interneurons in the rat perirhinal cortex. Photomicrographs showing interneurons stained with an antibody against PV in the perirhinal cortex of 3-week-old rats (A–C). Specifically, PV immunostaining is shown in a control, non-epileptic rat (A), and in pilocarpine-treated rats 7 (B) and 14 days (C) after pilocarpine treatment. (D) Normalized (respect to control) quantification of PV immunostained neurons in 3 and 8-week-old rats following pilocarpine treatment. Note in the 3-week-old animals (n = 3–6 for each time interval) that PV immunostained neurons decrease significantly 3 days as well as 7 and 14 days later. Note that similar findings were observed in 8-week-old rats (n = 4–5 for each time interval). **p < 0.01, analysis of variance followed by Tukey's test for multiple comparisons. Scale bar: 100 μm. Animal treatment is described in Biagini et al. (2008). Details of the immunostaining procedure and cell counts are in de Guzman et al. (2006, 2008); Bortel et al. (2010) and Benini et al. (2011).

Mentions: Recently, we have also studied interneuron damage in rats exposed to pilocarpine-induced status epilepticus at 3 weeks of age; these animals are more resistant to damage and have a tendency to develop chronic seizures of lower severity, compared with 8-week-old rats (Biagini et al., 2008). Results obtained from adult rats confirmed our previous findings regarding a decrease in PV-positive cells (Figure 6; cf., Benini et al., 2011). In addition, although rats exposed to pilocarpine-induced status epilepticus at 3 weeks of age were less prone to develop neuronal damage (Biagini et al., 2008), we found approximately a 50% decrease in PV interneurons 3 days after the pilocarpine administration; such reduction was maintained in the following time intervals of 7 and 14 days (Figures 6A–D), suggesting that this interneuron subtype is very sensitive to damage and that this occurs independently of brain maturation.


Perirhinal cortex and temporal lobe epilepsy.

Biagini G, D'Antuono M, Benini R, de Guzman P, Longo D, Avoli M - Front Cell Neurosci (2013)

Parvalbumin (PV)-immunopositive interneurons in the rat perirhinal cortex. Photomicrographs showing interneurons stained with an antibody against PV in the perirhinal cortex of 3-week-old rats (A–C). Specifically, PV immunostaining is shown in a control, non-epileptic rat (A), and in pilocarpine-treated rats 7 (B) and 14 days (C) after pilocarpine treatment. (D) Normalized (respect to control) quantification of PV immunostained neurons in 3 and 8-week-old rats following pilocarpine treatment. Note in the 3-week-old animals (n = 3–6 for each time interval) that PV immunostained neurons decrease significantly 3 days as well as 7 and 14 days later. Note that similar findings were observed in 8-week-old rats (n = 4–5 for each time interval). **p < 0.01, analysis of variance followed by Tukey's test for multiple comparisons. Scale bar: 100 μm. Animal treatment is described in Biagini et al. (2008). Details of the immunostaining procedure and cell counts are in de Guzman et al. (2006, 2008); Bortel et al. (2010) and Benini et al. (2011).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3756799&req=5

Figure 6: Parvalbumin (PV)-immunopositive interneurons in the rat perirhinal cortex. Photomicrographs showing interneurons stained with an antibody against PV in the perirhinal cortex of 3-week-old rats (A–C). Specifically, PV immunostaining is shown in a control, non-epileptic rat (A), and in pilocarpine-treated rats 7 (B) and 14 days (C) after pilocarpine treatment. (D) Normalized (respect to control) quantification of PV immunostained neurons in 3 and 8-week-old rats following pilocarpine treatment. Note in the 3-week-old animals (n = 3–6 for each time interval) that PV immunostained neurons decrease significantly 3 days as well as 7 and 14 days later. Note that similar findings were observed in 8-week-old rats (n = 4–5 for each time interval). **p < 0.01, analysis of variance followed by Tukey's test for multiple comparisons. Scale bar: 100 μm. Animal treatment is described in Biagini et al. (2008). Details of the immunostaining procedure and cell counts are in de Guzman et al. (2006, 2008); Bortel et al. (2010) and Benini et al. (2011).
Mentions: Recently, we have also studied interneuron damage in rats exposed to pilocarpine-induced status epilepticus at 3 weeks of age; these animals are more resistant to damage and have a tendency to develop chronic seizures of lower severity, compared with 8-week-old rats (Biagini et al., 2008). Results obtained from adult rats confirmed our previous findings regarding a decrease in PV-positive cells (Figure 6; cf., Benini et al., 2011). In addition, although rats exposed to pilocarpine-induced status epilepticus at 3 weeks of age were less prone to develop neuronal damage (Biagini et al., 2008), we found approximately a 50% decrease in PV interneurons 3 days after the pilocarpine administration; such reduction was maintained in the following time intervals of 7 and 14 days (Figures 6A–D), suggesting that this interneuron subtype is very sensitive to damage and that this occurs independently of brain maturation.

Bottom Line: The perirhinal cortex-which is interconnected with several limbic structures and is intimately involved in learning and memory-plays major roles in pathological processes such as the kindling phenomenon of epileptogenesis and the spread of limbic seizures.However, we have recently identified in pilocarpine-treated epileptic rats the presence of selective losses of interneuron subtypes along with increased synaptic excitability.Overall, these data indicate that perirhinal cortex networks are hyperexcitable in an animal model of temporal lobe epilepsy, and that this condition is associated with a selective cellular damage that is characterized by an age-dependent sensitivity of interneurons to precipitating injuries, such as status epilepticus.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Experimental Epileptology, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia Modena, Italy.

ABSTRACT
The perirhinal cortex-which is interconnected with several limbic structures and is intimately involved in learning and memory-plays major roles in pathological processes such as the kindling phenomenon of epileptogenesis and the spread of limbic seizures. Both features may be relevant to the pathophysiology of mesial temporal lobe epilepsy that represents the most refractory adult form of epilepsy with up to 30% of patients not achieving adequate seizure control. Compared to other limbic structures such as the hippocampus or the entorhinal cortex, the perirhinal area remains understudied and, in particular, detailed information on its dysfunctional characteristics remains scarce; this lack of information may be due to the fact that the perirhinal cortex is not grossly damaged in mesial temporal lobe epilepsy and in models mimicking this epileptic disorder. However, we have recently identified in pilocarpine-treated epileptic rats the presence of selective losses of interneuron subtypes along with increased synaptic excitability. In this review we: (i) highlight the fundamental electrophysiological properties of perirhinal cortex neurons; (ii) briefly stress the mechanisms underlying epileptiform synchronization in perirhinal cortex networks following epileptogenic pharmacological manipulations; and (iii) focus on the changes in neuronal excitability and cytoarchitecture of the perirhinal cortex occurring in the pilocarpine model of mesial temporal lobe epilepsy. Overall, these data indicate that perirhinal cortex networks are hyperexcitable in an animal model of temporal lobe epilepsy, and that this condition is associated with a selective cellular damage that is characterized by an age-dependent sensitivity of interneurons to precipitating injuries, such as status epilepticus.

No MeSH data available.


Related in: MedlinePlus