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PubMed1996

Calbindin-D28k mRNA expression in magnocellular hypothalamic neurons of female rats during parturition, lactation and following dehydration.

Recent studies indicate that calcium binding proteins may play a role in determining the electrical firing patterns of the hypothalamic magnocellular oxytocin (OT) and vasopressin (VP) neurons. In this study we have examined the calbindin-D28k mRNA content of magnocellular neurons in the supraoptic (SON) and paraventricular (PVN) nuclei and determined whether changes in expression correlate with the specific patterns of electrical activity displayed by these cells under different physiological circumstances. In situ hybridization with [35S]-labelled oligonucleotides revealed a heterogeneous pattern of calbindin-D28k mRNA expression in the SON and magnocellular PVN. Quantitative analysis demonstrated that the number of silver grains/cell in the dorsal half of the SON was approximately 30% higher (P < 0.05) than that of the ventral half of the nucleus. Within the PVN, calbindin-D28k mRNA-expressing neurons were detected in the medial magnocellular division of the PVN but not in magnocellular cells forming the core of the lateral magnocellular division. Dehydration for 24 h did not alter calbindin-D28k mRNA expression in the SON, PVN or cingulate cortex. In parturient and lactating rats, calbindin-D28k mRNA levels were significantly (P < 0.05) reduced in the medial magnocellular division of the PVN compared with virgin animals. No significant differences in calbindin-D28k mRNA expression were observed in either ventral or dorsal halves of the SON, or in the cingulate cortex of these animals. These results provide evidence for the differential expression of calbindin-D28k mRNA by hypothalamic magnocellular neurons and suggest that OT cells may express more calbindin-D28k mRNA than VP neurons. The reduction in calbindin-D28k mRNA expression by putative OT neurons of the PVN at the time of parturition and lactation supports the hypothesis of Li and colleagues (J. Physiol., 488 (1995) 601-608) that calbindin may play a part in determining the electrical firing patterns of magnocellular neurons. However, the absence of any similar decrease in the SON suggests that changes in calbindin-D28k mRNA expression are not essential for OT neurons to exhibit episodic bursting behavior.

Animals↗
PubMed2000

Concentration- and cell type-specific effects of calbindin D28k on vulnerability of hippocampal neurons to seizure-induced injury.

The calcium-binding protein calbindin D28k (CB) is expressed in limited subpopulations of neurons in the brain. In the hippocampus, CB is expressed in all dentate granule cells and a subpopulation of CA1 pyramidal neurons, but is absent from CA3 neurons. This pattern of CB expression is inversely correlated with neuronal vulnerability to seizure-induced damage suggesting the possibility that expression of CB confers resistance to excitotoxicity. While data from cell culture studies support an excitoprotective role for calbindin, it is not known whether CB is a key determinant of neuronal vulnerability in vivo. We therefore examined the pattern of damage to hippocampal neurons following intrahippocampal injection of the seizure-inducing excitotoxin kainate in CB homozygous (CB-/-) and CB heterozygous (CB+/-) knockout mice in comparison with wild-type mice (CB+/+). Whereas the extent of damage to CA1 neurons was similar in CB-/- and CB+/+ mice, damage to CA1 neurons was significantly reduced in CB+/- mice. Dentate granule neurons were not damaged following kainate-induced seizures in CB+/+, CB+/- or CB-/- mice. These findings suggest that CB can modify vulnerability of hippocampal CA1 neurons to seizure-induced injury, and that either CB is not a critical determinant of resistance of dentate granule neurons, or compensatory changes occur and lack of CB is not the only difference between CB-/- and CB+/+ mice.

Animals↗
PubMedDate not supplied

Calretinin and calbindin-D28K in male rats during postnatal development.

Calcium-binding proteins play potentially important roles in neurogenesis and neuroprotective mechanism(s). Some evidence exists that brain calbindin-D28K (CALB) is regulated by androgens. In the present study, calretinin (CALRET) and CALB patterns were determined by Western analysis in the medial basal hypothalamus (MBH) from male rats along with assaying plasma testosterone levels during postnatal development. Testosterone levels were very low in 7-, 10-, and 30-day-old animals (approximately 0.5 ng/mL), increased in a stair-step fashion to peak levels at 90 days (approximately 3.8 ng/mL), then declined with increasing age to very low levels at 300 days of age (approximately 0.3 ng/mL). At 7 and 10 days, MBH CALRET and CALB levels were low; however, at Day 30 a significant twofold increased was observed. Thereafter, in 60-, 120-, 180-, and 300-day-old animals MBH CALRET and CALB levels were, in general, comparable to 30-day-old values. These findings suggest that there is not a clear correspondence between the androgen status in male rats and the calcium-binding proteins (CALRET & CALB) expressed in the MBH. Therefore, it appears that brain CALRET and CALB are regulated in a developmental fashion with significant increases in expression occurring around the 4th postnatal week.

Aging↗
PubMed2000

Co-existence of calcium-binding proteins in neurons of the medullary dorsal horn of the rat.

Double immunofluorescence histochemistry for calcium-binding proteins was performed in the caudal subnucleus of the rat spinal trigeminal nucleus; for calbindin D28k (CB) and calretinin (CR), for CB and parvalbumin (PV), and for CB and CR. CB-immunoreactive (-ir) neurons were seen 1.7 times more frequently than CR-ir neurons and 5.5 times more frequently than PV-ir neurons. About 70-90% of these neurons were distributed in substantia gelatinosa. Co-existence of CB and CR was indicated in 2.3% of CB-ir and 3.9% of CR-ir neurons. Co-existence of CB and PV was indicated in 1.0% of CB-ir and 5.5% of PV-ir neurons. Co-existence of CR and PV was indicated in 1.4% of CR-ir and 5.1% of PV-ir neurons. In these doubly immunostained neurons, 59.5-69.5% were observed in substantia gelatinosa, 5.9-17.8% in the marginal zone, and 12.7-31.0% in the magnocellular part.

Animals↗
PubMed2000

Decreased calbindin-D28k immunoreactivity in aged rat sympathetic pelvic ganglionic neurons.

The rat major pelvic ganglion contains the majority of sympathetic and parasympathetic postganglionic neurons that innervate the pelvic viscera. Previous studies have indicated that it is only the sympathetic population of this ganglion that is susceptible to age-associated changes. We have examined the distribution of the neuronal calcium binding proteins calbindin-D28k, calretinin and parvalbumin by immunohistochemistry in young adult and aged rats and have discovered that calbindin-D28k is only present in the sympathetic neurons (identified by tyrosine hydroxylase immunostaining) and not in parasympathetic neurons (identified by VIP immunostaining). In the aged rats the number of calbindin-immunoreactive sympathetic neurons of the major pelvic ganglion was dramatically reduced. Calretinin and parvalbumin-immunoreactivity was present at a lower level of fluorescence than that of calbindin immunoreactivity in all the neurons of the major pelvic ganglion and this level was unchanged in aged rats. Thus we suggest that the decline of intracellular calbindin D28k levels may lead to impaired calcium buffering capacity which might be a contributory factor in the age-associated attrition of pelvic sympathetic neurons.

Aging↗
PubMed1996

Transient patterns of calbindin-D28k expression in the developing striatum of man.

In fetal and adult human brains, calbindin immunoreactivity (CB-ir) of neostriatal neuropil showed inhomogeneous pattern. A mosaic of CB-ir neuropil patches matching the acetylcholinesterase (AChE)-reactive patches and most of the encapsulated cell-dense islands was distributed in a lighter stained background matrix. During infancy, the pattern of CB expression changed from one of CB-rich patches to one of CB-poor striosomes and rich matrix. Furthermore, we observed a steady development of population of medium-sized neurons in the striatal matrix; in addition, a transient CB-expression was found in cells of the ganglionic eminence and presumably in a subset of striatal interneurons.

Acetylcholinesterase↗
PubMed1997

Immunohistochemical localization of calbindin D28k in the periodontal Ruffini endings of rat incisors.

It was examined whether calbindin D28k (CB) might be located in the rat incisor periodontal Ruffini ending, an essential mechanoreceptor in periodontal ligament, by light- and electron-microscopic immunohistochemistry. Some thick nerve fibers showing CB-like immunoreactivity (LI) entered the lingual half of the periodontal ligament of the incisor and showed the dendritic terminal arborization. Electron-dense immunoreaction products indicating CB-LI were distributed diffusely in axoplasm of the axon terminals, no mitochondria, however, were not labeled. Neither cell bodies nor cytoplasmic extensions of the terminal Schwann cells exhibited CB-LI. CB was presumed to be involved in the maintenance of Ca2+ homeostasis in the mechano-electric transduction in mechanoreceptors in the periodontal ligament.

Animals↗
PubMed1999

Relationship of calcium-binding protein containing neurons and projection neurons in the rat basolateral amygdala.

Two-laser and two-color approaches were used to observe the colocalization of the calcium-binding proteins, calbindin D28k and parvalbumin, and the retrograde tracer, Fluoro-Gold (FG) in the basolateral amygdala of the rat. The study was performed on five adult rats into which FG was injected to the frontal association cortex. Then, the localization of the retrogradely labeled neurons in the basolateral amygdala was compared with the localization of the neurons labeled by calcium-binding proteins. The present study showed that most of the retrogradely labeled neurons in the posterior part of the basolateral amygdala are also calbindin-positive. Even though a lot of parvalbumin-positive endings were present at the surface of the retrogradely labeled cells, we did not observe the colocalization of the parvalbumin and projective neurons.

Amygdala↗
PubMed1999

Maternal separation: hypothalamic-preoptic area and hippocampal calbindin-D28K and calretinin in male and female infantile rats.

Calcium-binding proteins (CaPs) potentially play important roles in neurogenesis and neuronal survival. Calbindin-D28K (CALB) and calretinin (CALRET) in the medial basal hypothalamic (and preoptic area) (MBH) and hippocampus (HIPPO) from control and maternally separated male and female infantile rats were examined by Western analysis. Significantly greater levels of the CaPs in the MBH vs. the HIPPO may suggest enhanced or decreased neuroprotection, respectively, during the stress hyporesponsive period (SHRP). Male infantile rats separated from their mother's from postnatal day 2-10 displayed significant changes in CALB and CALRET for the MBH (decrease) and HIPP (increase) brain sites suggesting possible modified (negative feedback) mechanism(s) in HPA dysfunction observed during postnatal life.

Animals↗
PubMed1999

Immunohistochemical evidence for the presence of calbindin containing neurones in the myenteric plexus of the guinea-pig stomach.

Using immunohistochemistry we studied the presence of calbindin in myenteric neurones of the guinea-pig stomach. A rabbit anti recombinant rat calbindin-D28k (CALB) stained 12, 12 and 25% of all myenteric neurones in the fundus, corpus and antrum, respectively. A rabbit anti recombinant human CALB stained 4, 4 and 16%, respectively. A mouse monoclonal antibody against the chicken intestinal CALB showed no labelling. In all regions most calbindin neurones were additionally choline acetyltransferase (ChAT) positive while only a small proportion exhibited nicotinamide adenosine dinucleatide phosphate (NADPH)-diaphorase-activity. Numerous calbindin-positive varicose nerve fibres were present within myenteric ganglia, rarely detectable in the muscle layers and virtually absent in the mucosa. This study demonstrated that a supopulation of cholinergic myenteric neurones in the stomach contain calbindin and suggested that many of these neurones fulfil interneuronal tasks.

Animals↗
PubMed2000

Calbindin-D28k immunoreactivity in the suprachiasmatic nucleus and the circadian response to constant light in the rat.

Recent studies in the hamster have led to the discovery that the expression of the calcium binding protein, calbindin-D28k, is a defining feature of neurons in the suprachiasmatic nucleus involved in the regulation of circadian rhythms by environmental light.(2,18, 19,32) To study further the involvement of calbindin-D28k, we examined the effect of exposure to constant light on calbindin-D28k immunoreactivity in the suprachiasmatic nucleus of intact rats and of rats treated neonatally with the retinal neurotoxin, monosodium glutamate. Exposure to constant light is known to disrupt circadian rhythms in rodents and we found previously that treatment with monosodium glutamate selectively prevents the disruptive effect of constant light on circadian rhythms in rats.(7,9) In the present study we found that exposure to light suppresses calbindin-D28k expression in the ventrolateral retinorecipient region of the suprachiasmatic nucleus of rats and that neonatal treatment with monosodium glutamate blocks the suppressive effect of constant light on calbindin-D28k expression. These findings are consistent with the proposed role of calbindin-D28k in photic signaling in the suprachiasmatic nucleus,(32) and point to the possibility that suppression of calbindin-D28k expression is linked to the mechanism by which constant light disrupts circadian rhythms.

Animals↗
PubMed2001

Chronic nicotine exposure reduces N-methyl-D-aspartate receptor-mediated damage in the hippocampus without altering calcium accumulation or extrusion: evidence of calbindin-D28K overexpression.

Neuronal accumulation of excess Ca2+ has been implicated in cellular death following several forms of physical and chemotoxic insult. Recent studies have suggested that exposure to agonists at brain nicotinic acetylcholine receptors reduces cytotoxic consequences of increased intracellular Ca2+ following some insults. In the present study, the ability of chronic exposure to (-)-nicotine to reduce cytotoxicity and attenuate increases in intracellular Ca2+ caused by exposure to N-methyl-D-aspartate were examined in organotypic cultures of rat hippocampus. Cultures were exposed to nicotine (0.1-10.0 microM) for five days prior to excitotoxic insult with N-methyl-D-aspartate. Exposure to N-methyl-D-aspartate produced concentration-dependent increases in both accumulation of 45Ca and in early and delayed cell death in the CA1, CA3 and dentate gyrus regions of cultures. The CA1 region of the hippocampus displayed the greatest sensitivity to cytotoxic effects of N-methyl-D-aspartate exposure; however, this regional difference was not associated with increased accumulation of 45Ca. Prior exposure to nicotine markedly attenuated N-methyl-D-aspartate-induced early and delayed cell death in each hippocampal region at concentrations as low as 0.1microM. However, nicotine did not alter the initial N-methyl-D-aspartate-stimulated influx of 45Ca or enhance extrusion of accumulated 45Ca measured at several time-points after insult. Five days of exposure to nicotine markedly increased immunoreactivity of the Ca2+ binding protein calbindin-D28K in each region of hippocampal cultures, effects reduced by mecamylamine co-exposure. These findings suggest that the potent protective effects of chronic nicotine exposure against neuronal overexcitation are not likely attributable to attenuations of Ca2+ accumulation, but are likely related to increased buffering of accumulated Ca2+.

Animals↗
PubMed2001

Immunohistochemical profiles of spinal lamina I neurones retrogradely labelled from the nucleus tractus solitarii in rat suggest excitatory projections.

Three morphologically distinct types of lamina I neurones, fusiform, flattened and pyramidal, project from the spinal cord to the caudal part of the nucleus tractus solitarii in the rat, and may represent a pathway whereby peripheral stimuli can modify autonomic functions. The neurochemistry of these three types of projection neurones was investigated using retrograde neuronal tracing with cholera toxin B-subunit combined with dual and triple immunofluorescence labelling for different neuroactive substances. None of the lamina I neurones with immunoreactivity for GABA or glycine were found to project to the nucleus tractus solitarii, whereas high levels of glutamate immunoreactivity, which may indicate a glutamatergic phenotype, were found in 18.4% of fusiform, 9.6% of pyramidal and 2.1% of flattened projection neurones. Immunoreactivity for calbindin-D28K was present in 34.9% of fusiform cells, 18.3% of pyramidal cells and 10.5% of flattened cells, and nitric oxide synthase immunoreactivity was detected in 13.8% of fusiform cells, 1.1% of pyramidal cells and 4.2% of flattened cells that had projections to the nucleus tractus solitarii. Calbindin immunoreactivity was co-localised in major subpopulations of projection neurones of each morphological type that contained glutamate immunoreactivity, whereas co-localisation of nitric oxide synthase immunoreactivity in these neurones was relatively uncommon. The pyramidal cell was the only retrogradely labelled cell type found to be immunoreactive for substance P, but few (<5%) of these neurones were immunolabelled. These data are consistent with the hypothesis that lamina I neurones projecting to the dorsal vagal complex are not inhibitory, and that some of them, belonging mostly to the fusiform and pyramidal types, may exert excitatory, glutamate- or substance P-mediated effects upon inhibitory interneurones in the nucleus tractus solitarii. Such excitatory pathways could be involved in the attenuation of the reflex control of blood pressure by both painful and innocuous peripheral stimuli, such as those arising in injury and exercise.

Afferent Pathways↗
PubMed2001

Colocalization of calcium-binding proteins and GABA in neurons of the rat basolateral amygdala.

The basolateral amygdala contains subpopulations of non-pyramidal neurons that express the calcium-binding proteins parvalbumin, calbindin-D28k (calbindin) or calretinin. Although little is known about the exact functions of these proteins, they have provided useful markers of specific neuronal subpopulations in studies of the neuronal circuitry of the cerebral cortex and other brain regions. The purpose of the present study was to investigate whether basolateral amygdalar non-pyramidal neurons containing parvalbumin, calbindin, or calretinin exhibit immunoreactivity for GABA, and to determine if calretinin is colocalized with parvalbumin or calbindin in the rat basolateral amygdala. Pyramidal neurons were distinguished from non-pyramidal neurons on the basis of staining intensity. Using immunofluorescence confocal laser scanning microscopy, as well as the 'mirror technique' on immunoperoxidase-stained sections, it was found that there was virtually no colocalization of calretinin with parvalbumin or calbindin, but that the great majority of basolateral amygdalar non-pyramidal neurons containing parvalbumin, calbindin, or calretinin exhibited GABA immunoreactivity. Calbindin-positive neurons constituted almost 60% of the GABA-containing population in both subdivisions of the basolateral nucleus and more than 40% of the GABA-containing population in the lateral nucleus. Parvalbumin-positive neurons constituted 19-43% of GABA-immunoreactive neurons in the basolateral amygdala, depending on the nucleus. Calretinin-positive non-pyramidal neurons constituted about 20% of the GABA-positive neuronal population in each nucleus of the basolateral amygdala. These findings indicate that non-pyramidal neurons containing parvalbumin, calbindin, or calretinin comprise the majority of GABA-containing neurons in the basolateral amygdala, and that the calretinin subpopulation is distinct from non-pyramidal subpopulations containing parvalbumin and calbindin. These separate neuronal populations may play unique roles in the inhibitory circuitry of the amygdala.

Amygdala↗
PubMed2001

Additive effect of glial cell line-derived neurotrophic factor and neurotrophin-4/5 on rat fetal nigral explant cultures.

Transplantation of embryonic dopaminergic neurons is an experimental therapy for Parkinson's disease, but limited tissue availability and suboptimal survival of grafted dopaminergic neurons impede more widespread clinical application. Glial cell line-derived neurotrophic factor (GDNF) and neurotrophin-4/5 (NT-4/5) exert neurotrophic effects on dopaminergic neurons via different receptor systems. In this study, we investigated possible additive or synergistic effects of combined GDNF and NT-4/5 treatment on rat embryonic (embryonic day 14) nigral explant cultures grown for 8 days. Contrary to cultures treated with GDNF alone, cultures exposed to NT-4/5 and GDNF+NT-4/5 were significantly larger than controls (1.6- and 2.0-fold, respectively) and contained significantly more protein (1.6-fold). Treatment with GDNF, NT-4/5 and GDNF+NT-4/5 significantly increased dopamine levels in the culture medium by 1.5-, 2.5- and 4.7-fold, respectively, compared to control levels, and the numbers of surviving tyrosine hydroxylase-immunoreactive neurons increased by 1.7-, 2.1-, and 3.4-fold, respectively. Tyrosine hydroxylase enzyme activity was moderately increased in all treatment groups compared to controls. Counts of nigral neurons containing the calcium-binding protein, calbindin-D28k, revealed a marked increase in these cells by combined GDNF and NT-4/5 treatment. Western blots for neuron-specific enolase suggested an enhanced neuronal content in cultures after combination treatment, whereas the expression of glial markers was unaffected. The release of lactate dehydrogenase into the culture medium was significantly reduced for GDNF+NT-4/5-treated cultures only. These results indicate that combined treatment with GDNF and NT4/5 may be beneficial for embryonic nigral donor tissue either prior to, or in conjunction with, intrastriatal transplantation in Parkinson's disease.

Animals↗
PubMed2002

Time course and manner of Purkinje neuron death following a single ethanol exposure on postnatal day 4 in the developing rat.

The present study was designed to evaluate the time course and manner of Purkinje cell death following a single ethanol dose delivered intragastrically on postnatal day (PN) 4 to rat pups. Analysis included immunolabeling of Purkinje cells with antibody specific for calbindin D28k and counting of Purkinje cells in each lobule of a mid-vermal slice. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling analysis and immunodetection for cleaved (activated) caspase-3 enzyme was used to identify apoptosis, with calbindin D28k co-immunolabeling to identify apoptotic Purkinje cells. Finally, immunodetection for cytochrome c, again with co-labeling using calbindin D28k antibody, identified intracellular release of cytochrome c from the mitochondria into the cytoplasm of Purkinje cells. The data demonstrate that a single dose of ethanol results in a significant and extensive, lobular dependent loss of Purkinje cells within 24 h after administration. Extensive loss in the early developing lobules (I-III, VIII-X) and less to no loss in the later developing lobules (IV-VII) is consistent with prior literature reports on the ethanol-induced effects on Purkinje cells at this age. Clear and consistent evidence of apoptotic Purkinje cells was identified and the pattern was transient in nature. Finally, cytochrome c is released from the mitochondria of Purkinje cells in a time course consistent with the activation of the mitochondrial pathway of apoptosis. These data support the hypothesis that ethanol-induced loss of Purkinje cells involves apoptotic mechanisms. Furthermore, the initiation of apoptosis by ethanol is consistent with ethanol-induced interruptions of Purkinje cell neurotrophic support leading to activation of the mitochondrial pathway of apoptosis.

Alcohol-Induced Disorders, Nervous System↗
PubMed2003

Selective age-related loss of calbindin-D28k from basal forebrain cholinergic neurons in the common marmoset (Callithrix jacchus).

A significant number of the cholinergic neurons in the basal forebrain of the primate, but not the rodent brain contain the calcium binding protein calbindin-D28k (CB). Previous experiments in our laboratory have demonstrated a substantial age-related loss of CB from the human basal forebrain cholinergic neurons (BFCN). The present study investigated the possible age-related loss of CB from the BFCN in a non-human primate species, the common marmoset (Callithrix jacchus). Quantitative analysis of matching sections as well as unbiased stereological determination of neuronal number were used in 16 adult marmosets ranging in age between 2 and 15 years. No significant changes were observed in the number of choline acetyltransferase-positive BFCN when a group of young animals (< or =4 years) was compared with a 6-8-year-old group and a 9-15-year-old group. Similarly, no age-related changes were observed in Nissl-stained magnocellular basal forebrain (putatively cholinergic) neurons. In contrast, the BFCN of the two older groups of animals displayed a significant loss of CB. The age-related loss of CB occurred in all sectors of the BFCN, but was greatest in the anterior sector of this cell group. The CB loss was neurochemically specific since the BFCN in the older groups of animals continued to express other markers such as high and low affinity neurotrophin receptors. The age-related loss of CB from the marmoset BFCN was also regionally selective as CB positive neurons in other structures, such as the cerebral cortex and the striatum displayed no apparent age-related changes. These results indicate that the marmoset BFCN display a significant and selective age-related loss of CB reminiscent of that observed in the human. Therefore, the common marmoset represents an appropriate animal model in which the consequences of BFCN CB loss can be investigated in depth. Loss of CB from the aged BFCN is likely to reduce the capacity of these neurons to buffer intracellular calcium and to leave them vulnerable to insults which can result in increased calcium levels. The vulnerability of the CB-negative BFCN in the aged marmoset to various insults which disturb calcium homeostasis remains to be investigated.

Aging↗
PubMed1997

Loss of Calbindin-D28K immunoreactivity from dentate granule cells in human temporal lobe epilepsy.

The loss of the calcium binding protein, Calbindin-D28k, from dentate granule cells has been observed in different animal models of epilepsy and in ischaemia. This decrease is accompanied by alterations of calcium and N-methyl-D-aspartate currents, which may explain the hyperexcitability of the dentate gyrus. In the present study, we found a loss of calbindin immunoreactivity from over 90% of the dentate granule cells in lobectomy samples from four of 10 temporal lobe epilepsy patients. In another four patients, over 50%, of dentate granule cells were devoid of calbindin immunoreactivity, whereas the remaining two cases showed a 20-30% decrease. Electron microscopy revealed a normal ultrastructure both in calbindin-containing and calbindin-negative granule cells. Both calbindin-positive and -negative mossy fibre collaterals participated in supragranular sprouting. As inferred from data in animal models, the lack of calbindin in dentate granule cells of human epileptic subjects is likely to result in hyperexcitability of the dentate gyrus, which may then function as a "motor" for seizures.

Adolescent↗