Cocaine treatment alters oxytocin receptor binding but not mRNA production in postpartum rat dams

Gestational cocaine treatment in rat dams results in decreased oxytocin (OT) levels, up-regulated oxytocin receptor (OTR) binding density and decreased receptor affinity in the whole amygdala, all concomitant with a significant increase in maternal aggression on postpartum day six. Rat dams with no gestational drug treatment that received an infusion of an OT antagonist directly into the central nucleus of the amygdala (CeA) exhibited similarly high levels of maternal aggression towards intruders. Additionally, studies indicate that decreased OT release from the hypothalamic division of the paraventricular nucleus (PVN) is coincident with heightened maternal aggression in rats. Thus, it appears that cocaine-induced alterations in OT system dynamics (levels, receptors, production, and/or release) may mediate heightened maternal aggression following cocaine treatment, but the exact mechanisms through which cocaine impacts the OT system have not yet been determined. Based on previous studies, we hypothesized that two likely mechanisms of cocaine's action would be, increased OTR binding specifically in the CeA, and decreased OT mRNA production in the PVN. Autoradiography and in situ hybridization assays were performed on targeted nuclei in brain regions of rat dams on postpartum day six, following gestational treatment twice daily with cocaine (15 mg/kg) or normal saline (1 ml/kg). We now report cocaine-induced reductions in OTR binding density in the ventromedial hypothalamus (VMH) and bed nucleus of the stria terminalis (BNST), but not the CeA. There was no significant change in OT mRNA production in the PVN following cocaine treatment.     

Restraint stress induces beta-amyloid precursor protein mRNA expression in the rat basolateral amygdala

Several studies have shown the involvement of beta-amyloid precursor proteins (APP) isoforms in physiological process like development of the central nervous system (CNS), functional roles in mature brain, and in pathological process like Alzheimer's disease, neuronal experimental damage, and stress, among others. However, the APP functions are still not clear. In the brain, APP(695) isoform is predominantly found in neurons while APP(751/770) isoforms are predominantly found in astroglial cells and have been associated to neurodegenerative processes. Acute or chronic stress in rats may trigger specific response mechanisms in several brain areas such as amygdala, hippocampus and cortex with the involvement of multiple neurotransmitters. Chronic stress may also induce neuronal injury in rat hippocampus. In situ hybridization (ISH) was used to investigate the expression of APP(695) and APP(751/770) mRNA in amygdala and hippocampus of male Wistar rats (n=4-6 per group) after acute (2 or 6h) or chronic (2h daily/7 days or 6h daily/21 days) restraint stress. Only the APP(695) mRNA expression was significantly increased in the basolateral amygdaloid nuclei following acute or chronic restraint. No APP isoform changed in hippocampus after any stress condition. These results suggest that restraint stress induces changes in gene expression of APP(695) in basolateral amygdaloid nucleus, an area related to stress response.     

Antipsychotics increase microtubule-associated protein 2 mRNA but not spinophilin mRNA in rat hippocampus and cortex

Antipsychotic (neuroleptic) drugs induce structural alterations in synaptic terminals and changes in the expression of presynaptic protein genes. Whether there are also changes in corresponding postsynaptic (dendritic) markers has not been determined. We describe the effect of 14-day treatment with typical (haloperidol, chlorpromazine) or atypical (clozapine, olanzapine, risperidone) antipsychotics on the expression of two dendritic protein genes, microtubule-associated protein 2 (MAP2) and spinophilin, using in situ hybridization, in the rat hippocampus, retrosplenial, and occipitoparietal cortices. MAP2 mRNA was increased modestly in the dentate gyrus and retrosplenial cortex by chlorpromazine, risperidone, and olanzapine and in the occipitoparietal cortex by chlorpromazine, haloperidol, and risperidone. None of the antipsychotics affected spinophilin mRNA in any area. Overall, these results show a modulation of MAP2 gene expression, likely reflecting functional or structural changes in the dendritic tree in response to some typical and atypical antipsychotics. The lack of change in spinophilin mRNA suggests that dendritic spines are not affected selectively by the drugs. The data provide further evidence that antipsychotics regulate genes involved in synaptic structure and function. Such actions may underlie their long-term effects on neural plasticity in areas of the brain implicated in the pathology of schizophrenia.     

Long-term stability of fear memory depends on the synthesis of protein but not mRNA in the amygdala

Synaptic modification supporting memory formation is thought to depend on gene expression and protein synthesis. Disrupting either process around the time of learning prevents the formation of long-term memory. Recent evidence suggests that memory also becomes susceptible to disruption upon retrieval. Whether or not the molecular events involved in the formation of new memory are the same as what is needed for memory to persist after retrieval has yet to be determined. In the present set of experiments, rats were given inhibitors of protein or messenger ribonucleic acid (mRNA) synthesis into the amygdala just after training or retrieval of fear memory. Results showed that blocking mRNA or protein synthesis immediately after learning prevented the formation of long-term memory, while stability of memory after retrieval required protein, but not mRNA, synthesis. These data suggest that the protein needed for memory reconsolidation after retrieval may be transcribed from pre-existing stores of mRNA.     

Confinement but not microgravity alters NMDA NR1 receptor expression in rat inner ear ganglia

Space flight produces changes in neuronal activity in the vestibular system. We studied the protein expression of the NMDA receptor subunit NR1 in the vestibular ganglia of rats exposed to microgravity for 17 days, beginning on postnatal day 8, as part of the NASA Neurolab mission. As a control, we studied the cochlear ganglia in the same way. NR1 expression in rats that had experienced microgravity (flight-FLT rats) was compared with that in two types of ground control. One control consisted of rats housed in regular cage conditions (VIV, vivarium); the other, asynchronous ground control (AGC), consisted of rats kept in cages similar to those used in flight (animal enclosure module, AEM), requiring no human care. After 8 days of flight, NR1 levels in the vestibular and cochlear neurons were similar in FLT, VIV and AGC rats. In contrast, 8 h after landing, the FLT and VIV animals showed similar, normal levels of NR1 staining, whereas the ganglia of the AGC animals displayed only very faint staining. Thus, microgravity did not modify NR1 expression in vestibular neurons. The lower levels of NR1 expression in the vestibular and cochlear neurons of AGC rats suggest an effect of confinement for 17 days in AEMs on the ground.     

Amyloid-beta peptide affects viability but not differentiation of embryonic and adult rat hippocampal progenitor cells

The neurological deficits that are characteristic of Alzheimer's Disease (AD) are ultimately a result of neuronal loss in distinct anatomical regions of the brain. This neuronal loss is thought to be due, in large part to the presence of the neurotoxic beta-amyloid (Abeta) deposits, that are characteristic of the AD brain. Transplantation therapy, in which neural stem cells (NSCs) or neural progenitor cells (NPCs) are introduced into damaged regions of the brain and induced to differentiate into replacement neurons, has been proposed as a possible therapeutic approach to treat AD. However, in the AD brain Abeta plaques, which remain in the area of neuronal degeneration, may affect the viability or differentiation potential of transplanted NSCs. Currently there is contradictory evidence concerning the effect of Abeta on NSCs. To further investigate the effect of Abeta on NSCs, we compared the mitochondrial function, proliferation and cellular differentiation of two populations of hippocampal NSCs (embryonic and adult derived) after Abeta exposure. Our results highlight the heterogeneity between different populations of NSCs even when derived from the same brain region. Our data also demonstrate that while mitochondrial function of NSCs is affected by Abeta, their proliferation and differentiation are not significantly influenced. Considered with previous studies, our results suggest that while NSCs do respond to the presence of Abeta, proliferation and differentiation of certain populations are not affected. Further study of the differences between susceptible vs. resistant populations of NSCs may provide crucial clues for the development of effective therapies to combat AD.     

Inflammation alters somatostatin mRNA expression in sensory neurons in the rat

Proinflammatory neuropeptides, such as substance P and calcitonin gene-related peptide, are up-regulated in primary afferent neurons in acute and chronic inflammation. While these neuropeptides have been intensively studied, potentially anti-inflammatory and/or anti-nociceptive neuropeptides such as somatostatin (SS) have been less widely investigated. Endogenous somatostatin is thought to exert a tonic antinociceptive effect. Exogenous SS is anti-inflammatory and antinociceptive and is thought to exert these actions through inhibition of proinflammatory neuropeptide release. In this study we have compared the expression of somatostatin in two inflammatory models: arthritis, a condition associated with increased nociception, and periodontitis, in which there is little evidence of altered nociceptive thresholds. In acute arthritis (< 24 h) SS mRNA was down-regulated in ipsilateral dorsal root ganglia (DRG; 52 +/- 7% of control, P < 0.05), and up-regulated in contralateral DRG (134 +/- 10% of control; P < 0.05). In chronic arthritis (14 days) this pattern of mRNA regulation was reversed, with SS being up-regulated ipsilaterally and down-regulated contralaterally. In chronic mandibular periodontitis (7-10 days), SS mRNA was up-regulated in only the mandibular division of the ipsilateral trigeminal ganglion (TG) (day 7, 219 +/- 9% and day 10, 217 +/- 12% of control; P < 0.02) but showed no change in other divisions of the trigeminal ganglion or in the mesencephalic nucleus. These data show that antinociceptive and anti-inflammatory neuropeptides are also regulated in inflammation. It is possible that the degree of inflammation and nociception seen may depend on the balance of pro- and anti-inflammatory and nociceptive peptide expression in a particular condition.     

Minocycline modulates chemokine receptors but not interleukin-10 mRNA expression in hypoxic-ischemic neonatal rat brain

Hypoxic-ischemic (HI) brain injury in the perinatal period causes significant morbidity. Minocycline (MN) is a tetracycline derivative that has reduced brain injury in various animal models of neurodegeneration, including perinatal ischemia. To determine whether MN can modulate the expression of chemokine receptors and interleukin-10 (IL10) in a model of neonatal brain injury, we produced an HI insult to the right cerebral hemisphere (ipsilateral) of the 7-day-old rat (PD7) by right common carotid artery ligation and 2.25 hr of hypoxia in 8% oxygen. MN (45 mg/kg, i.p.) or vehicle (PBS) was injected twice: 2 days and immediately before the HI insult. At 0, 1, 3, and 24 hr and 14 days after HI, total RNA from the ipsilateral and contralateral (exposed to hypoxia only) hemispheres was extracted, reverse transcribed, and amplified with gene-specific primers using a semiquantitative RT-PCR for macrophage inflammatory protein-1alpha), interferon-inducible protein (IP-10), C-C chemokine receptor 5 (CCR5; MIP-1alpha receptor), C-X-C chemokine receptor 3 (CXCR3; IP-10 receptor), and IL10. We found that, in the ipsilateral hemisphere, a significant (P < 0.05) increase in MIP-1alpha, IP-10, CCR5, and CXCR3 mRNA levels was observed. MN treatment decreased mRNA levels for CCR5 and CXCR3. In contrast, the levels of antiinflammatory cytokine IL10 were markedly decreased as a result of HI insult. Treatment with MN, however, had no effect on IL10. We conclude that MN decreased proinflammatory chemokine receptor expression but had little or no influence on the expression of antiinflammatory cytokine IL10. These effects confirm the antiinflammatory effect of MN in neonatal HI brain injury.     

Developmental changes of tau protein and mRNA in cultured rat brain oligodendrocytes

Oligodendrocytes elaborate an extensive network of multibranched processes and flat membranous sheets. Microtubules (MT) participate in the elaboration and stabilization of myelin-forming processes and are essential for cellular sorting processes. Microtubule-associated proteins (MAPs) are involved in the regulation and stabilization of the dynamic MT network. It has been shown previously that oligodendrocytes express the MAP tau, a phosphoprotein most abundant in neurons of the CNS. In this article, we demonstrate for the first time that oligodendrocytes contain all six tau isoforms, and that tau mRNA and protein expression is developmentally regulated. Immunoblot analysis reveals that tau protein is more abundant, and mature isoforms are more prominent at later stages of development. During the first week of culture maturation, a marked decrease in phosphorylation is observable. Using an RT-PCR approach, we can show that oligodendrocytes express small amounts of exon 3 containing isoforms and that during culture maturation, tau mRNA splice products with 3 MT-binding domains (3R) decrease and mRNA with 4 MT-binding domains (4R) increase. In situ hybridization study demonstrates that tau mRNA is present in precursor cells and in mature oligodendrocytes. Tau mRNA is actively transported into the cellular processes, is specifically present in the primary and some of the secondary processes, enriched at the turning and branching points and the growing tips, and often appears as small patches. Hence, localized tau translation at specific sites in the cellular extensions might contribute to the regulation of MT stability during process formation, early axonal contact establishment, and myelination.     

Overexpression of four-repeat tau mRNA isoforms in progressive supranuclear palsy but not in Alzheimer's disease.

Perturbations in the microtubule-associated protein tau occur in several human neurodegenerative diseases. In Alzheimer's disease and progressive supranuclear palsy (PSP), tau proteins assemble into straight and paired helical filaments that form intraneuronal deposits of neurofibrillary tangles (NFTs). The mechanisms underlying the aberrant assembly of tau into NFTs is unknown. To determine whether alterations in the expression of the carboxyl-terminal variants of tau contribute to NFT formation, we analyzed tau mRNA isoform expression in select regions of control, Alzheimer's disease, and PSP brains. In Alzheimer's disease, there were no alterations in tau mRNA isoform expression. However, in PSP, the levels of tau mRNA isoforms containing four microtubule binding domains were increased in the brainstem but not the frontal cortex or cerebellum. The brainstem in PSP has extensive NFT pathology, whereas the frontal cortex and cerebellum are relatively spared, suggesting that alterations in tau mRNA isoform expression occur in NFT-vulnerable regions in this disease. An increase in the four-repeat tau mRNA may lead to an increase in four-repeat tau protein isoforms and may contribute to the formation of NFTs in PSP. A similar increase in four-repeat tau mRNA has been reported for mutations associated with frontotemporal dementia and parkinsonism linked to chromosome 17.     

Increased expression of brain-derived neurotrophic factor but not neurotrophin-3 mRNA in rat brain after cortical impact injury

Levels of brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3) mRNA expression were measured in a rodent model of traumatic brain injury (TBI) following unilateral injury to the cerebral cortex. To obtain reliable data on the co-expression of neurotrophin genes, adjacent coronal sections from the same rat brains were hybridized in situ with BDNF and NT3 cRNA probes. BDNF mRNA increased at 1, 3, and 5 hr after unilateral cortical injury in the cortex ipsilateral to the injury site and bilaterally in the dorsal hippocampus. NT3 mRNA did not change significantly following injury. Our results suggest that TBI produces rapid increases in BDNF mRNA expression in rat brain without changes in NT3 mRNA expression, a finding which differs from studies of ischemia and seizures. It is possible that increased levels of BDNF mRNA rather than NT3 are important components of pathophysiological responses to TBI. © 1996 Wiley-Liss, Inc.     

Corticosterone regulates expression of BDNF and trkB but not NT-3 and trkC mRNA in the rat hippocampus

Corticosterone has profound effects on growth, differentiation, and synaptic transmission of hippocampal neurons by activation of mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs). In the present study we tested if neurotrophins can be implicated in these effects. For this purpose we injected 30, 300, and 1,000 μg corticosterone s.c. (per kg body weight) in adrenalectomized rats and measured the mRNA levels of brain-derived neurotrophic factor (BDNF), tyrosine receptor kinase (trk)B, neurotrophin (NT)-3, and trkC in hippocampal cell fields at 6 hr after steroid administration by in situ hybridization. NT-3 and trkC mRNA did not show significant changes in any hippocampal region after the various doses of conticosterone. BDNF mRNA decreased after corticosterone administration dose dependently, resulting in a maximal suppression of 35, 20, and 50% in dentate gyrus, CA3, CA1, respectively. Interestingly, trkB responded to corticosterone in an inverted U-shaped fashion in CA3 and dentate gyrus: the low dose of corticosterone increased trkB mRNA expression in both regions by approximately 30%, while the effect of the two higher doses was not different from the vehicle injected controls. In conclusion, we found differential effects of low and high doses of corticosterone on BDNF and trkB expression in hippocampus, which suggests involvement of a coordinated MR- and GR-mediated action. J. Neurosci. Res. 48:334–341, 1997. © 1997 Wiley-Liss, Inc.     

Thyroid hormone deficiency alters extracellular matrix protein expression in rat brain

The effects of thyroid hormone (T3) deficiency on extracellular matrix protein expression were analyzed in newborn rat brain. In hypothyroid animals, a marked increase in the expression of 62 kDa protein was observed in cerebral hemispheres and midbrain, while the 51.6 kDa protein was increased in cerebral hemispheres and decreased in midbrain and the 44.5 kDa protein was down regulated in both structures. On the basis of molecular weights, these proteins may be the proteoglycans cerebroglycan, glypican and N-Syndecan, respectively. In addition, hypothyroidism reduced fibronectin expression in midbrain (-59,7%), but not in cerebral hemispheres. T3 deficiency affects differently the expression of proteins in different brain regions. This may be involved in brain impairment caused by hypothyroidism.     

Aluminum induces tau aggregation in vitro but not in vivo

Etiological studies suggest that aluminum (Al) intake might increase an individual's risk of developing Alzheimer's disease (AD). Biochemical analysis data on the effects of Al, however, are inconsistent. Hence, the pathological involvement of Al in AD remains unclear. If Al is involved in AD, then it is reasonable to hypothesize that Al might be involved in the formation of either amyloid plaques or neurofibrillary tangles (NFTs). Here, we investigated whether Al might be involved in NFT formation by using an in vitro tau aggregation paradigm, a tau-overexpressing neuronal cell line (N2a), and a tau-overexpressing mouse model. Although Al induced tau aggregation in a heparin-induced tau assembly assay, these aggregates were neither thioflavin T positive nor did they resemble tau fibrils seen in human AD brains. With cell lysates from stable cell lines overexpressing tau, the accumulation of SDS-insoluble tau increased when the lysates were treated with at least 100 muM Al-maltolate. Yet Al-maltolate caused illness or death in transgenic mice overexpressing human tau and in non-transgenic littermates well before the Al concentration in the brain reached 100 muM. These results indicate that Al has no direct link to AD pathology.     

Repeated ECS induces GluR1 mRNA but not NMDAR1A-G mRNA in the rat hippocampus

The neural basis underlying the cognitive side effects of ECT is unknown. Recent studies suggest that the memory dysfunction may be caused by alterations in hippocampal synaptic efficacy [20]. In situ hybridization was used to examine the possible receptor mechanisms responsible for this effect. Repeated ECS markedly increased mRNA expression for the GluR1 subunit of the AMPA receptor, but not the NMDAR1A-G subtypes of the NMDA receptor, relative to control treatments. This effect was present 24 h after the last seizure and may be responsible for the expression of the ECS-induced increase in synaptic efficacy.     

Corticotropin-releasing factor (CRF), but not corticosterone, increases basolateral amygdala CRF-binding protein

Corticotropin-releasing factor (CRF) is a key mediator of the behavioral, autonomic, and endocrine responses to stress. CRF binds two receptors and a CRF-binding protein (CRF-BP), which may inactivate or modulate the actions of CRF at its receptors. The amygdala is an important anatomical substrate for CRF and contains CRF, its receptors, and CRF-BP. Our previous studies demonstrated that acute stress increases basolateral amygdala (BLA) CRF-BP mRNA. However, factors that may be responsible for this increase remain unclear. Both CRF and corticosterone are released during stress and are known to increase CRF-BP in vitro. However, the effects of these agents in vivo on brain CRF-BP have not been studied. Therefore, we examined the effects of CRF and corticosterone administration on BLA CRF-BP mRNA in rats. The findings demonstrate that intracerebroventricular CRF (5 microg) significantly increases BLA CRF-BP mRNA 9 h post-infusion, a time point consistent with that observed for the effects of acute stress-induced increases in CRF-BP. In contrast, injection of corticosterone at a dose mimicking acute stress (6.5 mg/kg sc) failed to increase BLA CRF-BP mRNA 9 h post-injection. Surprisingly, two different CRF antagonists failed to block CRF-induced increases in CRF-BP mRNA. These results suggest that CRF, but not corticosterone, may be responsible for stress-induced increases in BLA CRF-BP gene expression. Furthermore, this effect appears to be mediated by mechanisms other than the identified CRF receptors.     

Pregnancy alters lateral parabrachial nucleus but not hypothalamic Fos expression following hypotensive hemorrhage

The goal of these experiments was to determine if hemorrhage-induced Fos expression in the hypothalamus and lateral parabrachial nucleus (LPBN) is altered by reproductive cycle phase or pregnancy. Conscious unrestrained female Sprague-Dawley rats were subjected to a 16 ml/kg hemorrhage on the morning of the metestrus or proestrus phases of the estrous cycle, or on day 12-14 of pregnancy (mid-gestation). Hemorrhage induced a significant increase (p < 0.01) in the number of Fos-immunoreactive cell nuclei in the supraoptic nucleus, and in both the magnocellular and parvicellular components of the paraventricular hypothalamic nucleus, that did not differ between groups. In virgin females, hemorrhage also induced a significant increase in LPBN Fos expression that did not differ between metestrus and proestrus. In pregnant animals, there was an increase in basal LPBN Fos expression, but hemorrhage induced no further increase in the number of Fos-immunoreactive neurons in the LPBN. Mean arterial pressure decreased (p < 0.001) and plasma renin activity increased (p < 0.01) to a similar extent in all three groups after 16 ml/kg blood loss. In summary, the number of paraventricular and supraoptic nucleus neurons activated by hemorrhage is unaffected by estrous cycle phase or pregnancy. In contrast, pregnancy significantly attenuates the LPBN response to hemorrhage.     

Psychological stress increased corticotropin-releasing hormone mRNA and content in the central nucleus of the amygdala but not in the hypothalamic paraventricular nucleus in the rat

The central administration of corticotropin-releasing hormone (CRH) to experimental animals sets into motion a coordinated series of physiological and behavioral events that promote survival during threatening situation. A large body of evidence suggest that CRH in the central nucleus of the amygdala (CEA) induces fear-related behaviors and is essential to fear conditioning; however, evidence of CRH-mediated activation of the amygdala under physiological situation is still limited. We report here a study of the impact of a psychological stressor on hypothalamic and amygdala CRH systems in the rat. Non-footshocked rats placed in a floored compartment surrounded by footshocked rats were defined as the psychological stress group. Rats were exposed to psychological stress for 15 min, and then sacrificed 1.5 and 3 h after cessation of stress. We found that our psychological stressor induced an increase in both CRH mRNA levels, as assessed by in situ hybridization histochemistry, and CRH content, as assessed by micropunch RIA, in the CEA. Exposure to the psychological stressor also caused a significant increase in CRH mRNA levels with a trend for an increase in CRH content in the dorsolateral subdivision of the bed nucleus of the stria terminalis (BNST) which is anatomically associated with the CEA. In contrast, psychological stress induced a small, but significant increase in type-1 CRH receptor (CRHR-1) mRNA in the hypothalamic paraventricular nucleus (PVN), while it failed to elevate either PVN CRH mRNA levels or content, CRH content in the median eminence (ME), or levels of plasma ACTH or corticosterone (CORT). Thus, in the context of a psychological stressor, the activation of the amygdala CRH system can occur without robust activation of the hypothalamic CRH system. In the light of previous data that the psychological stress-induced loss of sleep was reversed by the central administration of a CRH antagonist, these data suggest that CRH in the CEA may contribute to the psychological stress-evoked fear-related behavior such as hyperarousal. These data also indicate that in response to a psychological stressor, the amygdala CRH system is much more sensitive than is the CRH system emanating from the PVN.     

Cochlear ablation alters acoustically induced c-fos mRNA expression in the adult rat auditory brainstem

Expression of c-fos mRNA was studied in the adult rat brain following cochlear ablations by using in situ hybridization. In normal animals, expression was produced by acoustic stimulation and was found to be tonotopically distributed in many auditory nuclei. Following unilateral cochlear ablation, acoustically driven expression was eliminated or decreased in areas normally activated by the ablated ear, e.g., the ipsilateral dorsal and ventral cochlear nuclei, dorsal periolivary nuclei, and lateral nucleus of the trapezoid body and the contralateral medial and ventral nuclei of the trapezoid body, lateral lemniscal nuclei, and inferior colliculus. These deficits did not recover, even after long survivals up to 6 months. Results also indicated that neurons in the dorsal cochlear nucleus could be activated by contralateral stimulation in the absence of ipsilateral cochlear input and that the influence of the contralateral ear was tonotopically organized. Results also indicated that c-fos expression rose rapidly and persisted for up to 6 months in neurons in the rostral part of the contralateral medial nucleus of the trapezoid body following a cochlear ablation, even in the absence of acoustic stimulation. This response may reflect a release of constitutive excitatory inputs normally suppressed by missing afferent input or changes in homeostatic gene expression related to sensory deprivation. Instances of transient, surgery-dependent increases in c-fos mRNA expression in the absence of acoustic stimulation were observed in the superficial dorsal cochlear nucleus and the cochlear nerve root on the ablated side. J. Comp. Neurol. 404:271–283, 1999. © 1999 Wiley-Liss, Inc.