Induction of heat shock (stress) genes in the mammalian brain by hyperthermia and other traumatic events: A current perspective

Brown, Ian R.

doi:10.1002/jnr.490270302

Cited by 180 publications

(116 citation statements)

References 96 publications

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“…Induction of a 72-kD heat shock protein (HSP72) is a sensitive marker of a variety of cellular stresses including ischemia, heat shock, hypoglycemia, and seizures (Brown, 1990) but is not necessarily pre dictive of neuronal death (Sloviter and Lowenstein, 1992). The distribution of HSP72 immunostained neurons at 24-72 h postischemia is similar to those that displayed altered T immunostaining within the first 2 h. It is of interest that in rats, heat shock results in increased somal T immunostaining similar to that observed following ischemia, except that phosphorylation of T is increased post-heat shock (Papasozomenos and Su, 1991).…”

Section: Discussionmentioning

confidence: 99%

Alterations in τ Immunostaining in the Rat Hippocampus following Transient Cerebral Ischemia

Geddes¹,

Schwab²,

Craddock³

et al. 1994

J Cereb Blood Flow Metab

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Summary: Previous studies in gerbils have shown that cytoskeletal disruption and a loss of the dendritic micro tubule-associated protein, MAP2, may occur after short periods of transient global ischemia. T, a predominantly axonal microtubule-associated protein, has not been ex amined following ischemia. We compared neuronal dam age with alterations in MAP2, T, and 72-kD heat shock protein (HSP72) immunostaining at various reperfusion times following 20 min of ischemia in the rat four-vessel occlusion model. T accumulated in neuronal cell bodies throughout the hippocampal formation 30 min to 2 h after the ischemic insult. Perikaryal T immunostaining was transient in most regions, but persisted in polymorphic hilar neurons. This was accompanied by a loss of immu no staining in the target of many hilar neurons, the inner Transient global ischemia is followed by a de layed loss of neurons in select brain regions, includ ing the hippocampus (for review see Schmidt Kastner and Freund, 1991). Using the rat four vessel occlusion model (Pulsinelli and Brierly, 1979), ischemia maintained for 20 min in halothane anesthetized animals results in neuronal damage in CAl and hilus, but not in CA3 (Jorgensen and Di emer, 1982; Pulsinelli et aI., 1982). The postisch emic rate of cell death is not uniform, with hilar neurons degenerating within a few hours, but CAl pyramidal cells degenerating 24-72 h following isch emia and reperfusion (Crain et aI., 1988; Hsu and Received August 3, 1993; final revision received October 28, 1993; accepted November 23, 1993. Address correspondence and reprint requests to Dr. James W. Geddes, 209 Sanders-Brown Building, University of Kentucky, Lexington, KY 40536-0230, U. S. A.Abbreviations used : HSP, heat shock protein; KA, kainic acid; MAP, microtubule-associated protein; TBS, Tris-buffered saline; 4VO, four-vessel occlusion. 554 molecular layer of the dentate gyrus. The same neuronal populations that exhibited increased T immunostaining of perikarya later displayed an induction of HSP72 immu noreactivity. In contrast, loss of MAP2 immunostaining was not consistently observed before neuronal death and did not correspond to HSP72 induction. The altered T immunostaining is not the direct result of excitotoxic in sult, as intrahippocampal injection of kainic acid did not cause the somal accumulation of T, but did cause disrup tion of MAP2 immunostaining. Taken together, the re sults suggest that the somal accumulation of T is an early, sensitive, and selective marker of ischemic insult.

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Section: Discussionmentioning

confidence: 99%

Alterations in τ Immunostaining in the Rat Hippocampus following Transient Cerebral Ischemia

Geddes¹,

Schwab²,

Craddock³

et al. 1994

J Cereb Blood Flow Metab

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“…Included in this family are the constitutive Hsp73, commonly referred to as Hsc70, and the inducible Hsp72, referred to as Hsp70. Most neurons contain high levels of the constitutive form and low levels of the inducible form (Brown 1991;Brown 1994). High levels of the constitutive Hsc70 in neurons may reflect their metabolic activity, which is one of the highest of all cells in the body.…”

Section: Introductionmentioning

confidence: 99%

Administration of Hsp70 in vivo inhibits motor and sensory neuron degeneration

Tidwell¹,

Houenou²,

Tytell³

2004

Cell Stress Chaper

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The induction of heat shock proteins (Hsps) serves not only as a marker for cellular stress but also as a promoter of cell survival, which is especially important in the nervous system. We examined the regulation of the constitutive and stress-induced 70-kD Hsps (Hsc70 and Hsp70, respectively) after sciatic nerve (SN) axotomy in the neonatal mouse. Additionally, the prevention of axotomy-induced SN cell death by administration of several preparations of exogenous Hsc70 and Hsp70 was tested. Immunohistochemistry and Western blot analyses showed that endogenous levels of Hsc70 and Hsp70 did not increase significantly in lumbar motor neurons or dorsal root ganglion sensory neurons up to 24 hours after axotomy. When a variety of Hsc70 and Hsp70 preparations at doses ranging from 5 to 75 g were applied to the SN stump after axotomy, the survival of both motor and sensory neurons was significantly improved. Thus, it appears that motor and sensory neurons in the neonatal mouse do not initiate a typical Hsp70 response after traumatic injury and that administration of exogenous Hsc/Hsp70 can remedy that deficit and reduce the subsequent loss of neurons by apoptosis.

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“…Moreover, it has been shown that female rats are more sensitive to the neurotoxicity of NMDA receptor antagonists than male rats (Fix et al 1995;Auer 1996). However, the precise mechanism underlying the neurotoxicity of NMDA receptor antagonists in rat retrosplenial cortex is currently unclear (reviews by Ellison 1995;Olney and Farber 1995;Farber et al 1998).It has been shown that 70 kDa heat shock protein HSP-70, which is not normally present in the rat brain, is induced within vulnerable brain cells in response to a number of different manipulations that induce cellular injury paradigms (reviews by Brown 1994;Sharp and Sagar 1994;Massa et al 1996). Furthermore, it has been reported that heat shock protein HSP-70, which is known as a sensitive marker of reversible neuronal injury, is induced in the retrosplenial cortex after administration of PCP, dizocilpine, or ketamine (Sharp et al 1991;Sharp and Sagar 1994;Hashimoto et al 1996;.…”

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confidence: 99%

Effects of Age and Gender on the Expression of Brain-Derived Neurotrophic Factor mRNA in Rat Retrosplenial Cortex Following Administration of Dizocilpine

Matsuki

Shirayama

Hashimoto

et al. 2001

Neuropsychopharmacology

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Using in situ hybridization, we studied the effects of age and gender on the expression of brain-derived neurotrophic factor (BDNF) mRNA and heat shock protein hsp-70 mRNA in the rat retrosplenial cortex following administration of the noncompetitive NMDA receptor antagonist ( ϩ )-MK-801 (dizocilpine). Male and female 12 weeks, or 10 months old) were given a single intraperitoneal injection of saline (1 ml/ kg) or dizocilpine (0.3, 1.0, or 3.0 mg/kg). No expression of BDNF mRNA and hsp-70 mRNA was detected in the rat retrosplenial cortex after administration of saline (1 ml/kg, IP). Administration of dizocilpine (0.3, 1.0, or 3.0 Several observations suggest that altered glutamatergic neurotransmission may play a role in the etiology and pathophysiology of schizophrenia (reviews by Javitt and Zukin 1991;Olney and Farber 1995;Coyle 1996;Tamminga 1998). Phencyclidine (PCP) and its analog ketamine have psychotomimetic properties in healthy human subjects and have been shown to cause a prolonged worsening of symptoms in stabilized chronic schizophrenic patients (Luby et al. 1959;Krystal et al. 1994). PCP and ketamine are noncompetitive antagonists of the ion-channel of the N-methyl-D-aspartate (NMDA) (Javitt and Zukin 1991). Ketamine is still used as an anesthetic in humans, and it is known that the ability of ketamine to induce psychosis is age dependent, with susceptibility to these effects not occurring in humans until adolescence and peak sensitivity occurring in early adulthood (Reich and Silvay 1989). In addition, it has also been suggested that PCP-induced psychosis may have a similar age-dependency profile (Baldridge and Bessen 1990;Welch and Correa 1980). Noncompetitive NMDA receptor antagonists such as PCP, ( ϩ )-MK-801 (dizocilpine), and ketamine have been reported to cause neurotoxicity in the retrosplenial cortex of rat brain after administration of a single dose (Olney et al. 1989). It has been shown that dizocilpine causes reversible pathological changes (neuronal vacuolization) in retrosplenial cortical neurons at doses of 2.5 mg/kg or less and that, at a dose of 5 mg/kg, dizocilpine induces irreversible necrosis of these neurons . Furthermore, it has been reported that vulnerability to dizocilpine-induced neurotoxicity in the rat retrosplenial cortex is age dependent, with the onset of sensitivity being approximately at puberty (45 days of age) and becoming maximal in early adulthood . Thus, rats display a gradual onset of susceptibility to NMDA receptor antagonist-induced neuronal injury in late adolescence just as humans become susceptible to ketamine (or PCP)-induced psychosis and to the symptomatic expression of schizophrenia in late adolescence . Moreover, it has been shown that female rats are more sensitive to the neurotoxicity of NMDA receptor antagonists than male rats (Fix et al. 1995;Auer 1996). However, the precise mechanism underlying the neurotoxicity of NMDA receptor antagonists in rat retrosplenial cortex is currently unclear (reviews by Ellison 1995;Olney and Farber 1995;Farb...

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Induction of heat shock (stress) genes in the mammalian brain by hyperthermia and other traumatic events: A current perspective

Cited by 180 publications

References 96 publications

Alterations in τ Immunostaining in the Rat Hippocampus following Transient Cerebral Ischemia

Alterations in τ Immunostaining in the Rat Hippocampus following Transient Cerebral Ischemia

Administration of Hsp70 in vivo inhibits motor and sensory neuron degeneration

Effects of Age and Gender on the Expression of Brain-Derived Neurotrophic Factor mRNA in Rat Retrosplenial Cortex Following Administration of Dizocilpine

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