Monoamine neurotransmitters in the evolution of infarction in ischemic striatum: morphologic correlation

Abstract

Evolution of infarction following cerebral ischemia is a delayed process, with spongiform degeneration of the neuropil occurring 6 to 8 hours after onset of ischemia. The brains of gerbils with stroke following unilateral carotid artery ligation were examined for catecholamine-derived fluorescence (CADF) by the Falck-Hillarp technique to study the relationship of catecholamine (CA) metabolism with damage to the neuropil. CADF could still be identified in the striatum for up to 16 hours after stroke and there appeared to be spongiform degeneration of the neuropil in relation to accumulations of CADF at 7 and 16 hours after stroke. Pretreatment of gerbils with a-methyl-p-tyrosine 400 mg/kg 6 hours prior to carotid ligation depleted the striatum of CADF until 16 hours after stroke and appeared to reduce the spongiform degeneration of the neuropil, though it did not affect ischemic degeneration of neuronal cell bodies. The continued presence of CADF in the striatum for up to 16 hours after stroke supports the previously reported findings that CA nerve terminals are still functional for 8 hours after stroke and that CA metabolism continues even though levels of CA are reduced immediately after onset of ischemia due to carotid artery ligation.

Neuroprotection by Alpha 2-Adrenergic Agonists in Cerebral Ischemia

“…It is well-documented that one of the initial responses in the central nervous system after cerebral ischemia is the massive release of norepinephrine, among many other neurotransmitters, in the hippocampus and striatum [24,25,55,79]. High concentrations of norepinephrine may trigger neuronal damage by inducing imbalances between cerebral oxygen demand and oxygen supply, increasing the sensitivity of pyramidal neurons to excitatory neurotrans-mitters such as glutamate and decreasing perfusion in the ischemic area.…”

Executive (dys)function after stroke: special considerations for behavioral pharmacology

“…Further, within both pre-clinical and clinical settings, executive function can be assessed either through laboratory-based or naturalistic/real-world situations (Chan et al, 2008). Among the stroke population, it is common for one or more neurotransmitter systems to be altered as a downstream result of the ischemic or hemorrhagic insult (Kanthan et al, 1996; Weinberger & Nieves-Rosa, 1988; Wurtman & Zervas, 1974), potentially leading to poor long-term cognitive outcomes in which patients struggle with high-level intellectual functioning and additional behavioral sequela (e.g., drug-abuse potential or drug-seeking behavior, an area in which evidence is currently lacking and in further need of research, as well as post-stroke depression), which will be discussed later in this review.…”

A non-oxidative electrochemical approach to online measurements of dopamine release through laccase-catalyzed oxidation and intramolecular cyclization of dopamine

“…While the basal level of brain extracellular DA was previously reported to be within 5-20 nM (Chena and Budygin, 2007;Shou et al, 2006;Sam and Justice, 1996) and was beyond the detection limit of our online method, the extracellular DA levels were reported to increase from several to several hundred times during some phys- iological and pathological processes, such as cocaine-associated (Zernig et al, 1997;Hsin et al, 2002) and electrical simulation (Tepper et al, 1991;Suaud-Chagny et al, 1992) as well as brain ischemia (Bhardwaj et al, 1990;Ooboshi et al, 1992;Weinberger and Nieves-Rosa, 1988;Weinberger, 2006), and could thus be monitored by the method demonstrated in this study.…”