Spreading Depression in Rabbit, Cat and Monkey

Abstract

Rabbits, cats and monkeys show species difference in the consistency and frequency with which spreading depression (SD) can be elicited during the first hours after exposure of the cortex. In the rabbit SD can be produced consistently at 6–10-minute intervals. In most of the preparations of the cat it is also possible to produce a series of SDs when using a longer interval (15–20 min.) between stimulations. Only rarely is it possible to obtain in the monkey a series of SDs even when long intervals are interjected between stimuli. However, the majority of preparations responded at least once with a SD. It has been possible to lead off SD in rabbits and cats with extradural electrodes implanted in the skull 5–7 days earlier. These electrodes were in most instances flush with the dural surface of the skull, resting on the undamaged dura. In the rabbit photo-Metrazol stimulation can produce SD which also has been recorded with the implanted electrodes. Since there is no reason to believe that the cortex in these latter experiments was damaged or in any other way abnormal, the conclusion was drawn that normal cortex can exhibit spreading depression.

Spreading Depolarization, A Pathophysiological Mechanism of Stroke and Migraine Aura

“…Similar observations were also made in an animal model for epileptogenesis following blood-brain barrier disruption [104]. In addition, there are differences in cytoarchitecture and tissue electrical resistivity between normal rodents and primates that render the former somewhat more susceptible to spreading depolarization [105]. In any case, all this indicates that much stronger triggers would have been necessary to induce spreading depolarizations in patients with chronic epilepsy than in healthy rats.…”

Mechanisms involved in the cerebrovascular dilator effects of cortical spreading depression

“…The veracity of these early observations by Leão (1944) on pial arteries and arterioles is such that they are very similar to more recent findings made in the same species over 40 years later (Shibata et al ., 1990). The pioneering research of Leão (1944) was soon followed by cerebral vascular studies in the rabbit and cat by Van Harreveld and Stamm (1952) and Van Harreveld and Ochs (1956), respectively. During this period, the characteristics and mechanisms of CSD were examined in detail (Grafstein, 1956; Van Harreveld, 1959).…”

“…As first described by Leão (1944), cortical spreading depression (CSD) represents a wave of neuronal depolarization followed by repolarization, which once initiated by a variety of chemical, electrical, and mechanical stimuli (Ayata and Moskowitz, 2006; Grafstein, 1956; Shibata et al ., 1990; Somjen, 2001; Van Harreveld, 1959; Verhaegen et al ., 1992; Verhaegen et al ., 1992) progresses outward across the surface of the cerebral cortex of both lissencephalic and gyrencephalic brains at a speed of approximately 2-5 mm/minutes (Leão, 1944; Van Harreveld et al ., 1956; Goadsby, 1996; Grafstein, 1956; Lauritzen, 1987; Shimizu et al ., 2000a; Shibata et al ., 1990; Smith et al ., 2006; Wahl et al ., 1996). Although leading to a transient depression of cortical activity, repeated CSDs in the healthy brain do not lead to pronounced neural damage (Nedergaard and Hansen, 1988) and may even be beneficial by promoting the development of protection against ischemic stress (Horiguchi et al ., 2005b; Kawahara et al ., 1995; Kiss et al ., 2004; Kobayashi et al ., 1995; Matsushima et al ., 1996; Otori et al ., 2003).…”

“…Spreading depression-like events occur in other brain locations such as cerebellum (Case et al ., 2002) and hippocampus (Herreras and Somjen, 1993; Kunkler and Kraig, 1998), and can also be induced in retina (de Oliveira Castro and Martins-Ferreira, 1970; Martins-Ferreira and de Oliveira Castro, 1966; 1971; Farkas et al ., 2008). Cortical spreading depression has been shown to occur in mature brains of all mammalian species studied including man (Van Harreveld et al ., 1956; Somjen, 2001; Lauritzen, 1987a; Goadsby, 1996; Yokota et al ., 2002; Shibata et al ., 1990; Fabricius et al ., 2006; Lauritzen, 1987 & 2001; Goadsby, 2005; Dalkara et al ., 2006), and is associated with major changes in extracellular levels of ions (Hansen and Zeuthen, 1981; Hansen et al ., 1980), neurotransmitters (Davies et al ., 1995), metabolic rate (Mayevsky and Weiss, 1991), and cerebral blood flow (CBF) (Table 1). For example, CSD is associated with a dramatic but short-lived rise in K + concentration from 3 to more than 50 mM (Hansen and Zeuthen, 1981).…”

Dynamic Diffusion Magnetic Resonance Imaging of Infarct Formation and Peri-infarct Spreading Depression after Middle Cerebral Artery Occlusion (MCAO) in macacca fasicularis

“…CSD has been demonstrated in experimental animal models by application of different types of stimuli to the cortex; mechanical (traumatic brain injury and stroke), chemical (direct potassium chloride solution application to the cortex) and electrical stimulation [2-8]. While experimental CSD induction in the normally perfused brain does not result in injury to the involved cortex, it has been hypothesized that CSDs in the vicinity of an ischemic lesion could add to the extent of the lesion, due to the increased metabolic demand during repolarization.…”