Dynamic thermal mapping of rat brain during sensory stimulation and spreading depression

Using both techniques of thermovision and statistical analysis of thermal imaging, dynamics of temperature distribution over the dorsal surface of the brain were investigated through the intact skull during acute experiments on white rats. Both diffuse and regionally specific cerebral thermal reactions were observed during visual, acoustic, and somatosensory stimulation, together with multiple local thermal response, often following a specific pattern. These outline thermal effects differing from the compartment of the brain to another in degree, stability, and point of onset. Temperature waves developed together with spreading depression, produced in the cortex by injecting KC1. Once investigations had been performed this response could be divided into diffuse and spatially ordered components. The possible mechanisms of this thermal imaging of brain processes are discussed, together with how they are linked with changes in cerebral blood flow and neuronal metabolic thermal production.Institute of Higher Nervous Activity and Neurophysiology, Academy of Sciences of the USSR, Moscow. Institute of Radio Engineering and Electronics, Academy of Sciences of the USSR, Moscow. Translated from Neirofiziologiya, Vol. 18, No. 1, pp. 26–35, January–February, 1986.     

Influence of air ions on brain activity induced by electrical stimulation in the rat

The brain induced activity was studied in 18 rats wearing chronically skull implanted electrodes. The stimulating factor was various electrical stimulations of the mesencephalic reticular activating formation, given during the slow wave state of sleep. The results of 300 stimulations were measured by amplitude and frequency changes in the EEG simultaneously recorded. Animals previously exposed to positive air ions (3 weeks 80,000 ions/ml) exhibited lowered excitability of the reticulocortical system. Significantly higher stimulations were necessary to induce arousal. Negative air ions induced more intricate effects: brain excitability was lowered when tested with weak stimulations, but normal when evaluated with medium high level stimilations. Sleep seems first more stable but as stimulation increases, arousal is soon as effective as in controls. These results are in agreement with others findings in behavioral fields and partly explains them.     

Cortical spreading depression modifies components of the inflammatory cascade

As more information becomes available regarding the role of inflammation following stroke, it is apparent that some inflammatory mediators are detrimental and others are beneficial to the progression of ischemic injury. Cortical spreading depression (CSD) is known to impart some degree of ischemic tolerance to the brain and to influence the expression of many genes. Many of the genes whose expression is altered by CSD are associated with inflammation, and it appears likely that modulation of the inflammatory response to ischemia by CSD contributes to ischemic tolerance. Understanding which inflammatory processes are influenced by CSD may lead to the identification of novel targets in the effort to develop an acute treatment for stroke.     

化学刺激或电刺激大鼠穹窿下器官诱发的饮水行为和脑内c-fos表达

目的对化学刺激和电刺激穹窿下器官(subfornical organ, SFO)诱发的饮水量和脑内c-fos表达的结果是否不同进行比较. 方法向大鼠SFO内微量注射L-谷氨酸作为化学刺激,用恒流刺激SFO作为电刺激,记录诱发的1 h内饮水量,用免疫组化方法检测脑内Fos蛋白表达.结果电刺激和化学刺激SFO均能诱导相似的饮水行为,其诱饮率分别为75%和85.7%,1 h平均饮水量分别为(0.28±0.22) ml 和(0.31±0.15) ml ,明显高于各自的对照组(P<0.05),并均能使前脑的 11个脑区(终板血管器官, 正中视前核,室旁核,视上核,下丘脑外侧区,丘脑室旁核,联合核和中央内侧核,终纹床核,穹窿周背区和无名质)和后脑的4个脑区(最后区,孤束核,臂旁外侧核和中缝背核)相似的Fos蛋白表达.结论刺激SFO所诱导的饮水行为和脑内Fos蛋白表达是激活其神经元胞体的结果.     

Cortical spreading depression aggravates early brain injury in a mouse model of subarachnoid hemorrhage

Cortical spreading depression (CSD) has been observed during the early phase of subarachnoid hemorrhage (SAH). However, the effect of CSD on the cerebral blood flow (CBF) and cerebral oxyhemoglobin (CHbO) during the early phase of SAH has not yet been assessed directly. We, therefore, used laser speckle imaging and optical intrinsic sinal imaging to record CBF and CHbO during CSD and cerebral cortex perfusion (CCP) at 24 hours after CSD in a mouse model of SAH. SAH was induced by blood injection into the prechiasmatic cistern. When CSD occurred, the change trend of CBF and CHbO in Sham group and SAH group was the same, but ischemia and hypoxia in SAH group was more significant. At 24 hours after SAH, the CCP of CSD group was lower than that of no CSD group, and the neurological function score of CSD group was lower. We conclude that induction of CSD further aggravates cerebral ischemia and worsens neurological dysfunction in the early stage of experimental SAH. Our study underscores the consequence of CSD in the development of early brain injury after SAH.     

Cortical and subcortical spreading depression in rats produced by focused ultrasound

Steady potential shifts produced by focused ultrasond were recorded in the cerebral cortex, hippocampus, thalamus, and caudate nucleus. Impulses of 50–100 msec duration were presented at a frequency of 5 and 10 Hz. Negative steady potential shifts were produced in each of the structures investigated, which gradually increased during rhythmic electrical reaction to reach –3 to –7 mV within 10–30 sec, often succeeded by a wave of spreading depression (SD). In each structure analyzed amplitude of SD waves measured 20–30 mV, lasting 30–40 sec in the cortex, the caudate nucleus and the thalamus, and 80–120 sec in the hippocampus. In unanesthetized and lightly anesthetized animals SD waves were on occasions the precursors of convulsive discharges forming under the action of focused ultrasound. Ultrasound at threshold doses proved ineffective for 5–7 min after the occurrence of an SD wave, but again evoked repeated SD waves once the refractory period had ended. Accordingly, local effects produced by focused ultrasound can result in functional blockage of the brain structures due to cortical and subcortical spreading depression.Institute of Higher Nervous Activity and Neurophysiology, Academy of Sciences of the USSR, Moscow. Institute of Brain Research, All-Union Research Center of Mental Health, Academy of Medical Sciences of the USSR, Moscow. N. N. Andreev Acoustic Institute, Academy of Sciences of the USSR, Moscow. Translated from Neirofiziologiya, Vol. 18, No. 1, pp. 55–61, January–February, 1986.     

Visual illusions induced by electrical stimulation of the labyrinth

In normal subjects, electrical stimulation of the labyrinth with surface electrodes located on the mastoid process induced illusions of shifting of a fixed point of light in darkness similar to the oculogyral illusion induced by rotatory vestibular stimulation. Monoaural anodal stimulation of the right labyrinth induced apparent shift of the target to the left; with cathodal stimulation, it shifted to the right; threshold current was 0.35–0.6 mA. When the current strength increased, the amplitude and rate of apparent movement of the target increased approximately linearly. With binaural, bipolar stimulation, the illusory movement of the target was toward the site of the cathode and the threshold decreased by 1.5–2.5 times. With binaural, monopolar stimulation, the target seemed to shift along the vertical and the threshold current was 1.4–3.0 mA. Eye movement appeared at substantially higher currents than those resulting in apparent movement of the target. It is suggested that visual illusions are linked not to vestibular eye-movement reactions, but to the effect vestibular signals have on the spatial perception system.Institute of Problems of Information Transmission, Academy of Sciences of the USSR, Moscow. Translated from Neirofiziologiya, Vol. 23, No. 3, pp. 321–327, May–June, 1991.     

Cortical activation induced by intraoral stimulation with water in humans

Studies of gustatory processing frequently utilize water as a control stimulus. However, the neural representations of intraoral stimulation with water have received little attention. We report a series of positron emission tomography studies involving intraoral stimulation with deionized distilled water. Attempting to taste water produced large, bilateral activations in insular, opercular, Rolandic and cerebellar cortices relative to resting with eyes closed or 'smelling' odorless air. The magnitude and volume of activation was substantially reduced when tasting water was contrasted with voluntary swallowing. This indicates that much of the activity induced by water reflects intraoral somatosensory or motor processing. Nevertheless, portions of the insula, operculum, post-central gyrus and cerebellum remained significantly activated in the contrast between 'tasting' water and swallowing. This activity appears to represent a specific neural correlate of fluid stimulation, and may reflect aspects of trigeminal, gustatory or thermal coding. These findings emphasize the large volume of cortex dedicated to intraoral processing, and highlight the importance of controlling for nongustatory factors in studies of gustation.     

Cortical alpha-adrenoceptor downregulation by tricyclic antidepressants in the rat brain

The aim of the present study was to examine the effect of chronic tricyclic antidepressants (TCAs) treatment on the density of -adrenoceptors in the rat brain. Density of ₁- and ₂-adrenoceptors was measured in cortex and hippocampus of rats treated with imipramine (IMI, 5 mg/kg body weight), desipramine (DMI, 10 mg/kg body weight), clomipramine (CMI, 10 mg/kg body weight) and amitriptyline (AMI, 10 mg/kg body weight), for 40 days, using [³H]prazosin and [³H]clonidine, respectively. The density of cortical ₁-adrenoceptors was significantly decreased with IMI (46%), DMI (21%), CMI (50%) and AMI (67%) treatment, without altering the affinity of the receptor. The density of cortical ₂-adrenoceptors was also significantly decreased with DMI (69%), CMI (81%) and AMI (80%) treatment, without affecting the affinity for [³H]clonidine. The density of hippocampal ₁-adrenoceptors was significantly decreased only with AMI treatment (47%), without affecting the affinity for [³H]prazosin. However, no change in hippocampal ₂-adrenoceptor density was observed with any of these TCAs. The results suggest that chronic antidepressant (AD) treatment downregulates the cortical, but not hippocampal, ₁- and ₂-adrenoceptors in rat brain. The region-specific downregulation of ₁- and ₂-adrenoceptors density, which occur after prolonged AD treatment, may underline the therapeutic mechanism of action.     

弱电刺激大鼠迷走神经中枢端在海马CA1区产生周期性theta电振荡

目的：观察弱电刺激迷走神经中枢端对正常大鼠海马细胞放电及场电的影响。方法：雄性成年大鼠45只．分离其颈部左侧迷走神经,结扎外周端,弱电（10Hz,0．5ms,1.5～5.0V,15-20／chain）刺激,每5min一次,共20串：记录右侧海马CAI细胞放电及双侧海马CAI场电。结果：双侧场电出现周期性theta电振荡（38／45,84．4％）,伴有theta—on（n=30）和theta—off（n=5）两种形式的非簇状紧张性细胞放电.结论：弱电刺激迷走神经中枢端激活海马CAI区网络,并对网络内细胞放电有紧张性调制作用.     

Thermal distribution over the cortical surface of the rat brain under direct electrical stimulation

The dynamics of thermal diffusion from the dorsal brain surface were studied in white rats through the intact skull during acute experiments on immobilized or Nembutal anesthetized white rats using a new thermovisualization technique involving direct electrical stimulation of the cortex. Local cortical heating of a 1–4 mm site in the vicinity of the electrodes set in within 160 msec after presentation of a single stimulus, reaching a maximum of 0.2°C by the 2nd-5th sec and slowly decaying to the initial level by the 2nd-3rd min. At the same time, but at a somewhat slower rate, the symmetrically opposite local site in the other hemisphere heated up, followed by a small area in the ipsilateral motor cortex and a number of other zones. Depending on the dose administered, Nembutal inhibits and decelerates the development of these effects and localizes them, raises the minimum threshold of their occurrence, and prolongs their closed state. As anesthesia deepened, the primary heat focus near the stimulating electrodes persisted the longest. The mechanisms underlying local cortical thermal responses and the time parameters of these are discussed and compared with those of the dynamics of standard electrographic effects.Institute of Higher Nervous Activity and Neurophysiology, Academy of Sciences of the USSR, Moscow. Translated from Neirofiziologiya, Vol. 19, No. 2, pp. 216–223, March–April, 1987.     

On the mechanism of the cortical depression induced by afferent stimulation

The cortical depression induced by the stimulation of some afferent fibers affects strychnine spikes elicited in two different ways: by direct electrical stimulation, and through the evoked potentials induced at the somatosensory area by single shocks to the radial nerve. The effects on these two types of responses were found to be very similar, which was taken to indicate that the site of action of the mechanism involved is the same, that is, the non-synaptic membranes of the dendrites of pyramidal neurons. It is suggested that the depressant action is mediated through the serotonergic neurons, since the previous administration of 5,6-Dihydroxytryptamine (5,6-DHT) blocked the changes. The 5-Hydroxytryptamine (5-HT) liberated would act as a neurohumoral agent, since the synaptic mechanisms do not seem to be involved and the effects are manifested in a diffuse manner.     

Enhanced extinction of aversive memories by high-frequency stimulation of the rat infralimbic cortex

Electrical stimulation of the rodent medial prefrontal cortex (mPFC), including the infralimbic cortex (IL), immediately prior to or during fear extinction training facilitates extinction memory. Here we examined the effects of high-frequency stimulation (HFS) of the rat IL either prior to conditioning or following retrieval of the conditioned memory, on extinction of Pavlovian fear and conditioned taste aversion (CTA). IL-HFS applied immediately after fear memory retrieval, but not three hours after retrieval or prior to conditioning, subsequently reduced freezing during fear extinction. Similarly, IL-HFS given immediately, but not three hours after, retrieval of a CTA memory reduced aversion during extinction. These data indicate that HFS of the IL may be an effective method for reducing both learned fear and learned aversion.