Neuronal Activity In Rats Research Articles

Inhibition of a hyperpolarization-activated current by clonidine in rat dorsal root ganglion neurons.

Whole cell voltage- and current-clamp recordings were carried out to investigate the effects of clonidine, an alpha 2-adrenoceptor agonist, in L4 and L5 dorsal root ganglion (DRG) neurons of the rat. In voltage-clamp mode, application of 20 microM clonidine reversibly reduced the inward current evoked by hyperpolarizing voltage steps. The "clonidine-sensitive current" was obtained by subtracting the current during clonidine application from the control current, and its properties were as follows. 1) It was a slowly activating inward current evoked by hyperpolarization. 2) The reversal potential in the standard extracellular solution ([K+]o = 5 mM, [Na+]o = 151 mM) was -38.3 mV, and reduction of [Na+]o shifted it to a more negative potential, whereas an increase of [K+]o shifted it to a more positive potential, indicating that the current was carried by Na+ and K+ (PNa/PK = 0.22). 3) The relationship between the chord conductance underlying the clonidine-sensitive current and voltage could be fitted by a Boltzmann equation. These results indicate that the clonidine-sensitive current corresponds to a hyperpolarization-activated current (Ih), i.e., clonidine inhibits Ih in rat DRG neurons. DRG neurons were classified as small (15.9-32.9 microns diam), medium-sized (33-42.9 microns), and large (43-63.6 microns), and 7 of 19, 24 of 25, and 22 of 22 of these types exhibited Ih with mean +/- SE clonidine-induced inhibition values of 36.1 +/- 3.5% (n = 7), 43.1 +/- 3.7% (n = 24), and 35.1 +/- 2.7% (n = 22), respectively. Clonidine application to L4 and L5 DRG neurons excised from rats the sciatic nerves of which had been transected 14-35 days previously (transected DRG neurons) also reduced Ih. In current-clamp mode, 9 of 13 intact and 4 of 6 transected medium-sized DRG neurons that exhibited Ih responded to clonidine with hyperpolarization (> 2 mV). Some medium-sized DRG neurons exhibited repetitive action potentials in response to a depolarizing current pulse, and clonidine reduced the firing discharge frequencies in 8 of 11 intact and 3 of 4 transected neurons tested. Injection of a hyperpolarizing current pulse produced time-dependent rectification in DRG neurons that exhibited Ih, and clonidine blocked this rectification in all intact and transected neurons tested. These results suggest that inhibition of Ih due to alpha 2-adrenoceptor activation contributes to modulation of DRG neuronal activity in rats. On the basis of our findings, we discuss the possible mechanisms whereby sympathetically released norepinephrine modulates the abnormal activity of DRG neuronal cell bodies after nerve injury.

Relation of cerebral blood flow to neuronal activity in rats with different susceptibilities to emotional stress as a predictor of cerebral ischemia severity

According to the results of 5-minute testing of free behavior in an open field carried out in different seasons, white laboratory rats were separated into three groups with high, medium, and low resistance to emotional stress, respectively (HR, MR, and LR rats), and it was found that the proportions of HR and MR rats, but not that of LR animals, varied with the season. Laser fluorimetry showed that local cerebral blood flow rates were highest in the HR group and lowest in the LR group. Conversely, wave amplitudes on the electroencephalogram (EEG) were lowest in the former group and highest in the latter. More significant differences among the three groups in levels of blood supply to the brain were revealed with a new method proposed to estimate blood flow per unit of EEG activity by calculating the ratio between the cerebral blood flow rate (expressed in ml/min/100 g brain tissue) and EEG activity (expressed in μV). HR rats proved to be more susceptible than their MR and LR counterparts to cerebral ischemia produced by occlusion of the common carotid arteries.

Hippocampal neuronal activity in rat and primate: Memory and movement

Hippocampal neuronal activity in rat and primate: Memory and movement

Role of nitric oxide in the coupling of cerebral blood flow to neuronal activation in rats.

Role of nitric oxide in the coupling of cerebral blood flow to neuronal activation in rats.

Cerebellar stimulation modulates thalamic noxious-evoked responses

Parafascicular (PF) neurons responding to noxious stimuli and focal electrical stimulation of midbrain, diencephalon, and hypothalamic nuclei, which send projections to PF, modulates the PF spontaneous and noxious-evoked responses. Some cerebellar efferents ascend to PF. This investigation attempted to study the effect of cerebellar stimulation on spontaneous and noxious-evoked PF neuronal activity in rats. It was observed that 26% (73/280) of PF neurons responded to a noxious stimulus. The PF neuronal population exhibits two cell types according to their response pattern following the noxious stimulus. One type of PF neurons were excited (n = 53) and were classified as nociceptive-on cells. The second type of PF neurons responded to noxious stimulus by a decrease in the ongoing firing rate (n = 20) and were classified as nociceptive-off cells. The responses of these two types of nociceptively identified cells were tested following cerebellar lateral nucleus stimulation (Lat.N.S.) utilizing several current intensities. Lat.N.S. with lower intensities (0.1-0.2 mA) elicited suppression of both spontaneous and nociceptive-evoked discharges of the nociceptive-on neurons, although higher intensities (0.4-0.6 mA) elicited excitation on both discharges of this type of neuron. In contrast, Lat.N.S. induced a monophasic intensity-dependent suppression of both the spontaneous and the nociceptive-evoked discharges of the nociceptive-off neurons. The results indicate that Lat.N.S. modulates the nociceptive-evoked responses of PF neurons. The possible role and related pathways of cerebellum in modulating noxious input were discussed.

Role of nitric oxide in the coupling of cerebral blood flow to neuronal activation in rats

We tested the hypothesis that nitric oxide (NO) is a mediator in the coupling of cerebral blood flow to neuronal activation. The production of NO was blocked in anesthetized rats with the NO-synthase inhibitor N ω- nitro- l-arginine ( l-NA). In controls, vibrissae stimulation for 60 s led to a fast (≤ 2 s), 17% increase in regional cerebral blood flow (rCBF) in the contralateral somatosensory cortex. Systemical (10 mg/kg) as well as topical (10 −3 M) application of l-NA reduced the response to stimulation by approximately 50%. Systemical application primarily attenuated the early component of the response, whereas topical application led to an attenuation throughout the whole 60-s stimulation interval. We conclude that NO is involved in rCBF coupling to neuronal activation.

The effects of a non-competitive NMDA receptor antagonist, MK-801, on behavioral hyperalgesia and dorsal horn neuronal activity in rats with unilateral inflammation

The involvement of NMDA receptors in rats with peripheral inflammation and hyperalgesia was evaluated by administration of the non-competitive NMDA receptor antagonist, MK-801. Inflammation and hyperalgesia was induced by intradermal injection of complete Freund's adjuvant (CFA) or carrageenan into the left hind paw. The latency of paw withdrawal from a thermal stimulus was used as a measure of hyperalgesia in awake rats. MK-801 (1.6 mg/kg, i.p., or 31.5 μg, intrathecal) significantly attenuated thermal hyperalgesia and reduced its duration in comparison to saline-injected rats ( P < 0.05). The receptive field size of nociceptive-specific and wide-dynamic-range neurons in the superficial and deep spinal dorsal horn recorded 24 h after injection of CFA was significantly reduced to 73 ± 6% ( P < 0.05, n = 8) and 74 ± 4% ( P < 0.05, n = 8) of control values, respectively, by a cumulative dose of 3 mg/kg of MK-801 (i.v.). MK-801 (2 mg/kg) prevented the expansion of the receptive fields of dorsal horn neurons recorded 5 ± 0.4 h (n = 5) after intradermal injection of CFA as compared to saline-injected rats ( P < 0.05). MK-801 had no significant effect on receptive field size of dorsal horn neurons in rats without CFA-induced inflammation but blocked a transient expansion of the receptive fields induced by 1 Hz, C-fiber intensity electrical stimulation of the sciatic nerve. The background activity and noxious heat-evoked response of dorsal horn neurons in rats with CFA-induced inflammation were primarily inhibited and noxious pinch-evoked activity was both facilitated and inhibited by the administration of MK-801. These results support the hypothesis that NMDA receptors are involved in the dorsal horn neuronal plasticity and behavioral hyperalgesia that follows peripheral tissue inflammation.

Effects of Thyrotropin-Releasing Hormone on Thermoregulatory Responses and Hypothalamic Neuronal Activity in Rats

Effects of Thyrotropin-Releasing Hormone on Thermoregulatory Responses and Hypothalamic Neuronal Activity in Rats

Effects of Thyrotropin-Releasing Hormone on Thermoregulatory Responses and Hypothalamic Neuronal Activity in Rats

Effects of Thyrotropin-Releasing Hormone on Thermoregulatory Responses and Hypothalamic Neuronal Activity in Rats

The functional states of the thalamus and the associated neuronal interplay.

The functional states of the thalamus and the associated neuronal interplay.

P-261 - Inhibitory effects of isofloxythepin on dopaminergic neuron activity in rats

P-261 - Inhibitory effects of isofloxythepin on dopaminergic neuron activity in rats

Functional properties of neurons in cat trigeminal subnucleus caudalis (medullary dorsal horn). I. Responses to oral-facial noxious and nonnoxious stimuli and projections to thalamus and subnucleus oralis.

Functional properties of neurons in cat trigeminal subnucleus caudalis (medullary dorsal horn). I. Responses to oral-facial noxious and nonnoxious stimuli and projections to thalamus and subnucleus oralis.

Supraoptic neuronal activity in rats during five days of water deprivation

Maintained single cell activity was recorded from rats deprived of water for 0, 1, 2, 3, 4, or 5 days; blood samples were obtained following recording. Mean supraoptic (Soa) cell firing rates were significantly elevated above Day 0 at Days 1, 3 and 4; rates of surrounding anterior hypothalamic (Haa) cells did not change with deprivation. Both plasma specific gravity and mean Soa cell firing rates showed increases on deprivation Day 1 and decreasing trends by Day 5, possibly suggesting a functional relationship. Significantly more Soa units (67%) than Haa units (15%) fired in a phasic pattern. The rate within bursts for Soa phasic neurons continued to rise with prolonged deprivation, much like plasma osmotic pressure, and may be more closely related to antidiuretic hormone depletion than overall mean rates.