Journal of Neurophysiology
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Astrocytic Glutamate Release-Induced Transient Depolarization and Epileptiform Discharges in Hippocampal CA1 Pyramidal Neurons A paroxysmal depolarization shift (PDS) has been suggested to be a hallmark for epileptic activity in partial-onset seizures. By monitoring membrane potentials and currents in pairs of pyramidal neurons and astrocytes with dual patch-clamp recording and exocytosis of vesicles from astrocytes with two-photon laser scanning microscopy in hippocampal slices, we found that infusion of inositol 1,4,5-trisphosphate (IP3 ) into astrocytes by patch pipettes induced astrocytic glutamate release that triggered a transient depolarization (TD) and epileptiform discharges in CA1 pyramidal neurons. The TD is due to a tetrodotoxin (TTX)-insensitive slowly decaying transient inward current (STC). Astrocytic glutamate release simultaneously triggers both the STC in pyramidal neurons and a transport current (TC) in astrocytes. The neuronal STC is mediated by ionotropic glutamate receptors leading to the TD and epileptiform discharges; while the astrocytic TC is a glutamate reuptake current resulting from transporting released glutamate into the patched astrocyte. Fusion of a large vesicle in astrocytes was immediately followed by an astrocytic TC, suggesting that the fused vesicle contains glutamate. Both fusion of large vesicles and astrocytic TCs were blocked by tetanus toxin (TeNT), suggesting that astrocytic glutamate release is via SNARE-dependent exocytosis of glutamate-containing vesicles. In the presence of TTX, the epileptogenic reagent, 4-AP, also induced similar neuronal STCs and astrocytic TCs, suggesting that astrocytic glutamate release may play an epileptogenic role in initiation of epileptic seizures under pathological conditions. Our study provides a novel mechanism, astrocytic release of glutamate, for seizure initiation.
Journal of Neurophysiology - Tập 94 Số 6 - Trang 4121-4130 - 2005
Sex-Related Differences in Human Pain and Rat Afferent Discharge Evoked by Injection of Glutamate Into the Masseter Muscle Animal studies have suggested that tissue injury–related increased levels of glutamate may be involved in peripheral nociceptive mechanisms in deep craniofacial tissues. Indeed, injection of glutamate (0.1–1 M, 10 μl) into the temporomandibular region evokes reflex jaw muscle responses through activation of peripheral excitatory amino acid receptors. It has recently been found that this glutamate-evoked reflex muscle activity is significantly greater in female than male rats. However, it is not known whether peripheral administration of glutamate, in the same concentrations that evoke jaw muscle activity in rats, causes pain in humans or activates deep craniofacial nociceptive afferents. Therefore we examined whether injection of glutamate into the masseter muscle induces pain in male and female volunteers and, since masseter afferent recordings were not feasible in humans, whether glutamate excites putative nociceptive afferents supplying the masseter muscle of male and female rats. Injection of glutamate (0.5 M or 1.0 M, 0.2 ml) into the masseter muscle of both men and women caused significantly higher levels of peak pain, duration of pain, and overall pain than injection of isotonic saline (0.2 ml). In addition, glutamate-evoked peak and overall muscle pain in women was significantly greater than in men. In rats of both sexes, glutamate (10 μl, 0.5 M) evoked activity in a subpopulation of masseter muscle afferents ( n = 36) that projected to the subnucleus caudalis, an important relay of noxious input from the craniofacial region. The largest responses to glutamate were recorded in muscle afferents with the slowest conduction velocities (2.5–5 m/s). Further, glutamate-evoked masseter muscle afferent activity was significantly greater in female than in male rats. These results indicate that glutamate injection into the masseter muscle evokes pain responses that are greater in women than men and that one possible mechanism for this difference may be a greater sensitivity to glutamate of masseter muscle afferents in females. These sex-related differences in acute experimental masseter muscle pain are particularly interesting given the higher prevalence of many chronic muscle pain conditions in women.
Journal of Neurophysiology - Tập 86 Số 2 - Trang 782-791 - 2001
Characteristics of Glutamate-Evoked Temporomandibular Joint Afferent Activity in the Rat Injection of glutamate into the rat temporomandibular joint (TMJ) capsule can reflexly induce a prolonged increase in the electromyographic (EMG) activity of the jaw muscles, however, the characteristics of TMJ afferents activated by glutamate have not been investigated. In the present study, we examined the effect of glutamate injection into the TMJ capsule on jaw muscle EMG activity and the extracellularly recorded activity of single trigeminal afferents that had receptive fields in the TMJ tissue and antidromically identified projections to the brain stem subnucleus caudalis (Vc) in rats of both sexes. Glutamate (0.05–1.0 M, 10 μl) injection into the TMJ capsule evoked EMG activity in a dose-related manner; however, at concentrations of 0.5 and 1.0 M, glutamate-evoked digastric muscle responses were greater in female than in male rats. In experiments where jaw muscle EMG and afferent activity were recorded simultaneously, glutamate (0.5 M, 10 μl) injection into the TMJ capsule evoked activity in the jaw muscles as well as in 27 (26 Aδ and 1 C-fiber afferent) of 34 trigeminal afferents that could be activated by blunt mechanical stimulation of the TMJ tissue. In these experiments, glutamate-evoked jaw muscle activity was significantly increased for 6 min after the glutamate injection, whereas afferent activity was significantly increased only during the first minute after the glutamate injection. The glutamate-evoked afferent activity was inversely related to conduction velocity and, in afferents with conduction velocities <10 m/s, was significantly greater in female ( n = 6) than in male ( n = 10) rats. These results suggest that glutamate excites putative nociceptive afferents within the TMJ to a greater degree in female than in male rats. This sex-related difference in afferent discharge may, in part, underlie sex-related differences in glutamate-evoked jaw muscle EMG activity.
Journal of Neurophysiology - Tập 85 Số 6 - Trang 2446-2454 - 2001
Activation of Peripheral GABA<sub>A</sub> Receptors Inhibits Temporomandibular Joint–Evoked Jaw Muscle Activity Activation of peripheral GABAA receptors inhibits temporomandibular joint–evoked jaw muscle activity. We have previously shown that injection of mustard oil or glutamate into rat temporomandibular joint (TMJ) tissues, an experimental model of acute TMJ injury, can reflexly induce a prolonged increase in the activity of both digastric (jaw-opener) and masseter (jaw-closer) muscles. In this study, GABA was applied to the TMJ region by itself or in combination with glutamate, and the magnitude of evoked jaw muscle electromyographic (EMG) activity was measured. Application of GABA alone to the TMJ region did not evoke significant jaw muscle EMG activity when compared with normal saline controls. In contrast, co-application of GABA and glutamate into the TMJ region decreased the magnitude of glutamate-evoked EMG activity. This GABA-mediated inhibition of glutamate-evoked EMG activity followed an inverse dose-response relationship with an estimated median inhibitory dose (ID50 ) of 0.17 ± 0.05 (SE) μmol and 0.031 ± 0.006 μmol for the digastric and masseter muscles, respectively. Co-administration of the GABAA receptor antagonist bicuculline (0.05 μmol) but not the GABAB receptor antagonist phaclofen (0.05 or 0.15 μmol) reversed the suppressive actions of GABA, indicating that this action of GABA may be mediated by peripheral GABAA receptors located within the TMJ region. Our results suggest that activation of peripheral GABAA receptors located within the TMJ region could act to decrease the transmission of nociceptive information.
Journal of Neurophysiology - Tập 81 Số 4 - Trang 1966-1969 - 1999
HIPPOCAMPAL ELECTRICAL ACTIVITY IN AROUSAL
Journal of Neurophysiology - Tập 17 Số 6 - Trang 533-557 - 1954
RABBIT EEG "THETA" RHYTHM: ITS ANATOMICAL SOURCE AND RELATION TO ACTIVITY IN SINGLE NEURONS
Journal of Neurophysiology - Tập 23 Số 4 - Trang 403-420 - 1960
Strategies for Dynamic Stability During Locomotion on a Slippery Surface: Effects of Prior Experience and Knowledge Falls due to slips are prevalent in everyday life. The purpose of this study was to determine the reactive recovery responses used to maintain dynamic stability during an unexpected slip, establish the time course of response adaptation to repeated slip perturbations, and distinguish the proactive strategies for negotiating a slippery surface. Twelve young adults participated in the study in which a slip was generated following foot contact on a set of steel free-wheeling rollers. Surface electromyographic (EMG) data were collected from rectus femoris, biceps femoris, tibialis anterior, and the medial head of gastrocnemius on the perturbed limb. Whole body kinematics were recorded using an optical imaging system: from this the center of mass, foot angle, and medial-lateral stability margins were determined. In addition, braking/loading and accelerating/unloading impulses while in contact with the rollers and the rate of loading the rollers were determined from ground reaction forces. Results demonstrate that the reactive recovery response to the first slip consisted of a rapid onset of a flexor synergy (146–199 ms), a large arm elevation strategy, and a modified swing limb trajectory. With repeated exposure to the slip perturbation, the CNS rapidly adapts within one slip trial through global changes. These changes include the attenuation of muscle response magnitude, reduced braking impulse, landing more flat-footed, and elevating the center of mass. Individuals implement a “surfing strategy” while on the rollers when knowledge of the surface condition was available before hand. Furthermore, knowledge of a slip results in a reduced braking impulse and rate of loading, a shift in medial-lateral center of mass closer to the support limb at foot contact on the rollers and a more flat foot landing. In conclusion, prior experience with the perturbations allows subsequent modification and knowledge of the surface condition results in proactive adjustments to safely traverse the slippery surface.
Journal of Neurophysiology - Tập 88 Số 1 - Trang 339-353 - 2002
The Pedunculopontine Tegmental Nucleus: A Second Cholinergic Source for Frequency-Specific Auditory Plasticity Cholinergic modulation is essential for many brain functions and is an indispensable component of the prevalent models attempting to understand the neural mechanism responsible for learning-induced auditory plasticity. Unlike the cholinergic basal forebrain, the cholinergic pedunculopontine tegmental nucleus (PPTg) has received little attention. This study was designed to confirm whether the PPTg enables frequency-specific plasticity in the ventral division of the medial geniculate body of the thalamus (MGBv). Using the mouse model, we paired electrical stimulation of the PPTg with tone stimulation to help define the role of the PPTg. The receptive fields of MGBv neurons were examined before and after the paired stimulation; they were quantified in this study by best frequency (BF), response threshold, dynamic range, and spike number. We found that the electrical stimulation of the PPTg together with a tone presentation shifted the BFs of MGBv neurons upward when the frequency of the paired tone was higher than that of the control BF. Similarly, the BFs shifted downward when the frequency of the paired tone was lower than that of the control BF. The BFs of MGBv neurons, however, remained unchanged when the frequency of the paired tone was the same as that of the control BF. There was a linear relationship between the BF shift of MGBv neurons and the difference between the frequency of the paired tone and the control BF of MGBv neurons. Highly frequency specific changes were also observed in the response threshold, dynamic range, and spike number. This frequency-specific plasticity was largely eliminated by the microinjection of the muscarinic receptor antagonist atropine into the MGBv before the paired stimulation. Our findings suggest that the PPTg, like the cholinergic basal forebrain, is an important cholinergic source that enables frequency-specific plasticity in the central auditory system.
Journal of Neurophysiology - Tập 105 Số 1 - Trang 107-116 - 2011
CHEMICAL TRANSMITTER SUBSTANCES IN BRAIN STEM OF CAT
Journal of Neurophysiology - Tập 24 Số 1 - Trang 80-90 - 1961
Nicotinic acetylcholine receptor subunit α<sub>7</sub>-knockout mice exhibit degraded auditory temporal processing The CHRNA7 gene that encodes the α7 -subunit of the nicotinic acetylcholine receptor (α7 -nAChR) has been associated with some autism spectrum disorders and other neurodevelopmental conditions characterized, in part, by auditory and language impairment. These conditions may include auditory processing disorders that represent impaired timing of neural activity, often accompanied by problems understanding speech. Here, we measure timing properties of sound-evoked activity via the auditory brainstem response (ABR) of α7 -nAChR knockout mice of both sexes and wild-type colony controls. We find a significant timing delay in evoked ABR signals that represents midbrain activity in knockouts. We also examine spike-timing properties of neurons in the inferior colliculus, a midbrain nucleus that exhibits high levels of α7 -nAChR during development. We find delays of evoked responses along with degraded spiking precision in knockout animals. We find similar timing deficits in responses of neurons in the superior paraolivary nucleus and ventral nucleus of the lateral lemniscus, which are brainstem nuclei thought to shape temporal precision in the midbrain. In addition, we find that other measures of temporal acuity including forward masking and gap detection are impaired for knockout animals. We conclude that altered temporal processing at the level of the brainstem in α7 -nAChR-deficient mice may contribute to degraded spike timing in the midbrain, which may underlie the observed timing delay in the ABR signals. Our findings are consistent with a role for the α7 -nAChR in types of neurodevelopmental and auditory processing disorders and we identify potential neural targets for intervention. NEW & NOTEWORTHY Disrupted signaling via the α7 -nicotinic acetylcholine receptor (α7 -nAChR) is associated with neurodevelopmental disorders that include impaired auditory processing. The underlying causes of dysfunction are not known but a common feature is abnormal timing of neural activity. We examined temporal processing of α7 -nAChR knockout mice and wild-type controls. We found degraded spike timing of neurons in knockout animals, which manifests at the level of the auditory brainstem and midbrain.
Journal of Neurophysiology - Tập 122 Số 2 - Trang 451-465 - 2019
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