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Russell, Noah A.; Horii, Arata; Smith, Paul F.; Darlington, Cynthia L.; Bilkey, David K.
doi: 10.1152/jn.00953.2005pmid: 16772515
The hippocampus has a major role in memory for spatial location. Theta is a rhythmic hippocampal EEG oscillation that occurs at ∼8 Hz during voluntary movement and that may have some role in encoding spatial information. We investigated whether, as part of this process, theta might be influenced by self-movement signals provided by the vestibular system. The effects of bilateral peripheral vestibular lesions, made ≥60 days prior to recording, were assessed in freely moving rats. Power spectral analysis revealed that theta in the lesioned animals had a lower power and frequency compared with that recorded in the control animals. When the electroencephalography (EEG) was compared in epochs matched for speed of movement and acceleration, theta was less rhythmic in the lesioned group, indicating that the effect was not a result of between-group differences in this behavior. Blood measurements of corticosterone were also similar in the two groups indicating that the results could not be attributed to changes in stress levels. Despite the changes in theta EEG, individual neurons in the CA1 region of lesioned animals continued to fire with a periodicity of ∼8 Hz. The positive correlation between cell firing rate and movement velocity that is observed in CA1 neurons of normal animals was also maintained in cells recorded from lesion group animals. These findings indicate that although vestibular signals may contribute to theta rhythm generation, velocity-related firing in hippocampal neurons is dependent on nonvestibular signals such as sensory flow, proprioception, or motor efference copy. Address for reprint requests and other correspondence: D. K. Bilkey, Dept. of Psychology and Neuroscience Research Centre, University of Otago, 95 Union St., PO Box 56, Dunedin, New Zealand (E-mail: [email protected] )
Ricci-Tersenghi, F.; Minneci, F.; Sola, E.; Cherubini, E.; Maggi, L.
doi: 10.1152/jn.01202.2005pmid: 16598063
We developed and analytically solved a simple and general stochastic model to distinguish the univesicular from the multivesicular mode of glutamate release. The model solution gives analytical mathematical expressions for average values of quantities that can be measured experimentally. Comparison of these quantities with the experimental measures allows one to discriminate the release mode and to determine the most probable values of model parameters. The model has been validated at glutamatergic CA3–CA1 synapses in the hippocampus from newborn (P1–P5 old) rats. Our results strongly support a multivesicular type of release process requiring a variable pool of immediately releasable vesicles. Moreover, computing quantities that are functions of the model parameters, the mean amplitude of the synaptic response to the release of a single vesicle ( q ) was estimated to be 5–10 pA, in very good agreement with experimental findings. In addition a multivesicular type of release was supported by the following experimental evidences: 1 ) a high variability of the amplitude of successes, with a coefficient of variation ranging from 0.12 to 0.73; 2 ) an average potency ratio a 2 /a 1 between the second and first response to a pair of stimuli >1; and 3 ) changes in the potency of the synaptic response to the first stimulus when the release probability was modified by increasing or decreasing the extracellular calcium concentration. Our results indicate that at Schaffer collateral–CA1 synapses of the neonatal rat hippocampus a single action potential may induce the release of more than one vesicle from the same release site. Address for reprint requests and other correspondence: L. Maggi, Dipartimento di Fisiologia Umana e Farmacologia, University "La Sapienza," Piazzale A. Moro 5, 00185 Rome, Italy (E-mail: [email protected] )
Berryman, L. J.; Yau, J. M.; Hsiao, S. S.
doi: 10.1152/jn.01190.2005pmid: 16641375
In this study we investigate the haptic perception of object size. We report the results from four psychophysical experiments. In the first, we ask subjects to discriminate the size of objects that vary in surface curvature and compliance while changing contact force. We show that objects exhibit size constancy such that perception of object size using haptics does not change with changes in contact force. Based on these results, we hypothesize that size perception depends on the degree of spread between the digits at initial contact with objects. In the second experiment, we test this hypothesis by having subjects continuously contact an object that changes dynamically in size. We show that size perception takes into account the compliance of the object. In the third and fourth experiments we attempt to separate the individual contributions of proprioceptive and cutaneous input. In the third, we test the ability of subjects to perceive object size after altering the sensitivity of cutaneous receptors with adapting vibratory stimuli. The results from this experiment suggest that initial contact is signaled by the cutaneous slowly adapting type 1 afferents (SA1) and/or the rapidly adapting afferents (RA). In the last experiment, we block cutaneous input at the site of contact by anesthetizing the digital nerves and show that proprioceptive information alone provides only a rough estimate of object size. We conclude that the perception of object size depends on inputs from SA1 and possibly RA afferents, combined with inputs from proprioceptive afferents that signal the spread between digits. Address for reprint requests and other correspondence: S. Hsiao, Zanvyl Krieger Mind/Brain Institute, Johns Hopkins University, 338 Krieger Hall, 3400 N. Charles St., Baltimore, MD 21218 (E-mail: [email protected] )
Williford, Tori; Maunsell, John H. R.
doi: 10.1152/jn.01207.2005pmid: 16772516
Previous single-unit studies of visual cortex have reported that spatial attention modulates responses to different orientations and directions proportionally, such that it does not change the width of tuning functions for these properties. Other studies have suggested that spatial attention causes a leftward shift in contrast response functions, such that its effects on responses to stimuli of different contrasts are not proportional. We have further explored the effects of attention on stimulus-response functions by measuring the responses of 131 individual V4 neurons in two monkeys while they did a task that controlled their spatial attention. Each neuron was tested with a set of stimuli that spanned complete ranges of orientation and contrast during different states of attention. Consistent with earlier reports, attention scaled responses to preferred and nonpreferred orientations proportionally. However, we did not find compelling evidence that the effects were best described by a leftward shift of the contrast response function. The modulation of neuronal responses by attention was well described by either a leftward shift or proportional scaling of the contrast response function. Consideration of differences in experimental design and analysis that may have contributed to this discrepancy suggests that it was premature to exclude a proportional scaling of responses to different contrasts by attention in favor of a leftward shift of contrast response functions. The current results reopen the possibility that the effects of attention on stimulus-response functions are well described by a single proportional increase in a neuron's response to all stimuli. Address for reprint requests and other correspondence: J.H.R. Maunsell, Harvard Medical School, Department of Neurobiology, 220 Longwood Ave., Boston, MA 02115 (E-mail: [email protected] )
Onimaru, Hiroshi; Kumagawa, Yuko; Homma, Ikuo
doi: 10.1152/jn.01175.2005pmid: 16495360
There are at least two respiration-related rhythm generators in the medulla: the pre-Bötzinger complex, which produces inspiratory (Insp) neuron bursts, and the parafacial respiratory group (pFRG), which produces predominantly preinspiratory (Pre-I) neuron bursts. The pFRG Pre-I neuron activity has not been correlated with motor neuron activity in slice or block preparations of rostral medulla. In this study, we attempted to detect pFRG Pre-I activity as motor output in the rostral medulla. We recorded respiratory activity of the facial nerve in the brain stem–spinal cord preparation of 0- to 2-day-old rats. Facial nerve activity consisted of preinspiratory, Insp, and postinspiratory activity. Pre- and postinspiratory activity corresponded well with membrane potential trajectories of Pre-I neurons in the rostral ventrolateral medulla. In response to perfusion of 1 µM DAMGO (a µ-opiate agonist), fourth cervical ventral root (C4) Insp activity was depressed and facial nerve activity continued to synchronize with Pre-I neuron bursts. After transverse sectioning between the levels of the pre-Bötzinger complex and the pFRG, C4 Insp activity recovered within 15 min, but facial nerve activity was inhibited. When DAMGO was applied, C4 Insp activity was inhibited, and rhythmic facial nerve activity recovered. Subsequent elevation of K + concentration reinduced C4 activity, but facial nerve activity was inhibited. Whole cell recordings in the rostral block revealed the presence of putative Pre-I neurons, the activity of which was synchronized with facial nerve activity. These results show that the rostral medulla, not including the pre-Bötzinger complex, produces Pre-I–like rhythmic activity that can be monitored as facial nerve motor output in newborn rat in vitro preparations. Address for reprint requests and other correspondence: H. Onimaru, Department of Physiology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142, Japan (E-mail: [email protected] )
Mölle, Matthias; Yeshenko, Oxana; Marshall, Lisa; Sara, Susan J.; Born, Jan
doi: 10.1152/jn.00014.2006pmid: 16611848
Slow oscillations originating in the prefrontal neocortex during slow-wave sleep (SWS) group neuronal network activity and thereby presumably support the consolidation of memories. Here, we investigated whether the grouping influence of slow oscillations extends to hippocampal sharp wave-ripple (SPW) activity thought to underlie memory replay processes during SWS. The prefrontal surface EEG and multiunit activity (MUA), along with hippocampal local field potentials (LFP) from CA1, were recorded in rats during sleep. Average spindle and ripple activity and event correlation histograms of SPWs were calculated, time-locked to half-waves of slow oscillations. Results confirm decreased prefrontal MUA and spindle activity during EEG slow oscillation negativity and increases in this activity during subsequent positivity. A remarkably close temporal link was revealed between slow oscillations and hippocampal activity, with ripple activity and SPWs being also distinctly decreased during negative half-waves and increased during slow oscillation positivity. Fine-grained analyses of temporal dynamics revealed for the slow oscillation a phase delay of approximately 90 ms with reference to up and down states of prefrontal MUA, and of only approximately 60 ms with reference to changes in SPWs, indicating that up and down states in prefrontal MUA precede corresponding changes in hippocampal SPWs by approximately 30 ms. Results support the notion that the depolarizing surface-positive phase of the slow oscillation and the associated up state of prefrontal excitation promotes hippocampal SPWs via efferent pathways. The preceding disfacilitation of hippocampal events temporally coupled to the negative slow oscillation half-wave appears to serve a synchronizing role in this neocorticohippocampal interplay. Address for reprint requests and other correspondence: Dr. M. Mölle, Department of Neuroendocrinology, University of Lübeck, Ratzeburger Allee 160, Haus 23a, 23538 Lübeck, Germany (E-mail: [email protected] )
Kittelberger, J. Matthew; Land, Bruce R.; Bass, Andrew H.
doi: 10.1152/jn.00067.2006pmid: 16598068
Midbrain structures, including the periaqueductal gray (PAG), are essential nodes in vertebrate motor circuits controlling a broad range of behaviors, from locomotion to complex social behaviors such as vocalization. Few single-unit recording studies, so far all in mammals, have investigated the PAG's role in the temporal patterning of these behaviors. Midshipman fish use vocalization to signal social intent in territorial and courtship interactions. Evidence has implicated a region of their midbrain, located in a similar position as the mammalian PAG, in call production. Here, extracellular single-unit recordings of PAG neuronal activity were made during forebrain-evoked fictive vocalizations that mimic natural call types and reflect the rhythmic output of a known hindbrain–spinal pattern generator. The activity patterns of vocally active PAG neurons were mostly correlated with features related to fictive call initiation. However, spike trains in a subset of neurons predicted the duration of vocal output. Duration is the primary feature distinguishing call types used in different social contexts and these cells may play a role in directly establishing this temporal dimension of vocalization. Reversible, lidocaine inactivation experiments demonstrated the necessity of the midshipman PAG for fictive vocalization, whereas tract-tracing studies revealed the PAG's connectivity to vocal motor centers in the fore- and hindbrain comparable to that in mammals. Together, these data support the hypotheses that the midbrain PAG of teleosts plays an essential role in vocalization and is convergent in both its functional and structural organization to the PAG of mammals. Address for reprint requests and other correspondence: J. M. Kittelberger, Dept. of Neurobiology and Behavior, Seeley G. Mudd Hall, Cornell University, Ithaca, NY 14853 (E-mail: [email protected] )
doi: 10.1152/jn.01282.2005pmid: 16611839
Two main forms of neurotransmitter release are known: action potential-evoked and spontaneous release. Action potential-evoked release depends on Ca 2+ entry through voltage-gated Ca 2+ channels, whereas spontaneous release is thought to be Ca 2+ -independent. Generally, spontaneous and action potential-evoked release are believed to use the same release machinery to release neurotransmitter. This study shows, using the whole cell patch-clamp technique in rat cerebellar slices, that at the interneuron- Purkinje cell synapse activation of presynaptic group II metabotropic glutamate receptors suppresses spontaneous GABA release through a mechanism independent of voltage-gated Ca 2+ channels, store-operated Ca 2+ channels, and Ca 2+ release from intracellular Ca 2+ stores, suggesting that the metabotropic receptors target the release machinery directly. Voltage gated Ca 2+ channel-independent release following increased presynaptic cAMP production is similarly inhibited by these metabotropic receptors. In contrast, both voltage-gated Ca 2+ channel-dependent and presynaptic N -methyl- D -aspartate receptor-dependent GABA release were unaffected by activation of group II metabotropic glutamate receptors. Hence, the mechanisms underlying spontaneous and Ca 2+ -dependent GABA release are distinct in that only the former is blocked by group II metabotropic glutamate receptors. Thus the same neurotransmitter, glutamate, can activate or inhibit neurotransmitter release by selecting different receptors that target different release machineries. Address for reprint requests and other correspondence: Dept. of Physiology, Anatomy and Genetics, Oxford University, Sherington Bldg., Parks Rd., Oxford OX1 3PT, UK (E-mail: [email protected] )
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