Biomedical subjects

J S Yeomans

Publications and source records attributed to J S Yeomans.

18 recordsLinked to original sources

PubMed1992

Electrically evoked turning: asymmetric and symmetric collision between anteromedial cortex and striatum.

Electrical stimulation of the anteromedial cortex (AMC) or striatum of rats evoked contraversive eye, head and body movements. In these experiments we test which neurons and which pathways are responsible for the turning by delivering conditioning (C) pulses to one site and test (T) pulses to the second site, and measuring the frequency of pulse pairs required to evoke a full turn in 10 s. Decreases in the required frequency were usually found at C-T intervals from 0.6 to 1.0 ms, whether the C pulses were delivered to the AMC or to the striatum. This symmetric effect is attributed to collision in fast-conducting axons connecting cortex and striatum. Symmetric collision at C-T intervals of 2-4 ms was observed between cortex and 3 dorsal striatal sites, suggesting slower axons from cortex to these dorsal striatal sites. In several animals, asymmetric changes in required frequency also occurred. When the C pulses were presented via the striatal electrode, the recovery in required frequency occurred at C-T intervals of 1-4 ms, but when the C pulses were presented via the cortical electrode, recovery occurred at C-T intervals of 2-50 ms. This asymmetry is attributed to indirect (i.e., transynaptic) activation of corticostriatal or striatal output axons. These results suggest that in both cortex and striatum there are synapses, transmitting from rostral to caudal, which are important for electrically evoked turning. When C and T pulses were delivered to the same site, decreases in required frequency occurred at C-T intervals from 0.4 to 4 ms, attributable to recovery from refractoriness. In 3 striatal sites, however, large changes were also seen at C-T intervals from 6 to 50 ms. In all 3 sites, asymmetric collision occurred at these same intervals. The recovery at long C-T intervals could be due to transynaptic collision also, resulting from the simultaneous activation of presynaptic and postsynaptic axons by a single striatal electrode.

Animals↗

PubMed1990

Differential effects of atropine, procaine and dopamine in the rat ventral tegmentum on lateral hypothalamic rewarding brain stimulation.

Microinjections of the muscarinic antagonist, atropine, of dopamine, or of the local anesthetic, procaine, in the ventral tegmentum elevated frequency thresholds for lateral hypothalamic self-stimulation. The largest and most robust effects were observed following atropine (30 or 60 micrograms) microinjections. The most sensitive sites for the atropine effect were near dopamine cells. In order to determine if the effects of atropine can be reversed by pretreatment with a cholinergic agonist, carbachol (1-3 micrograms) was microinjected 15 min prior to atropine. Carbachol pretreatment attenuated the frequency threshold elevation of atropine by 47-95%. Since atropine is a local anesthetic, the effects of procaine on self-stimulation thresholds were tested as well. Procaine (100 or 250 micrograms) in ventral tegmentum elevated frequency thresholds by much less than atropine. Therefore, while atropine attenuates reward primarily through blockade of muscarinic receptors, the local anesthetic effect of atropine may enhance the threshold elevation. Dopamine (1-10 micrograms) also elevated frequency thresholds, but when dopamine injections were repeated daily, the threshold elevations were attenuated. This attenuation contrasted with the robust effects of atropine, and may reflect the development of autoreceptor subsensitivity. Hence, both dopaminergic and muscarinic receptors in ventral tegmentum are involved in lateral hypothalamic brain stimulation reward.

Animals↗

PubMed1990

"Temporal summation decay" in hypothalamic self-stimulation: threshold changes at long intrapair intervals due to axonal subnormal periods.

Rats were trained to bar press for trains of conditioning (C) and test (T) pulses delivered via lateral hypothalamic electrodes. As intrapair (C-T) intervals increased from 10 ms to 100 ms, the frequency of pulses required for self-stimulation increased, similar to results of Smith and Coons (1970). This effect was observed only for electrode placements where self-stimulation was obtained at frequencies below 16 Hz and currents of 600 microA and higher. The effect was larger when the train duration was increased from 0.5 s to 2.0 s. The threshold increase was abolished when the T pulses were greater in current than the C pulses but not when C pulses were larger than T pulses. The larger T pulses also removed relative refractory period effects at a C-T interval of 1.0 ms. Therefore, the increase in required current or frequency at long C-T intervals appears to be due to a decline in axonal excitability (i.e., the subnormal period) rather than a decay in synaptic temporal summation. Possible flaws in other reports of paired-pulse "temporal summation decay" at long C-T intervals using 2 electrodes are discussed.

Animals↗

PubMed1989

Double-pulse stimulation of startle-like responses in rats: refractory periods and temporal summation.

A startle-like response was evoked by electrical stimulation with one pulse in several brainstem sites of the primary acoustic startle circuit. If a second pulse was delivered 0.4-10 ms after the first pulse, a stronger response or a decreased current threshold resulted. The facilitatory effect of the second pulse increased as interpulse (C-T) interval increased from 0.4 to 2.0 ms in cochlear nucleus or ventral lateral lemniscus sites. In caudal pontine reticular formation sites, the effect of the second pulse increased sharply from 0.3 to 0.5 ms. These results suggest that very short refractory period axons mediate electrically elicited startle in reticular formation, and that longer refractory period axons mediate startle in cochlear nucleus or ventral lateral lemniscus. In reticular formation sites, the effect of the second pulse declined nearly exponentially from 2.0 to 50 ms with a time constant of about 4 ms. Stimulation of similar reticular formation sites in cats evokes monosynaptic EPSPs in spinal motoneurons with an almost identical time course, as reported by other investigators. This suggests that the startle response evoked from the reticular formation results from monosynaptic activation of spinal motoneurons. Temporal summation declined more slowly and irregularly in cochlear nucleus and ventral lateral lemniscus sites, suggesting that these sites are not monosynaptically connected with spinal motoneurons, a conclusion consistent with anatomical data. In reticular formation sites near the facial nerve, a second peak in the two-pulse curve was observed at a C-T interval of 10 ms. The second peak was blocked by local anesthesia of the face ipsilateral to the stimulating electrode, suggesting that a single twitch of facial muscles facilitates startle.

Action Potentials↗

PubMed1988

Excitability properties of medial forebrain bundle axons of A9 and A10 dopamine cells.

A9 and A10 units identified as dopaminergic were recorded with extracellular micropipettes. The units were antidromically activated by electrical stimulation at the level of the preoptic area. The absolute refractory periods ranged from 1.2 to 2.5 ms. During the 2-8 ms of the relative refractory period, conduction was slower than normal by up to 1.5 ms. The time constant, C, of the strength-duration curve ranged from 0.4 to 0.6 ms. The current (I)-distance (D) relationship, tested by moving the stimulating electrode past the axon, was approximately parabolic (I = K D exp 2), with the constant of the equation, K, ranging from 900 to 2000 microA/mm exp 2, for 0.5 ms pulses. This relationship allows calculation of the radius of the field of dopamine axon excitation at any current. These high K values show that axons of dopamine cells cannot be activated unless high current densities are delivered, even when electrodes are placed near the axons. These data allow determination of the extent to which dopamine axons can be the directly activated substrates for behaviors, such as self-stimulation and circling, which are evoked by electrical stimulation of the medial forebrain bundle or internal capsule.

Action Potentials↗

PubMed1988

Contraversive circling elicited from the internal capsule and substantia nigra: evidence for a continuous axon bundle mediating circling.

Electrical stimulation of many brain sites (e.g., anteromedial cortex, internal capsule, substantia nigra, superior colliculus, rostro-medial tegmentum, and medial pons) evokes circling. The collision method of Shizgal et al. (J. Comp. Physiol. Psychol., 94 (1980) 227-237) was used to determine whether these sites are functionally connected for the production of circling in rats. If connectivity was evidenced, then refractory period and conduction velocity distributions were determined for axons passing through the connected stimulation sites. Collision of up to 90% was found between electrodes placed in internal capsule and substantia nigra, suggesting that these sites are connected by continuous axons that mediate circling. The refractory periods of these axons ranged from 0.5 to 4.5 ms, and the conduction velocities of these axons ranged from 0.9 to 4.4 ms. These velocities are similar to those of striatonigral axons. No collision was found between anteromedial cortex and any other sites tested, nor between pontine sites and internal capsule or substantia nigra.

Animals↗

PubMed1988

Cholinergic antagonists in ventral tegmentum elevate thresholds for lateral hypothalamic and brainstem self-stimulation.

Frequency thresholds for lateral hypothalamic self-stimulation are elevated following microinjections of atropine into ventral tegmentum (73). Many self-stimulation sites in brainstem are situated near cholinergic cell groups and axons, and ventral tegmentum receives cholinergic afferents terminals. To test the hypothesis that ventral tegmental muscarinic receptors are involved in lateral hypothalamic and brainstem self-stimulation, stimulating electrodes were placed in lateral hypothalamus and dorsal tegmentum near the midbrain-pons border, and cannulae were implanted in ventral tegmentum. Microgram injections of muscarinic antagonists, atropine or scopolamine, or a choline uptake blocker, hemicholinium-3, elevated frequency thresholds for both self-stimulation sites in a dose-dependent and time-dependent fashion. In addition, summation and collision between the two self-stimulation sites was tested using paired-pulse methods (53). Summation ranged from 31 to 87% (i.e., 24 to 47% reductions in frequency threshold were observed at long intrapair intervals), but no collision-like effects were observed at short intrapair intervals. The ventral tegmentum is a likely site for the convergence of dorsal tegmental and lateral hypothalamic self-stimulation pathways.

Animals↗

PubMed1988

Turning responses evoked by stimulation of visuomotor pathways.

Lateral eye, head, and body movements are produced by electrical stimulation of many brain regions from frontal cortex to pons. A new collision method shows that at least 5 separate axon bundles mediate stimulation-elicited lateral head and body movements in rats. One bundle passes between the rostromedial tegmentum and medial pons, with conduction velocities of 0.8-18 m/s. A second bundle passes between the superior colliculus and contralateral medial pons, with conduction velocities of 1.7-13 m/s. A third bundle passes between the superior colliculus and ventrolateral pons, with conduction velocities of 1.3-20 m/s. A fourth bundle passes between the internal capsule and medial substantia nigra, with conduction velocities of 0.9-4.4 m/s. A fifth bundle passes between the anteromedial cortex and rostral striatum, with conduction velocities of 2.4-36 m/s. Collision effects have not been observed between the anteromedial cortex and the internal capsule, medial substantia nigra, superior colliculus, rostromedial tegmentum, or medial pons, which suggests that these sites are not connected by axons mediating turning. Possible synaptic linkages between the 5 bundles and possible transmitters are discussed.

Animals↗

PubMed1987

Circling elicited from the anteromedial cortex and medial pons: refractory periods and summation.

Contraversive circling is evoked by stimulating the anteromedial cortex (AMC) of rats, and ipsiversive circling is evoked by stimulating the medial pons (PONS). During AMC circling, lateral and vertical head movements and vibrissae movements were exhibited. During PONS circling, although lateral head movements were exhibited, vertical head movements and vibrissae movements were not exhibited. Refractory periods were estimated by delivering trains of paired pulses and measuring the frequency thresholds for circling at various intrapair intervals. Refractory periods at AMC circling sites were much longer (range 1.4-3.3 ms) than at PONS circling sites (range 0.5-1.0 ms). To determine the degree of summation between the AMC and contralateral PONS, the two sites were stimulated concurrently. Summation of 95-100% was observed for AMC and PONS circling. No collision was observed at short intrapair intervals of paired pulses. Thus, the AMC and PONS are not connected axonally but are related, perhaps serially, for the production of circling.

Animals↗

PubMed1986

Two converging brainstem pathways mediating circling behavior.

Ipsiversive circling results from stimulation of the rostromedial tegmentum (RMT) or medial pons (PONS), and contraversive circling results from stimulation of the superior colliculus (SC). To determine whether these sites are functionally connected, the collision method of Shizgal, Bielajew, Corbett, Skelton and Yeomans (1980) was used in rats. Pairs of stimulation pulses were presented to two sites, and the degree of collision between stimulation-evoked action potentials was assessed by measuring the frequency required for circling at short and long intrapair conditioning-testing (C-T) intervals. Collision was evidenced when the required frequencies were higher at short C-T intervals than at long C-T intervals. Collision of 46-62% was observed between RMT and PONS, and collision of 15-29% was observed between SC and PONS. Sites from which collision was obtained were located along the trajectories of the medial tegmental tract and the crossed tectospinal pathway. Refractory periods in all sites were similar, ranging from 0.3 to 1.7 ms. Conduction velocities of axons connecting RMT and PONS and SC and PONS were comparable, ranging from 0.8 to 13.3 m/s and 1.7 to 13.8 m/s, respectively, with lower conduction velocities associated with more ventral pontine sites. Thus, RMT and PONS, and SC and PONS are connected by myelinated axons that mediate circling.

Animals↗

PubMed1985

Cholinergic involvement in lateral hypothalamic rewarding brain stimulation.

Rats were implanted with stimulating electrodes in the lateral hypothalamus, and cannulae for chemical injections in the ventral tegmentum. Injections of atropine, a muscarinic antagonist, increased thresholds for self-stimulation in a dose-dependent fashion, without slowing bar pressing rates. Thresholds increased less for a self-stimulation site contralateral to the atropine injection. In a conditioned place preference test, the rats preferred compartments in which they received carbachol, a cholinergic agonist. Muscarinic receptors in ventral tegmentum therefore seem critical for medial forebrain bundle (MFB) reward. The possible cholinergic cells of origin are discussed.

Animals↗

PubMed1985

Longitudinal brainstem axons mediating circling: behavioral measurement of conduction velocity distributions.

Current applied near the midline brainstem elicits rapid ipsiversive circling. Pontine and midbrain sites were stimulated concurrently with paired pulses and the number of pulse pairs required to produce 3 complete circles in 10 s was measured at various intrapair (C-T) intervals. The same results were obtained when C pulses were presented via the midbrain electrode and T pulses via the pontine electrode, or vice versa: as C-T interval increased from 0.4 to 2.0 ms, the number of pulse pairs required decreased gradually. These decreases occurred at longer C-T intervals than the refractory period decreases observed in single-electrode tests. These results imply that collision occurred in the directly stimulated axons and that a longitudinal bundle of uninterrupted axons mediates the circling behavior. The sites from which collision was obtained overlap with both medial longitudinal fasciculus and crossed tectobulbar and tectospinal tracts. The axons mediating circling appear to have conduction velocities from 2 to roughly 20 m/s. By comparison, superior colliculus units antidromically driven from contralateral electrode sites that produce circling had conduction velocities from 0.7 to 40 m/s.

Animals↗

PubMed1979