Effect of direct and transcallosal stimulation on inhibition of unit activity in the cat association cortex

Inhibition of association cortical neurons (in the form of inhibition of spontaneous activity or of IPSPs) during direct and transcallosal stimulation was studied in cats immobilized with muscle relaxants. The duration of inhibition of stimulation and the number of stimuli. With an increase in the strength of stimulation inhibition deepened to a certain level for a particular neuron, after which it could be further lengthened with an increase in the number of stimuli. In the case of repeated stimulation by volleys of stimuli, very prolonged inhibition developed gradually in the neurons, during which spontaneous activity was inhibited for 2–5 sec. The duration of the IPSP depended on the intensity of stimulation and number of stimuli and its amplitude depended on the intensity and frequency of stimulation and on the number of stimuli. In some cases the amplitude of the IPSP continued to rise after a short volley of stimuli, even after the end of stimulation. An increase in the number of stimuli in the volley lengthened the IPSPs, but their amplitude remained constant throughout the period of stimulation. Prolonged inhibition (up to a few seconds) was connected with the development of a hyperpolarization postsynaptic potential in the neurons. It is suggested that neurons exerting a monosynaptic inhibitory influence on cells of the association cortex may be located in the opposite hemisphere.A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 13, No. 2, pp. 133–141, March–April, 1981.     

刺激大鼠下丘脑背内侧核对丘脑束旁核痛相关神经元放电的影响

本文在 79只清醒麻痹大鼠身上,用玻璃微电极记录丘脑束旁核痛兴奋(PfPE)和痛抑制(PfPI)单位的放电及其对刺激下丘脑背内侧核(DMH)的反应,并观察切割脊髓背外侧束的效应。主要结果如下:(1)刺激DMH使PfPE 单位的自发放电及痛放电有明显的抑制作用,而使PfPI 单位的自发放电增多,并解除伤害性刺激引起的抑制效应;(2)刺激DMH引起PfPE 单位的抑制效应,在切割脊髓背外侧束后仍然出现。上述结果提示:DMH 对丘脑束旁核在处理痛觉信息上具有调制作用,这种调制作用可能不通过脑干下行性抑制系统完成,而主要是通过脊髓上联系抑制丘脑束旁核神经元对痛传入的反应。     

外侧臂旁核神经元对穹窿下器逆向刺激和孤束核顺向剌激的反应

Single unit discharges were extracellularly recorded from the neurons in the lateral parabrachial nucleus (LPBN) and responses of the recorded units to antidromic stimulation of the subfornical organ (SFO) and to orthodromic stimulation of the nucleus tractus solitarius (NTS) were observed in urethane-anesthetized rats. Following electrical stimulation of the SFO, 9.9% (51/151) of the LPBN units were antidromically activated. After activation of peripheral baroreceptors by raising arterial blood pressure with an intravenous injection of phenylephrine, 40.7% (22/54) of the LPBN units were inhibited and 27.8% (17/54) excited. Following orthodromic stimulation of the depressor area in the NTS, 55.6% (94/169) of the LPBN units showed an increase and 22.5% (38/169) a decrease in firing rates. Among the LPBN neurons antidromically activated by SFO stimulation, 2 units were inhibited by phenylephrine administrated i.v.; of the 8 units tested, when the NTS was stimulated, 6 were excited and 2 inhibited. The results suggest that the LPBN neurons may receive inhibitory or excitatory baroreceptive inputs from the NTS and then relay it directly to SFO.     

Electrical potentials from the eye and optic nerve of Strombus: effects of electrical stimulation of the optic nerve.

1. Photic stimulation of the mature eye of Strombus can evoke in the optic nerve 'on' activity in numerous small afferent fibres and repetitive 'off' bursts of afferent impulses in a smaller number of larger fibres. 2. Synchronous invasion of the eye by electrically evoked impulses in small optic nerve fibres (apparently the 'on' afferents, antidromically activated) can evoke a burst of impulses in the larger 'off' fibres which propagate away from the eye. Invasion of the eye via one branch of optic nerve can evoke an answering burst in another branch. 3. Such electrically evoked bursts are similar to light-evoked 'off' bursts with respect to their impulse composition, their ability to be inhibited by illumination of the eye, and their susceptibility to MgCl2 anaesthesia. 4. Invasion of the eye by a train of repetitive electrically evoked impulses in the absence of photic stimulation can give rise to repetitive 'off' bursts as well as concomitant oscillatory potentials in the eye which are similar to those normally evoked by cessation of a photic stimulus. 5. The electrically evoked 'off' bursts appear to be caused by an excitatory rebound following the cessation of inhibitory synaptic input from photoreceptors which can be antidromically activated by electrical stimulation of the optic nerve. 6. The experimental results suggest that the rhythmic discharge of the 'off' fibres evoked by the cessation of a photic stimulus is mediated by the abrupt decrease of inhibitory synaptic input from the receptors.     

Extensive dual innervation and mutual inhibition by forelimb and hindlimb inputs to ventroposterolateral nucleus projection neurons in the rat

The stimulation of brachial plexus and sciatic nerve resulted in a precisely timed, synchronous volley of inputs to ventroposterolateral (VPL) neurons from either forelimb or hindlimb. Such stimulation activated sensory fibers of all modalities and was therefore modality-nonspecific. Extracellular recordings of modality-nonspecific single-unit evoked responses from VPL showed that 13% of VPL projection neurons responded to both forelimb and hindlimb inputs. We also demonstrated mutually inhibitory interactions between inputs from forelimb and hindlimb in 45% of VPL units. Unlike the somatotopic map produced by others using modality-specific inputs, the modality-nonspecific evoked response map of VPL had a broadly overlapping distribution of evoked responses. This was especially true for the more caudal aspects of VPL. When the delivery of stimuli was appropriately timed, forelimb inputs caused the inhibition of responses to forelimb stimulation; similarly, hindlimb inputs inhibited responses to forelimb stimulation. The inhibition had a variable duration that may reflect a combination of processes, including recurrent inhibitory collateral input from the thalamic reticular nucleus (TRN) or an intrinsic hyperpolarizing inhibitory afterpotential of the VPL neuron. The presence of an extensive converging input on VPL neurons and an inhibitory correlate to this overlapping of inputs may explain the shifting of VPL maps following lesions of peripheral nerve, spinal cord, or dorsal column nuclei (DCN).     

Partly shared spinal cord networks for locomotion and scratching

Animals produce a variety of behaviors using a limited number of muscles and motor neurons. Rhythmic behaviors are often generated in basic form by networks of neurons within the central nervous system, or central pattern generators (CPGs). It is known from several invertebrates that different rhythmic behaviors involving the same muscles and motor neurons can be generated by a single CPG, multiple separate CPGs, or partly overlapping CPGs. Much less is known about how vertebrates generate multiple, rhythmic behaviors involving the same muscles. The spinal cord of limbed vertebrates contains CPGs for locomotion and multiple forms of scratching. We investigated the extent of sharing of CPGs for hind limb locomotion and for scratching. We used the spinal cord of adult red-eared turtles. Animals were immobilized to remove movement-related sensory feedback and were spinally transected to remove input from the brain. We took two approaches. First, we monitored individual spinal cord interneurons (i.e., neurons that are in between sensory neurons and motor neurons) during generation of each kind of rhythmic output of motor neurons (i.e., each motor pattern). Many spinal cord interneurons were rhythmically activated during the motor patterns for forward swimming and all three forms of scratching. Some of these scratch/swim interneurons had physiological and morphological properties consistent with their playing a role in the generation of motor patterns for all of these rhythmic behaviors. Other spinal cord interneurons, however, were rhythmically activated during scratching motor patterns but inhibited during swimming motor patterns. Thus, locomotion and scratching may be generated by partly shared spinal cord CPGs. Second, we delivered swim-evoking and scratch-evoking stimuli simultaneously and monitored the resulting motor patterns. Simultaneous stimulation could cause interactions of scratch inputs with subthreshold swim inputs to produce normal swimming, acceleration of the swimming rhythm, scratch-swim hybrid cycles, or complete cessation of the rhythm. The type of effect obtained depended on the level of swim-evoking stimulation. These effects suggest that swim-evoking and scratch-evoking inputs can interact strongly in the spinal cord to modify the rhythm and pattern of motor output. Collectively, the single-neuron recordings and the results of simultaneous stimulation suggest that important elements of the generation of rhythms and patterns are shared between locomotion and scratching in limbed vertebrates.     

5－羟色胺对大鼠下丘脑脑片弓状核神经元自发电活动的影响

在７４张大鼠下丘脑脑片上,用玻璃微电极记录到弓状核自发放电单位１７６个,其放电形式有三种：慢不规则型（１１９个,６７．６％）;快连续型（４６个,２６．１％）;位相型（１１个,６．３％）。５－ＨＴ（１０－６ｍｏｌ／Ｌ,３ｍｉｎ）对不同形式放电单位的作用均以抑制为主：对部分慢不规则单位（９／１１９）则表现为先抑制后兴奋的双相性反应,对少数神经元有兴奋作用。１２个被５－ＨＴ抑制的单位,其抑制作用不能被噻庚啶（ＣＨＤ,１０－５ｍｏｌ／Ｌ）阻断,４个被５－ＨＴ抑制的的单位中,其抑制作用可被二甲基麦角新碱（ＭＳＧ１０－６ｍｏｌ／Ｌ）部分或完全阻断。７个被５－ＨＴ抑制的单位,其中４个单位中,５－ＨＴ的抑制作用可被特异性５－ＨＴ１Ａ受体阻断剂Ｐｉｎｄｏｂｉｎｄ－５－ＨＴ１Ａ部分阻断;但另外３个单位的阻断效果不明显。上述结果表明：５－ＨＴ对弓状核不同形式放电单位的作用均以抑制为主,其作用可能是通过５－羟色胺（５－ＨＴ１）受体介导的,部分还可能是通过５－ＨＴ１Ａ受体介导的。     

Responses of neurons in the rat nucleus submedius to noxious and innocuous mechanical cutaneous stimulation

Extracellular recordings were used to characterize responses to cutaneous mechanical stimulation of 78 neurons in the rat nucleus submedius (SM). Thirty-nine of these units were activated by some type of cutaneous mechanical stimulation. Eighteen cells were activated exclusively by noxious stimuli. In 13 of these cells, responses were of swift onset and relatively rapid termination following stimulus application. In contrast, in three neurons responses were delayed both in onset and termination, and in two the response was immediate, but the markedly increased evoked activity outlasted stimulus application by 13 min. Receptive fields (RFs) of these nociceptive neurons were generally large, although none were bilateral. Four SM neurons were activated by innocuous stimuli, but their maximal response was obtained only after noxious stimulation. Responses of all of these neurons were of immediate onset and recovery, and their RFs were large (two were bilateral). Twelve SM neurons were activated maximally by innocuous stimuli. Responses of seven of these cells were immediate in onset and termination, while that of three were delayed in both onset and termination. Two of the 12 innocuous-only neurons quickly became unresponsive to repeated stimulus applications, and could be reactivated only after a rest period during which no stimuli were applied. RFs of these units were also generally large, and in three cases were bilateral. Five SM neurons responded by decreasing, or completely ceasing, their firing subsequent to noxious-only (n = 2), or innocuous-only (n = 3) stimulation. Four of these units had large RFs (two were bilateral). The remaining 39 SM neurons could not be activated by any type of mechanical cutaneous stimulation we tried. Electrical stimulation of the ventrolateral orbital cortex (VLO) was employed to examine frontal cortical projections of 21 SM neurons. Ten of these units were activated, although all of them synaptically rather than antidromically, and two were inhibited. There was no clear-cut relationship between neuronal location, physiological type, RF site, or VLO stimulation effects among the 39 SM neurons. These results provide further support for the involvement of SM neurons in nociceptive information signaling, and suggest additionally that the role of the nucleus is not limited to nociception but encompasses a wider range of cutaneous sensations.     

Botzinger complex region role in phrenic-to-phrenic inhibitory reflex of cat

Neuronal recordings, microstimulation, and electrolytic and chemical lesions were used to examine the involvement of the B?tzinger Complex (B?tC) in the bilateral phrenic-to-phrenic inhibitory reflex. Experiments were conducted in decerebrate cats that were paralyzed, ventilated, thoracotomized, and vagotomized. Microelectrode recordings within the B?tC region revealed that some neurons were activated by phrenic nerve stimulation (15 of 69 expiratory units, 9 of 67 inspiratory units, and 19 nonrespiratory-modulated units) at average latencies similar to the onset latency of the phrenic-to-phrenic inhibition. In addition, microstimulation within the B?tC caused a short latency transient inhibition of phrenic motor activity. In 17 cats phrenic neurogram responses to threshold and supramaximal (15 mA) stimulation of phrenic nerve afferents were recorded before and after electrolytic B?tC lesions. In 15 animals the inhibitory reflex was attenuated by bilateral lesions. Because lesion of either B?tC neurons or axons of passage could account for this attenuation, in eight experiments the phrenic-to-phrenic inhibitory responses were recorded before and after bilateral injections of 5 microM kainic acid (30-150 nl) into the B?tC. After chemical lesions, the inhibitory response to phrenic nerve stimulation remained; however, neuronal activity typical of the B?tC could not be located. These results suggest that axons important in producing the phrenic-to-phrenic reflex pass through the region of the B?tC, but that B?tC neurons themselves are not necessary for this reflex.     

Responses of Neurons in the Rat Nucleus Submedius to Noxious and Innocuous Mechanical Cutaneous Stimulation

Extracellular recordings were used to characterize responses to cutaneous mechanical stimulation of 78 neurons in the rat nucleus submedius (SM). Thirty-nine of these units were activated by some type of cutaneous mechanical stimulation. Eighteen cells were activated exclusively by noxious stimuli. In 13 of these cells, responses were of swift onset and relatively rapid termination following stimulus application. In contrast, in three neurons responses were delayed both in onset and termination, and in two the response was immediate, but the markedly increased evoked activity outlasted stimulus application by 13 min. Receptive fields (RFs) of these nociceptive neurons were generally large, although none were bilateral. Four SM neurons were activated by innocuous stimuli, but their maximal response was obtained only after noxious stimulation. Responses of all of these neurons were of immediate onset and recovery, and their RFs were large (two were bilateral). Twelve SM neurons were activated maximally by innocuous stimuli. Responses of seven of these cells were immediate in onset and termination, while that of three were delayed in both onset and termination. Two of the 12 innocuous-only neurons quickly became unresponsive to repeated stimulus applications, and could be reactivated only after a rest period during which no stimuli were applied. RFs of these units were also generally large, and in three cases were bilateral. Five SM neurons responded by decreasing, or completely ceasing, their firing subsequent to noxious-only (n = 2), or innocuous-only (n = 3) stimulation. Four of these units had large RFs (two were bilateral). The remaining 39 SM neurons could not be activated by any type of mechanical cutaneous stimulation we tried.

Electrical stimulation of the ventrolateral orbital cortex (VLO) was employed to examine frontal cortical projections of 21 SM neurons. Ten of these units were activated, although all of them synaptically rather than antidromically, and two were inhibited. There was no clear-cut relationship between neuronal location, physiological type, RF site, or VLO stimulation effects among the 39 SM neurons.

These results provide further support for the involvement of SM neurons in nociceptive information signaling, and suggest additionally that the role of the nucleus is not limited to nociception but encompasses a wider range of cutaneous sensations.     

外侧臂旁核神经元对穹隆下器逆向刺激和孤束核顺向刺激的反应

细胞外记录大鼠外侧臂旁核(LPBN)神经元单位放电,观察了刺激穹隆下器(SFO)在记录单位诱发的逆向反应和静脉注射新福林兴奋外周压力感受器和刺激孤束核(NTS)减压区诱发的顺向反应。实验发现:刺激 SFO,9.9%(15/151)的 LPBN 神经元有逆向反应。静脉注射新福林,40.7%(22/54)的 LPBN 神经元有抑制反应,27.8%(17/54)有兴奋反应。刺激 NTS,55.6%(94/169)的 LPBN 神经元呈现顺向兴奋反应;22.5%(38/169)呈现顺向抑制反应。观察静脉注射新福林对 SFO 刺激有逆向反应的 LPBN 神经元自发放电的影响,在两个受试单位均见抑制反应。观察刺激 NTS 对逆向反应单位自发放电的影响,在8个受试单位中,6个呈兴奋反应;2个呈抑制反应。以上结果表明:LPBN 接受来自 NTS 的兴奋性或抑制性压力感受性传入,并把这种信息经 LPBN-SFO 直接通路传输到 SFO。     

Response of Human Thalamic Neurons to High-Frequency Stimulation

Thalamic deep brain stimulation (DBS) is an effective treatment for tremor, but the mechanisms of action remain unclear. Previous studies of human thalamic neurons to noted transient rebound bursting activity followed by prolonged inhibition after cessation of high frequency extracellular stimulation, and the present study sought to identify the mechanisms underlying this response. Recordings from 13 thalamic neurons exhibiting low threshold spike (LTS) bursting to brief periods of extracellular stimulation were made during surgeries to implant DBS leads in 6 subjects with Parkinson''s disease. The response immediately after cessation of stimulation included a short epoch of burst activity, followed by a prolonged period of silence before a return to LTS bursting. A computational model of a population of thalamocortical relay neurons and presynaptic axons terminating on the neurons was used to identify cellular mechanisms of the observed responses. The model included the actions of neuromodulators through inhibition of a non-pertussis toxin sensitive K⁺ current (I_KL), activation of a pertussis toxin sensitive K⁺ current (I_KG), and a shift in the activation curve of the hyperpolarization-activated cation current (I_h). The model replicated well the measured responses, and the prolonged inhibition was associated most strongly with changes in I_KG while modulation of I_KL or I_h had minimal effects on post-stimulus inhibition suggesting that neuromodulators released in response to high frequency stimulation are responsible for mediating the post-stimulation bursting and subsequent long duration silence of thalamic neurons. The modeling also indicated that the axons of the model neurons responded robustly to suprathreshold stimulation despite the inhibitory effects on the soma. The findings suggest that during DBS the axons of thalamocortical neurons are activated while the cell bodies are inhibited thus blocking the transmission of pathological signals through the network and replacing them with high frequency regular firing.     

Modification of the pattern of central neurons by sensory inputs from the reproductive organs in Aplysia depilans L

In the abdominal ganglion of Aplysia a number of motoneurons regulating visceral organs reacted to the stimulation of the reproductive organs. The response was mostly biphasic and often delayed. The multifunctional interneuron I (cell L10) reacted to the stimulation of the reproductive organs with burst firing, followed by an inhibitory phase. The interneuron II, involved in the regulation of visceral functions, was also activated during stimulation of the reproductive organs and its burst-pattern could be identified on a number of other neurons. Several members of the neurosecretory cell group reacted to the stimulation of reproductive organs. The response was, as a rule, biphasic and similar to the hormone action, long-lasting. Three further cells (near the cell L12, above the cell L21, and the neuron between R2 and R7 with unknown function) showed a stereotyped response to the stimulation of the reproductive organs. All the neurons reacting to the stimulation of the reproductive organs also received inputs from the cardiorenal system. The data support the existence of common networks composing variable units in the regulation of visceral functions of gastropods.     

Convergence of antennal and ocellar inputs in the insect brain

Summary Unitary responses were recorded from the brain of the fleshfly, Boettcherisca peregrina, during olfactory or mechanical stimulation of the antenna, and simultaneous photic stimulation of the ocelli. Convergence from the two inputs, the antenna and the ocelli, was observed. The response to antennal stimulation was facilitated by photic stimulation in most units. The responses to the antennal stimuli were facilitated greatly at the peak of the photic response. Some units responded both to ocellar illumination and antennal stimulation. Their response to antennal stimulation seemed independent of the light-condition during the light-adapted state, but was facilitated at the onset of the ocellar illumination, and occluded just after its cessation. In addition, there were some units which responded to antennal stimulation but not to the ocellar illumination; some of them also showed facilitation of the response to antennal stimulation during ocellar illumination.     

c-Fos expression in rat brain stem and spinal cord in response to activation of cardiac ischemia-sensitive afferent neurons and electrostimulatory modulation

The purpose of this study was to identify central neuronal sites activated by stimulation of cardiac ischemia-sensitive afferent neurons and determine whether electrical stimulation of left vagal afferent fibers modified the pattern of neuronal activation. Fos-like immunoreactivity (Fos-LI) was used as an index of neuronal activation in selected levels of cervical and thoracic spinal cord and brain stem. Adult Sprague-Dawley rats were anesthetized with urethane and underwent intrapericardial infusion of an "inflammatory exudate solution" (IES) containing algogenic substances that are released during ischemia (10 mM adenosine, bradykinin, prostaglandin E2, and 5-hydroxytryptamine) or occlusion of the left anterior descending coronary artery (CoAO) to activate cardiac ischemia-sensitive (nociceptive) afferent fibers. IES and CoAO increased Fos-LI above resting levels in dorsal horns in laminae I-V at C2 and T4 and in the caudal nucleus tractus solitarius. Dorsal rhizotomy virtually eliminated Fos-LI in the spinal cord as well as the brain stem. Neuromodulation of the ischemic signal by electrical stimulation of the central end of the left thoracic vagus excited neurons at the cervical and brain stem level but inhibited neurons at the thoracic spinal cord during IES or CoAO. These results suggest that stimulation of the left thoracic vagus excites descending inhibitory pathways. Inhibition at the thoracic spinal level that suppresses the ischemic (nociceptive) input signal may occur by a short-loop descending pathway via signals from cervical propriospinal circuits and/or a longer-loop descending pathway via signals from the nucleus tractus solitarius.     

刺激家兔扣带回前部对丘脑腹后外侧核痛敏神经元放电的作用

131只家兔在三碘季铵酚麻痹下,用玻璃微电极在腹后外侧核(VPL)记录对伤害性刺激有反应的单位。在786个 VPL 单位中,对伤害性刺激有反应的单位共128个,占总数16.3%.其中116今对伤害性刺激呈兴奋效应,占90.6%。其余12个呈抑制效应,占9.4%。静脉注射吗啡可以取消这些神经元对伤害性刺激的放电反应。78次的测试结果表明扣带回前部的刺激可以抑制32%VPL 神经元的自发放电活动。同样,也可以抑制由于伤害性刺激而引起的 VPL 神经元的放电反应。这种抑制程度和扣带回的刺激频率有关;8Hz 的刺激频率所引起的抑制效应最佳。上述实验结果说明,扣带回可以通过其下行纤维的活动;影响伤害性冲动在丘脑 VPL水平上的传递。     

Tonic inhibition of dorsal pontine neurons during the postural atonia produced by an anticholinesterase in the decerebrate cat.

1. Experiments performed in precollicular decerebrate cats indicate that neurons located in the caudal part of the locus coeruleus and locus subcoeruleus as well as in the surrounding reticular formation were greatly depressed during the cataplectic episodes induced by i.v. injection of 0.1 mg/kg of eserine sulphate. 2. These units actually showed a slow regular firing rate when the rigidity was present. Moreover their firing rate greatly decreased during the episodes of postural atonia produced by the anticholinesterase. In some instances a complete abolition of firing occurred during these episodes. The depression of unit discharge anticipated the onset of postural atonia and lasted throughout the episodes. 3. Some of the neurons described above responded with steady changes in their discharge rate to natural stimulation of macular labyrinthine receptors during postural rigidity. However, the response of these neurons to lateral tilts was suppressed during the episodes of postural atonia induced by the anticholinesterase, This and other arguments suggested that these units were tonically inhibited during the induced cataplectic episodes. 4. The time course of the rate deceleration shown by these neurons during transition from postural rigidity to muscular atonia represents a mirror image of the rate acceleration which affects most of the pontine reticular neurons located in the gigantocellular tegmental field (FTG) during the induced cataplectic episodes. These reciprocal rate relations suggest that a functional interaction exists between the two cell groups. In particular it is postulated that the pontine FTG neurons are self-excitatory and excitatory to the locus coeruleus neurons, while the last neurons may be self-inhibitory and inhibitory to FTG neurons. These findings can be related to previous observations showing that neurons located in the region of locus coeruleus undergo a rate deceleration during desynchronized sleep which mimics the time course of firing to the pontine reticular neurons. 5. In conclusion it appears that the decerebrate rigidity is present in so far as the cholinergic reticular neurons, which trigger the bulbospinal inhibitory system, are tonically inhibited by neurons located in the monoaminergic structures of the dorsolateral pontine tegmentum. On the other hand the suppression of the decerebrate rigidity ,which occurs during the cholinergically induced cataplectic episodes results from activation of the cholinergic reticular neurons, which escape tonic inhibition from monoaminergic structures.     

Excitatory and inhibitory responses of the ongoing sympathetic discharge in single renal neurons to liminal stimulation of aortic C-fibres in the rabbit

Excitatory and inhibitory responses of sympathetic discharge were recorded in single renal postganglionic neurons of rabbits anaesthetized with urethane and chloralose. The animals were vagotomized and had transected aortic nerves. Responses were elicited by single volleys in the aortic C-fibres. Excitatory responses consisted in short-lasting increase in the rate of ongoing sympathetic discharge and were followed by inhibitory responses. Excitatory effects together with inhibitory responses were seen in 68% of units (19/28). Only excitatory effects appeared in 2 neurons (7.1%) and only inhibitory effects in 7 neurons (25%). In renal neurons exhibiting both effects, the excitatory responses appeared after latency of 172 +/- 8 ms (x +/- S.D.) and had duration of 64 +/- 11 ms. Inhibitory effects had latency o f 257 +/- 10 ms and their duration amounted to 265 +/- 22 ms. In more than half of recordings the excitatory responses were separated from the inhibitory effects by discharge lasting 33 +/- 4 ms. Significant correlations between latencies of excitatory and inhibitory responses and between duration of excitatory and latency of inhibitory responses suggest interaction between both effects. Increase in the number of afferent volleys (1 through 5) evoked relatively small changes in duration of the excitatory effect indicating that temporal facilitation is of minor importance in generating this response. Temporal facilitation was found to play an important role in determining duration of the inhibitory response. Comparison of effects of unilateral and bilateral stimulation of the aortic C-fibres showed larger occlusion of durations of the excitatory than inhibitory responses.     

Participation of alpha and beta adrenoreceptors in facilitating and inhibiting the action of the sympathetic nervous system in parasympathetic bradycardia

Electrical stimulation of the distal vagal cervical end in urethane chloralose anesthetized cats caused bradycardia that could be both enhanced and inhibited during sympathetic activation. Sympathetic activation was induced by electrical stimulation of the sympathetic outflow of the spinal cord at the level of Th 1-Th 3 in pitched cats or by an intravenous injection of tyramine. It has been proved pharmacologically that alpha-adrenoceptors are involved in potentiation. The inhibitory influences are realized via both alpha- and beta-adrenoceptors.     

Capsaicin-sensitive muscle afferents modulate the monosynaptic reflex in response to muscle ischemia and fatigue in the rat

The role of muscle ischemia and fatigue in modulating the monosynaptic reflex was investigated in decerebrate and spinalized rats. Field potentials and fast motoneuron single units in the lateral gastrocnemious (LG) motor pool were evoked by dorsal root stimulation. Muscle ischemia was induced by occluding the LG vascular supply and muscle fatigue by prolonged tetanic electrical stimulation of the LG motor nerve. Under muscle ischemia the monosynaptic reflex was facilitated since the size of the early and late waves of the field potential and the excitability of the motoneuron units increased. This effect was abolished after L3-L6 dorsal rhizotomy, but it was unaffected after L3-L6 ventral rhizotomy. By contrast, the monosynaptic reflex was inhibited by muscle fatiguing stimulation, and this effect did not fully depend on the integrity of the dorsal root. However, when ischemia was combined with repetitive tetanic muscle stimulation the inhibitory effect of fatigue was significantly enhanced. Both the ischemia and fatigue effects were abolished by capsaicin injected into the LG muscle at a dose that blocked a large number of group III and IV muscle afferents. We concluded that muscle ischemia and fatigue activate different groups of muscle afferents that are both sensitive to capsaicin, but enter the spinal cord through different roots. They are responsible for opposite effects, when given separately: facilitation during ischemia and inhibition during fatigue; however, in combination, ischemia enhances the responsiveness of the afferent fibres to fatigue.