RESUMEN
The interaction of dopamine and glutamate in the nucleus accumbens in the regulation of locomotion was investigated. Microinjection of N-methyl-D-aspartic acid (NMDA, a glutamatergic NMDA receptor agonist) or alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA, a quisqualic receptor agonist which is a glutamatergic non-NMDA receptor agonist) into the nucleus accumbens caused a substantial increase in locomotor activity. This increase in locomotor activity was significantly reduced by prior administration of the dopamine D2 agonist quinpirole, but not the D1 agonist, SKF 38393, into the same brain sites. The reduction in locomotion produced by quinpirole was dose dependent. Eight days after the ventral tegmental area was lesioned with 6-hydroxydopamine to destroy the dopamine projection and the axon terminals of the mesolimbic dopamine neurons in nucleus accumbens, the hyperkinetic effects produced by injections of NMDA and AMPA into the nucleus accumbens were substantially reduced. These results suggested that the glutamate agonist induced locomotion is mediated by dopamine. Thus, it appears that NMDA- or AMPA-induced locomotion is due to the activation of glutamate receptors on the mesolimbic dopamine terminals in the nucleus accumbens which release dopamine and subsequently increase locomotion.
Asunto(s)
Dopamina/fisiología , Glutamatos/fisiología , Locomoción/fisiología , Núcleo Accumbens/fisiología , Animales , Encefalopatías/inducido químicamente , Encefalopatías/fisiopatología , Dopaminérgicos/farmacología , Ergolinas/farmacología , Ácido Glutámico , Hipercinesia/inducido químicamente , Inyecciones Intraventriculares , Sistema Límbico/fisiología , Locomoción/efectos de los fármacos , Masculino , N-Metilaspartato/farmacología , Neuronas/fisiología , Núcleo Accumbens/efectos de los fármacos , Oxidopamina , Terminales Presinápticos/fisiología , Quinpirol , Ratas , Ratas Wistar , Receptores de Dopamina D1/efectos de los fármacos , Receptores de Dopamina D1/fisiología , Receptores de Dopamina D2/efectos de los fármacos , Receptores de Dopamina D2/fisiología , Ácido alfa-Amino-3-hidroxi-5-metil-4-isoxazol Propiónico/farmacologíaRESUMEN
The mesencephalic locomotor region is defined as a functional region sending signals to the spinal cord generators of rhythmical limb movements for locomotion. It has been shown that the mesencephalic locomotor region plays a critical role in locomotion initiated from the nucleus accumbens or from the subpallidal region. However, there are conflicting data on whether synaptic input from the nucleus accumbens--subpallidal region to the mesencephalic locomotor region mediates locomotion. The purpose of the study was to determine the role of synaptic input to different subregions of the mesencephalic locomotor region in locomotion induced by injecting dopamine into the nucleus accumbens or by injecting picrotoxin into the subpallidal region in freely behaving rats. Synaptic transmission in the mesencephalic locomotor region was eliminated by excitotoxic lesions or was reversibly interrupted by injecting cobalt chloride, which can block synaptic transmission. Excitotoxic lesions or injections of cobalt into subregions of the mesencephalic locomotor region significantly decreased, although did not completely block, locomotion. The most effective sites for cobalt- and lesion-induced reduction in locomotion were consistent with localization of the mesencephalic locomotor region. Effective sites for cobalt and lesions markedly overlapped but were not identical. The results indicate that synaptic transmission within the mesencephalic locomotor region contributes to dopamine- or picrotoxin-induced locomotion.
Asunto(s)
Locomoción/fisiología , Mesencéfalo/fisiología , Neuronas/fisiología , Transmisión Sináptica/fisiología , Animales , Encefalopatías/inducido químicamente , Encefalopatías/fisiopatología , Cobalto/farmacología , Dopamina/farmacología , Globo Pálido/anatomía & histología , Globo Pálido/fisiología , Ácido Iboténico/farmacología , Ácido Kaínico/farmacología , Masculino , Mesencéfalo/anatomía & histología , Actividad Motora/fisiología , Núcleo Accumbens/fisiología , Picrotoxina/farmacología , Ratas , Ratas Wistar , Transmisión Sináptica/efectos de los fármacosRESUMEN
Effects of dopamine D1 and D2 receptor agonists (SKF 38393 and quinpirole, respectively) on locomotion were studied in two behavioural situations characterized by low and high level of exploratory locomotor activity. Administration of quinpirole bilaterally into the nucleus accumbens increased locomotor activity at the low initial level of activity and decreased locomotor activity at the high activity level, while the administration of SKF 38393 increased locomotor activity in both behavioural situations. It was concluded that quinpirole has differential effects on locomotion, depending on the initial level of activity.
Asunto(s)
Ergolinas/farmacología , Actividad Motora/efectos de los fármacos , Núcleo Accumbens/fisiología , 2,3,4,5-Tetrahidro-7,8-dihidroxi-1-fenil-1H-3-benzazepina/administración & dosificación , 2,3,4,5-Tetrahidro-7,8-dihidroxi-1-fenil-1H-3-benzazepina/farmacología , Animales , Dopaminérgicos/farmacología , Ergolinas/administración & dosificación , Conducta Exploratoria/efectos de los fármacos , Masculino , Núcleo Accumbens/efectos de los fármacos , Quinpirol , Ratas , Ratas Wistar , Receptores de Dopamina D1/efectos de los fármacos , Receptores de Dopamina D1/fisiología , Receptores de Dopamina D2/efectos de los fármacos , Receptores de Dopamina D2/fisiología , Técnicas EstereotáxicasRESUMEN
Locomotor activity measured in an open-field apparatus was increased by adding partitions to enhance exploratory locomotion and by injecting amphetamine into the nucleus accumbens. Administration of the dopamine D2 agonist, quinpirole, into the nucleus accumbens reduced significantly both exploratory and amphetamine-elicited locomotion. It is suggested that these effects of quinpirole are mediated by different presynaptic mechanisms.
Asunto(s)
Anfetamina/farmacología , Ergolinas/farmacología , Conducta Exploratoria/efectos de los fármacos , Actividad Motora/efectos de los fármacos , Anfetamina/antagonistas & inhibidores , Animales , Dopaminérgicos/farmacología , Ergolinas/administración & dosificación , Masculino , Microinyecciones , Quinpirol , Ratas , Ratas Endogámicas , Técnicas EstereotáxicasRESUMEN
The interaction of the cholecystokinin octapeptide (CCK-8) with dopamine (DA) and dopamine agonists on neurons in the nucleus accumbens was investigated using single unit recording and iontophoretic techniques in urethane-anaesthetized rats. Neurons in the nucleus accumbens were activated by single pulse stimulation of amygdala. Using seven-barrel microelectrodes, the effects of iontophoretic application of CCK-8, DA, dopamine D1 and/or D2 receptor agonists (SKF 38393 and LY 171555 respectively) were compared. The iontophoretic application of DA, LY 171555 and LY 171555 + SKF 38393 attenuated by 50-60% the excitatory responses of accumbens neurons to electrical stimulation of basolateral amygdala whereas SKF 38393 attenuated the response by less than 30%. The iontophoretic application of CCK reduced these attenuating effects of DA, LY 171555 and SKF 38393 + LY 171555. With CCK there was a rather small reduction of the attenuating effect of SKF 38393. These observations provide additional electrophysiological evidence of the interaction of CCK and dopamine and suggest that the interaction is associated mainly with dopamine D2 mechanisms.
Asunto(s)
2,3,4,5-Tetrahidro-7,8-dihidroxi-1-fenil-1H-3-benzazepina/farmacología , Amígdala del Cerebelo/fisiología , Benzazepinas/farmacología , Dopaminérgicos/farmacología , Dopamina/farmacología , Ergolinas/farmacología , Neuronas/fisiología , Núcleo Accumbens/fisiología , Receptores Dopaminérgicos/fisiología , Sincalida/farmacología , Amígdala del Cerebelo/efectos de los fármacos , Animales , Estimulación Eléctrica , Potenciales Evocados/efectos de los fármacos , Masculino , Neuronas/efectos de los fármacos , Núcleo Accumbens/efectos de los fármacos , Quinpirol , Ratas , Ratas Endogámicas , Receptores Dopaminérgicos/efectos de los fármacosRESUMEN
Injections of the dopamine D2 agonist quinpirole (LY 171555) into the nucleus accumbens reduced exploratory locomotion in a dose-dependent manner. Injections of the dopamine D1 agonist SKF 38393 had no effect on exploratory locomotion. The results are consistent with observations from recent electrophysiological and behavioral experiments which suggest a presynaptic action of the D2 agonist. It is proposed that quinpirole activates D2 receptors on the axon terminals of glutamatergic hippocampal-accumbens neurons that are associated with exploratory locomotion.
Asunto(s)
Dopaminérgicos/farmacología , Ergolinas/farmacología , Conducta Exploratoria/efectos de los fármacos , Actividad Motora/efectos de los fármacos , Animales , Relación Dosis-Respuesta a Droga , Masculino , Quinpirol , Ratas , Ratas Endogámicas , Factores de TiempoRESUMEN
Dopamine has been shown to modulate responses of accumbens neurones to excitatory inputs from the amygdala. The demonstration that cholecystokinin (CCK) co-exists and appears to be co-released with dopamine in the accumbens suggests that the modulatory action of dopamine in the accumbens may in turn be modified by CCK. This possibility was investigated in the present study. Single unit recordings were obtained in the medial and caudal accumbens of urethane-anaesthetized rats. These neurones were strongly excited by amygdala stimulation, and concurrent stimulation of the ventral tegmental area (VTA) at 10 Hz attenuated the responses, presumably due to dopamine release. Iontophoretic application of proglumide (PRG) at 30 nA enhanced the attenuating effect of VTA stimulation on the excitatory response to amygdala stimulation. Exogenous dopamine produced a similar attenuation in response and the attenuation was in turn suppressed by concurrent iontophoresis of sulphated CCK fragments applied at a current titrated not to produce significant effect on the spontaneous activity of the neurone nor its response to amygdala stimulation. These results demonstrate that exogenous and endogenous CCK can modify the postsynaptic action of dopamine in the nucleus accumbens in addition to modulating its release shown in other studies, and further suggests that CCK is likely an endogenous functional antagonist of dopamine, serving a comodulatory role in regulating synaptic transmission in the ventral striatum.
Asunto(s)
Colecistoquinina/farmacología , Dopamina/farmacología , Núcleo Accumbens/efectos de los fármacos , Amígdala del Cerebelo/fisiología , Animales , Interacciones Farmacológicas , Estimulación Eléctrica , Electrofisiología , Potenciales Evocados/efectos de los fármacos , Iontoforesis , Masculino , Neuronas/fisiología , Núcleo Accumbens/citología , Núcleo Accumbens/fisiología , Proglumida/farmacología , Ratas , Ratas Endogámicas , Tegmento Mesencefálico/fisiologíaRESUMEN
The contribution of hippocampal glutamatergic and VTA dopaminergic inputs to the nucleus accumbens and the role of accumbens--ventral and subpallidal GABAergic pathway in integrating the limbic signals into motor responses via pedunculopontine nucleus were examined with electrophysiological and behavioural techniques. Stimulation of hippocampal input to the accumbens activates GABAergic output to the subpallidal area which leads to suppression of spontaneous firing of subpallidal neurons, while activation of dopamine receptors in the accumbens suppresses GABAergic output to subpallidal area and thus increases the firing of picrotoxin-sensitive ventral pallidal neurons. However, both treatments induced hypermotility suggesting the functional heterogeneity of the ventral and subpallidal areas in "limbic-motor integration". Furthermore, both hippocampal output signals and dopaminergic input to the accumbens descend via ventral and subpallidal areas serially to the pedunculopontine nucleus, the region of the mesencephalic locomotor region. In addition, a parallel ascending pathway from the subpallidal area to the mediodorsal nucleus, and subsequently to the medial prefrontal cortex, probably mediates behaviour, e.g. food hoarding, that requires higher cognitive processing.
Asunto(s)
Sistema Límbico/fisiología , Motivación , Actividad Motora/fisiología , Neuronas/fisiología , Prosencéfalo/fisiología , Animales , Globo Pálido/fisiología , Humanos , Mesencéfalo/fisiología , Modelos Biológicos , Enfermedades del Sistema Nervioso/fisiopatologíaRESUMEN
The neuromodulatory action of dopamine (DA) on acetylcholine (ACh)-evoked responses of prefrontal cortex (PFC) neurones were investigated electrophysiologically in rats anaesthetised with a combination of urethane and ketamine. Iontophoretic application of ACh-excited prefrontal cortex neurones. Concurrent application of DA (5-15 nA) resulted in complex changes in the ACh-evoked responses: (1) DA depressed spontaneous background discharges (designated as noise) proportionally more than the ACh-evoked discharges (designated as input signals), thus yielding an enhanced signal/noise ratio. This increase in signal/noise ratio by dopamine was reversed by iontophoretic application of the Da D2 antagonist sulpiride (20-50 nA). Nevertheless, iontophoretic application of D2 agonist quinpirole (5-35 nA) enhanced the ACh-evoked response, but was accompanied by some increase in spontaneous discharge, thus yielding no change in the signal/noise ratio. (2) DA also increased the signal/noise ratio by inducing a net increase of the ACh-evoked response but simultaneously suppressed the spontaneous activity of PFC neurones. This effect was more prominent following blockade of D1 receptors by SCH23390 (6 mg/kg, i.p.), suggesting that D1 receptors may normally inhibit D2 receptor function in the PFC. In addition, endogenous DA in the PFC did not play a significant part in modifying the ACh-evoked responses since the modulation of ACh-evoked response by DA or its D1 and D2 agonists was similar in both saline control and alpha-methyl-p-tyrosine-pretreated rats. (3) When ejected with larger iontophoretic current (16-35 nA), DA suppressed both the ACh-evoked and spontaneous discharge and this effect was mimicked by D1 agonist SKF38393 (5-15 nA). Taken together, these results suggest that complex dopaminergic modulation of the cholinergic responses of prefrontal cortex neurones are mediated by D1 and D2 receptors. This DA action may have a functional role in the cognitive-integrative processes occurring in the prefrontal cortex.
Asunto(s)
Acetilcolina/farmacología , Corteza Cerebral/fisiología , Dopamina/farmacología , Neuronas/fisiología , 2,3,4,5-Tetrahidro-7,8-dihidroxi-1-fenil-1H-3-benzazepina/farmacología , Animales , Benzazepinas/farmacología , Corteza Cerebral/efectos de los fármacos , Dopaminérgicos/farmacología , Electrofisiología/métodos , Ergolinas/farmacología , Potenciales Evocados/efectos de los fármacos , Iontoforesis , Masculino , Metiltirosinas/farmacología , Neuronas/efectos de los fármacos , Quinpirol , Ratas , Ratas Endogámicas , Tirosina 3-Monooxigenasa/antagonistas & inhibidores , alfa-MetiltirosinaRESUMEN
The role of the glutamatergic hippocampal-nucleus accumbens pathway in relaying hippocampal information via the nucleus accumbens to the motor system was investigated behaviorally using the radial-arm maze paradigm in rats. Bilateral injections of kynurenic acid, a glutamate antagonist, into the nucleus accumbens increased the latency to initiate movement during performance of an 8-arm radial maze with all arms baited and with 4 arms baited. Injections of kynurenic acid did not change the number of visits to previously visited arms (i.e. working memory errors) on both versions of the 8-arm radial maze. However, on the 8-arm radial maze with 4 arms baited, injections increased the number of visits to unbaited arms (i.e. reference memory errors). Similar injections were made in rats with ibotenic acid lesions of the prefrontal cortex in order to eliminate the glutamatergic prefrontal cortex-nucleus accumbens pathway so as to investigate the glutamatergic hippocampal-nucleus accumbens pathway. These rats displayed similar deficits on the radial-arm maze as non-lesioned rats (i.e. enhanced latency to initiate movement and reference memory errors). These findings suggest that the glutamatergic hippocampal-accumbens pathway plays a role in radial-arm maze performance by transferring information required for performing a radial-arm maze to the motor system.
Asunto(s)
Aprendizaje Discriminativo/fisiología , Hipocampo/fisiología , Ácido Quinurénico , Núcleo Accumbens/metabolismo , Núcleos Septales/metabolismo , Conducta Espacial/fisiología , Animales , Masculino , Memoria/fisiología , Núcleo Accumbens/efectos de los fármacos , RatasRESUMEN
Recordings were made of the electrical activity of neurons in the subpallidal area of urethane-anesthetized rats. Output neurons from the subpallidal area to the pedunculopontine nucleus were identified by antidromic activation. The inputs to subpallidal neurons to single-pulse stimulation of the amygdala and hippocampus were investigated. More than two-thirds of the subpallidal neurons antidromically activated by pedunculopontine stimulation were inhibited by hippocampal stimulation and activated by amygdala stimulation. Subpallidal neurons not antidromically activated by pedunculopontine stimulation also responded to stimulation of the amygdala and hippocampus but no differential effects were observed. The relation of these findings to limbic influences on locomotor activity is discussed.
Asunto(s)
Amígdala del Cerebelo/fisiología , Globo Pálido/fisiología , Hipocampo/fisiología , Tegmento Mesencefálico/fisiología , Potenciales de Acción , Animales , Estimulación Eléctrica , Masculino , Vías Nerviosas/fisiología , Ratas , Ratas EndogámicasRESUMEN
The possible role of ventral pallidum (VP) in expressing dopaminergic actions in the nucleus accumbens was studied electrophysiologically using extracellular single unit recording and iontophoretic techniques in urethane-anaesthetized rats. Microinjections of dopamine (130 mM, 5-10 micrograms/0.2-0.4 microliters) into the nucleus accumbens resulted in a gradual, but prolonged, increase in the firing rate of VP neurones. Injections of the D1 agonist SKF38393 (34 mM, 2 micrograms/0.2 microliters), followed by the D2 agonist quinpirole (40 mM, 2 micrograms/0.2 microliters) into the accumbens, but not in the reverse order, resulted in a similar increase in the activity of VP neurones, mimicking the dopaminergic effect. Injections of either the D1 or the D2 agonist alone into the accumbens, however, produced no significant changes. Furthermore, iontophoretic application of picrotoxin, a gamma-aminobutyric acid (GABA) antagonist, or naloxone, an opiate (including enkephalin) antagonist on the same VP neurone which responded to accumbens dopamine injection also increase its spontaneous firing rate. Thus, pre-activation of D1 receptors in the accumbens was essential for the subsequent physiological expression of D2 receptors in inducing an increase in the firing rate of VP neurones. Dopamine in the accumbens may suppress the tonic inhibitory GABAergic and enkephalinergic outputs to the VP, resulting in an increase in firing rate of VP neurones. Since previous behavioural studies have shown that dopaminergic stimulation in the accumbens increases locomotor activity, the increased firing rate of ventral pallidal neurones may be expressing the postsynaptic actions of dopamine receptor stimulations in the accumbens as initiation of locomotor activity.
Asunto(s)
Benzazepinas/farmacología , Dopaminérgicos/farmacología , Ergolinas/farmacología , Globo Pálido/fisiología , Núcleo Accumbens/fisiología , Receptores Dopaminérgicos/fisiología , Núcleos Septales/fisiología , 2,3,4,5-Tetrahidro-7,8-dihidroxi-1-fenil-1H-3-benzazepina , Potenciales de Acción/efectos de los fármacos , Animales , Naloxona/farmacología , Núcleo Accumbens/efectos de los fármacos , Picrotoxina/farmacología , Quinpirol , Ratas , Receptores Dopaminérgicos/efectos de los fármacosRESUMEN
The contribution of the pedunculopontine nucleus to exploratory locomotion was investigated in rats. Locomotor activity recorded in a standard open-field apparatus was increased more than two-fold when wooden panels were inserted. This novelty-elicited locomotion was reduced significantly when procaine was injected bilaterally into the pedunculopontine nucleus but not when procaine was injected bilaterally into the mediodorsal thalamus, a second major projection site of the subpallidal area. These results support observations from earlier studies implicating hippocampal-accumbens-subpallidal-pedunculopontine projections in exploratory locomotion.
Asunto(s)
Conducta Exploratoria/fisiología , Globo Pálido/fisiología , Puente/fisiología , Núcleos Talámicos/fisiología , Animales , Masculino , Ratas , Ratas EndogámicasRESUMEN
The effect of pharmacological stimulation of the amygdala on spontaneous locomotor activity in the rat and its modulation by accumbens dopamine were investigated. Bilateral injection of N-methyl-D-aspartic acid into the basolateral nucleus of the amygdala produced a dose-dependent suppression of spontaneous locomotor activity in the rat. The suppression of locomotor activity was reversed completely by injection of L-glutamic acid diethyl ester, a putative glutamatergic antagonist, into the nucleus accumbens but partially enhanced by injection of nipecotic acid, a GABA uptake inhibitor, into the ventral pallidum. Furthermore, low doses of dopamine injected into the accumbens, which by itself did not elicit hyperactivity in the animals, completely reversed the suppression of locomotor activity following amygdala stimulation. These results show that the projection from the amygdala to nucleus accumbens has an inhibitory effect on spontaneous locomotor activity in rats and that dopamine in the accumbens attenuated this suppression effect possibly due to its neuromodulatory action as demonstrated in previous electrophysiological experiments.
Asunto(s)
Amígdala del Cerebelo/fisiología , Ácido Aspártico/análogos & derivados , Dopamina/farmacología , Conducta Exploratoria/efectos de los fármacos , Núcleo Accumbens/fisiología , Núcleos Septales/fisiología , Amígdala del Cerebelo/efectos de los fármacos , Animales , Ácido Aspártico/farmacología , Interacciones Farmacológicas , Antagonistas de Aminoácidos Excitadores , Glutamatos/farmacología , Masculino , Microinyecciones , Actividad Motora/efectos de los fármacos , N-Metilaspartato , Ácidos Nipecóticos/farmacología , Núcleo Accumbens/efectos de los fármacos , Ratas , Ratas Endogámicas , Valores de ReferenciaRESUMEN
Intracellular recordings were made from neurons in the nucleus accumbens in situ to determine how dopamine produces the selective neuromodulatory action in the accumbens observed in previous studies. Electrical stimulation of the basolateral nucleus of the amygdala was found to produce monosynaptically evoked depolarizing and hyperpolarizing postsynaptic potential sequences in a large proportion of the accumbens neurons sampled. Dopamine applied iontophoretically or released endogenously by stimulation of the ventral tegmental area produced consistent membrane depolarization and an increase in membrane conductance but not an increase in spontaneous activity of the accumbens neurons. Stimulation of the ventral tegmental area with trains of 10 pulses at 10 Hz prior to stimulation of the amygdala produced 8-58% reduction in the amplitude of the depolarizing postsynaptic potential but no change in the late hyperpolarizing postsynaptic potential. Although attenuation of the depolarizing postsynaptic potential amplitude from ventral tegmental area stimulation was often accompanied by membrane depolarization, it appeared that the two responses were not causally related. The effect of ventral tegmental area stimulation on the evoked depolarizing postsynaptic potential and the membrane potential were blocked by haloperidol indicating the involvement of dopamine. Iontophoretically applied dopamine produced responses similar to ventral tegmental area stimulation with two exceptions: (i) iontophoretically applied dopamine produced consistently stronger maximal attenuation of the depolarizing postsynaptic potential than did ventral tegmental area stimulation; and (ii) iontophoretically applied dopamine always attenuated both the depolarizing postsynaptic potential and hyperpolarizing postsynaptic potential whereas ventral tegmental area stimulation produced selective attenuation of the depolarizing postsynaptic potential only. These electrophysiological results are complementary to those from pharmacological experiments and suggest that one of several physiological functions of dopamine in the nucleus accumbens is a neuromodulatory one involving presynaptic action on non-dopaminergic terminals.
Asunto(s)
Dopamina/farmacología , Núcleo Accumbens/fisiología , Núcleos Septales/fisiología , Potenciales de Acción/efectos de los fármacos , Amígdala del Cerebelo/fisiología , Animales , Estimulación Eléctrica , Haloperidol/farmacología , Masculino , Potenciales de la Membrana/efectos de los fármacos , Neuroglía/fisiología , Núcleo Accumbens/efectos de los fármacos , Ratas , Ratas Endogámicas , Tegmento Mesencefálico/fisiologíaRESUMEN
The pedunculopontine nucleus (PPN) is a major component of the mesencephalic locomotor region. There is little known, however, about neurotransmitters in the PPN associated with locomotor activity. The purpose of the present study was to investigate a possible modulatory effect of the cholinergic system on locomotion. The effects of application of carbachol (CCh) into the PPN on locomotor activity of freely moving rats were studied. Unilateral injections of CCh into the PPN decreased spontaneous locomotor activity of rats. On the other hand, an increase in locomotor activity resulted from CCh injections into sites surrounding the PPN. These CCh-induced changes in locomotion were no longer observed after pretreatment of the PPN with atropine. Locomotor activity induced by injections of amphetamine into the nucleus accumbens was also reduced to control levels by ipsilateral injections of CCh into the PPn, whereas contralateral injections of CCh were ineffective. The results suggest that the muscarinic cholinergic system has a modulatory influence on locomotor activity presumably by affecting PPN cells involved in relaying locomotion-associated signals. The PPN receives signals from higher structures involved in initiation of locomotion while the muscarinic system seems to play a role in attenuation or inhibition of locomotor behaviour.
Asunto(s)
Carbacol/farmacología , Locomoción/efectos de los fármacos , Mesencéfalo/fisiología , Anfetamina/farmacología , Animales , Masculino , Núcleo Accumbens/fisiología , Ratas , Ratas EndogámicasRESUMEN
The locomotor activity of freely moving rats was increased by electrical stimulation of brainstem sites, including the pedunculopontine nucleus, a major component of the mesencephalic locomotor region (MLR), and sites located in the subthalamic locomotor region (SLR), which is in the area of the zona incerta (ZI) dorsomedial to the subthalamic nucleus. Injections to the MLR of glycine, an inhibitory transmitter of the spinal cord and brainstem, had no effect on locomotion, nor did strychnine sulfate, a glycine antagonist. Unilateral injections of the excitatory amino acid, N-methyl-D-aspartic acid (NMDA), and kainic acid, a glutamate analogue, into the MLR produced an increase in locomotion not seen with glutamate, an excitatory amino acid, into the same area. A still greater response, having a later onset than NMDA but also a longer duration, was produced by administration of picrotoxin and bicuculline methiodide, GABA antagonists, to the MLR. Carbachol injections into the MLR produced two types of responses: either increased or decreased locomotion. Hypermotility resulted from microinjections of glutamate, and picrotoxin and bicuculline, into the ZI. The short latency, short duration response to glutamate resulted in a greater increase in locomotion than with picrotoxin or bicuculline when each was administered into the SLR. These results provide further evidence for the functional role of the MLR and SLR in the initiation of locomotor activity in the intact, freely behaving rat.
Asunto(s)
Tronco Encefálico/fisiología , Actividad Motora/fisiología , Aminoácidos/farmacología , Animales , Bicuculina/farmacología , Mapeo Encefálico , Tronco Encefálico/efectos de los fármacos , Carbacol/farmacología , Estimulación Eléctrica , Masculino , Actividad Motora/efectos de los fármacos , Picrotoxina/farmacología , Ratas , Ratas Endogámicas , Estricnina/farmacologíaRESUMEN
Experiments were done in urethan-anesthetized rats to investigate the effect of plasma angiotensin II (ANG II) and hypernatremia on the excitability of subfornical organ (SFO) neurons projecting directly to paraventricular nucleus of the hypothalamus (PVH), supraoptic nucleus (SON), and nucleus medianus (NM). Extracellular recordings were made from 106 antidromically identified neurons in the SFO. The firing frequency of 53 (50%) was increased by the intracarotid infusion of ANG II and/or 0.5 M hypertonic NaCl. The intracarotid infusion of isotonic saline or the intravenous infusion of phenylephrine did not alter the discharge rate of these SFO neurons. Of 38 PVH projecting neurons, 21 (55%) responded to ANG II and/or hypertonic NaCl: 9 to ANG II only, 8 to hypertonic NaCl only, and 4 to both. Similarly, of 42 SON projecting neurons, 30 (71%) responded to ANG II and/or hypertonic NaCl: 10 to ANG II only, 15 to hypertonic NaCl only, and 5 to both. Finally, of 26 NM projecting neurons, one increased its firing frequency to ANG II and one other to 0.5 M NaCl. An additional eight SFO neurons were found to send collateral axons to both the PVH and SON (n = 6) and PVH and NM (n = 2): four responded in various combinations to intracarotid infusion of ANG II and 0.5 M NaCl. These data suggest that blood-borne ANG II and plasma hypernatremia can influence arterial pressure and the release of vasopressin from the neurohypophysis by altering the discharge rate of SFO neurons projecting to forebrain structures that contain magnocellular neurosecretory vasopressin neurons and neurons that are components of sympathoexcitatory pathways.
Asunto(s)
Angiotensina II/sangre , Hipernatremia/fisiopatología , Neuronas/fisiopatología , Sistemas Neurosecretores/fisiopatología , Órgano Subfornical/fisiopatología , Animales , Estimulación Eléctrica , Electrofisiología , Hipernatremia/sangre , Masculino , Modelos Neurológicos , Núcleo Hipotalámico Paraventricular/fisiología , Fenilefrina/farmacología , Área Preóptica/fisiología , Ratas , Ratas Endogámicas , Cloruro de Sodio/farmacología , Núcleo Supraóptico/fisiologíaRESUMEN
The contributions of accumbens-subpallido-mediodorsal thalamus (MD) projections to food hoarding were investigated. The number of food pellets hoarded was reduced by bilateral injections of haloperidol into the accumbens, by bilateral injections of GABA into the subpallidal region and by bilateral injections of procaine into the mediodorsal thalamus. Food hoarding was not reduced by bilateral injections of procaine into the pedunculopontine nucleus. It appears that subpallido-mediodorsal thalamus projections are associated with hoarding behavior but not subpallido-pedunculopontine projections.
Asunto(s)
Conducta Animal/fisiología , Globo Pálido/fisiología , Núcleo Accumbens/fisiología , Núcleos Septales/fisiología , Tálamo/fisiología , Animales , Conducta Animal/efectos de los fármacos , Alimentos , Haloperidol/farmacología , Inyecciones , Procaína/farmacología , Ácido gamma-Aminobutírico/farmacologíaRESUMEN
A comparison was made of the contributions to locomotor activity of output projections of the subpallidal region to the mediodorsal thalamus (MD) and to the pedunculopontine nucleus (PPN). Locomotor activity elicited by injections of picrotoxin into the subpallidal region was reduced by the administration of procaine to the pedunculopontine nucleus but not by the administration of procaine to mediodorsal thalamus. Since the pedunculopontine nucleus is part of the mesencephalic locomotor region (MLR) it appears that subpallido-pedunculopontine projections contribute to the locomotor component of adaptive behaviors associated with limbic integrative activities.