Role of the limbic system in hypothalamically elicited attack behavior

The present review summarizes our research findings concerning the role of the limbic system in hypothalamically-elicited aggression in the cat. Utilizing a dual-stimulation procedure, our results indicate that much of the limbic system suppresses quiet biting attack behavior. The most potent inhibitory effects were obtained from the basomedial amygdala and the prefrontal cortex. Other structures displaying suppression of attack following electrical stimulation include the dorsal hippocampus, pyriform cortex, lateral septal nucleus, lateral aspect of substantia innominata, and anterior cingulate gyrus. Sites producing facilitation of attack include the ventral hippocampus, far lateral aspect of the lateral septal nucleus, medial aspect of the substantia innominata, and lateral amygdaloid nucleus. Anatomical studies suggest that the medial forebrain bundle and stria terminalis are utilized by limbic structures to provide direct modulation of the hypothalamus while the substantia innominata, mediodorsal thalamic nucleus and bed nucleus of the stria terminalis contain important interneurons in the control of quiet biting attack. Further studies indicate that the amygdala, ventral hippocampus, and substantia innominata may control aggressive behavior by modulating the trigeminal sensory components of the attack response.     

Respiratory pumping: Neuronal control of a centrally commanded behavior in aplysia

Respiratory pumping in Aplysia californica is a relatively stereotyped behavioral pattern with three components: (1) withdrawal of gill, siphon and mantle shelf; (2) closing of parapodia; (3) heart inhibition accompanied by a decrease in vasomotor tone. This phasic behavior is triggered by a central burst-generating network of interneurons in the abdominal ganglion. During respiratory pumping, motor neurons innervating the several effector organs receive a burst of either excitatory or inhibitory synaptic input which has previously been attributed to an unidentified central command cell called Interneuron II. Several of these motor cells are also concomitantly release from tonic synaptic input, which is opposite in sign to that which they receive from Interneuron II. This tonic input has been attributed to an unidentified cell called Interneuron XI. In this paper we identify and describe some of the neurons which contribute to the burst generating network; specifically, we focus on the neurons that produce the synaptic action attributed to Interneurons II and XI. The synaptic actions attributed to Interneuron XI are produced by a single, spontaneously active neuron, cell L24. This cell is a multi-action interneuron: it produces inhibitory synaptic potentials in some follower motor neurons, excitatory synaptic potentials in other follower cells, and a conjoint excitatory-inhibitory synaptic action onto gill motor neuron L7. At low frequency, L24 is excitatory to L7. With high frequency firing of L24, the synaptic potential produced in L7 converts from excitatory to inhibitory. In contrast to Interneuron XI, which is a single cell, the synaptic potentials previously attributed to Interneuron II are actually produced by a cluster of at least 3 respiratory command cells which we call L25, L26 and L27. Each of these cells accounts for only a limited portion of the synaptic input that drives the motor neurons during respiratory pumping. For most motor neurons innervated by both the respiratory command cells and Interneuron XI, the two synaptic inputs are opposite in sign. Mutually inhibitory connections between Interneuron XI and some of the central respiratory command cells ensure that the synaptic potentials from these two sources are constrained to occur at different times. Thus, centrally commanded synaptic inhibition or excitation of these motor neurons is made more effective by simultaneous disexcitation or disinhibition of Interneuron XI input. In addition to their role in generating respiratory pumping, L24 and L26 also contribute to the mediation of the defensive gill and siphon withdrawal reflex.     

Effects of stimulation of the substantia innominata upon attack behavior elicited from the hypothalamus in the cat

Experiments were undertaken in order to determine the role of the substantia innominata and surrounding regions in quiet biting attack elicited from electrical stimulation of the hypothalamus in the cat. Stimulation from sites in the lateral aspect of the substantia innominata resulted in a suppression of quiet biting attack and in a constriction of the 'effective trigeminal sensory fields' established during hypothalamic attack site stimulation. Stimulation from sites situated more medially in the substantia innominata resulted in a facilitation of quiet biting attack and in an expansion of the 'effective trigeminal sensory fields'. The motor component of the jaw opening response was altered in only 50% of the cases in contrast to the consistent effects observed upon the 'effective sensory fields'. Electrical stimulation of the substantia innominata had little effect upon affective display elicited from the ventromedial hypothalamus. Stimulation from sites located in the nucleus accumbens had no effect upon hypothalamically-elicited quiet biting attack and inhibited the occurrence of affective display in 2 to 5 animals tested. These studied suggest that the substantia innominata differentially modulates quiet biting attack and accomplishes this, at least in part, through its effects upon sensory mechanisms associated with the jaw opening reflex.     

Corticospinal control of antagonistic muscles in the cat

We recently suggested that movement-related inter-joint muscle synergies are recruited by selected excitation and selected release from inhibition of cortical points. Here we asked whether a similar cortical mechanism operates in the functional linking of antagonistic muscles. To this end experiments were done on ketamine-anesthetized cats. Intracortical microstimulation (ICMS) and intramuscular electromyographic recordings were used to find and characterize wrist, elbow and shoulder antagonistic motor cortical points. Simultaneous ICMS applied at two cortical points, each evoking activity in one of a pair of antagonistic muscles, produced co-contraction of antagonistic muscle pairs. However, we found an obvious asymmetry in the strength of reciprocal inhibition; it was always significantly stronger on physiological extensors than flexors. Following intravenous injection of a single bolus of strychnine, a cortical point at which only a physiological flexor was previously activated also elicited simultaneous activation of its antagonist. This demonstrates that antagonistic corticospinal neurons are closely grouped, or intermingled. To test whether releasing a cortical point from inhibition allows it to be functionally linked with an antagonistic cortical point, one of three GABA(A) receptor antagonists, bicuculline, gabazine or picrotoxin, was injected iontophoretically at one cortical point while stimulation was applied to an antagonistic cortical point. This coupling always resulted in co-contraction of the represented antagonistic muscles. Thus, antagonistic motor cortical points are linked by excitatory intracortical connections held in check by local GABAergic inhibition, with reciprocal inhibition occurring at the spinal level. Importantly, the asymmetry of cortically mediated reciprocal inhibition would appear significantly to bias muscle maps obtained by ICMS in favor of physiological flexors.     

Differential control of hypothalamically elicited flight behavior by the midbrain periaqueductal gray in the cat

The purpose of the present study was to determine the role of the midbrain periaqueductal gray (PAG) and thalamic centrum medianum-parafascicular complex (CM-Pf) in the regulation of hypothalamically elicited flight behavior in the cat. The experimental paradigm involved a comparison of the differences in response latencies between single stimulation of the hypothalamus and concurrent stimulation of the hypothalamus and sites in the PAG or the CM-Pf. Dual stimulation of the ventral and dorsal aspects of the PAG resulted in differential modulation of flight behavior. Stimulation of the dorsal PAG suppressed hypothalamically elicited flight behavior while stimulation of the ventral aspects of the PAG facilitated flight behavior. Facilitation of flight behavior was also found from stimulation of ventral portions of the CM-Pf.     

Neural pathways mediating hypothalamically elicited flight behavior in the cat

This study has sought to identify hypothalamic pathways mediating flight behavior in the cat. Flight behavior, characterized by an initial pupillary dilatation and followed by vigorous attempts to leap out of the observation chamber, was elicited primarily by electrical stimulation of the medial preoptic region and dorsomedial hypothalamus, and to a lesser extent from the perifornical region. A [14C]-2-deoxyglucose analysis was utilized to examine brain regions functionally activated by stimulation of hypothalamic sites which elicited flight behavior. In a second series of experiments, [3H]leucine injected into regions surrounding electrode tips from which flight had previously been elicited, permitted identification of pathways arising from such functionally characterized sites. We describe for the first time pathways arising from the hypothalamus which mediate flight behavior. In spite of individual variation in placement of electrodes eliciting flight, a consistent pattern of labeling was observed following injection of either [14C]-2-deoxyglucose systemically or [3H]amino acids into the hypothalamus. The primary rostral target structures receiving inputs from flight electrode sites included the nuclei of the diagonal band, bed nucleus of the stria terminalis, medial amygdaloid nucleus, lateral septal nucleus, and anterior medial preoptico-hypothalamus. Caudal to the level of stimulation, the principal target nuclei involved the centrum medianum-parafascicular complex and the midbrain central gray substance. Possible roles of these nuclear regions in organization and regulation of flight behavior is discussed.     

Possible mechanisms involved in the stereotyped behavior elicited by amphetamine.

In a variety of animals, amphetamine administration produces an increase in locomotor behavior and an induction of repetitive, stereotyped behaviors. There is now considerable evidence to suggest that the induction of stereotyped behaviors is accomplished, in part, by alterations in catecholaminergic transmission in the central nervous system. By recording the spontaneous activity of neurons in the rat brain substantia nigra, reticular formation, basal ganglia, and elsewhere during systemic administration of amphetamine and related drugs, or during administration by means of microinfusions directly into these brain regions, relationships may be drawn between the biochemical and behavioral effects of these drugs and drug-induced changes in neuronal activity in the central nerovous system. Current evidence, for example, suggests that amphetamine produces an inhibition of neuronal activity in the neostriatum and pars compacta of the substantia nigra by means of dopamine released from dopaminergic terminals in the neostriatum and dopaminergic dendrites in the substantia nigra respectively. In addition, current evidence suggests the possibility of a GABA-mediated functional antagonism between excitatory cortical and/or thalamic input to the neostriatum and dopaminergic input from the substantia nigra which could be involved in the apparently mutually exclusive occurrence of amphetamine-induced locomotion and stereotyped behaviors that follow amphetamine administration. Such evidence may also have relevance to a variety of behavioral disorders involving the basal ganglia and catecholaminergic transmission in the central nervous system.