Neuropsychological outcome of GPi pallidotomy and GPi or STN deep brain stimulation in Parkinson's disease

This paper highlights the neuropsychological sequelae of posteroventral pallidotomy (PVP) and deep brain stimulation (DBS) of the subthalamic nucleus (STN) and the internal segment of the globus pallidus (GPi) at 3/6 months postoperatively. Results are based on our extensive experience with PVP and our preliminary observations with DBS. Patients with borderline cognitive or psychiatric functioning risk postoperative decompensation. Nonlateralizing attentional and hemisphere-specific impairments of frontostriatal cognitive functions followed unilateral PVP. "Frontal" behavioral dyscontrol was observed in approximately 25% of patients. Three cases of staged bilateral PVP suggest that premorbid factors may predict outcome, although lesion size and location are also critical. Older patients are at risk for significant cognitive and behavioral decline after bilateral STN DBS, while GPi DBS may be safer.     

‘Telepathic’ phenomena and separation anxiety

By discussing a treatment characterized by its difficult ending, the author strives to show the dynamic impact of separation on phenomena that can be seen as ‘telepathic’. Led to develop some inalienable attachment to her analyst in the primary transference, the analysand found herself caught up in the contradiction of her visceral dread of dependency, which compelled her to interrupt the work in progress. She then began to work out her analyst's comings and goings and to run into him in public places, as if to be assured of his immovability. This phenomenon arose with high frequency as the effect of some idealization of the maternal object aiming to deny the spatiotemporal gap. The chance that the experience of rejection via indifference may be repeated also entailed the transferential unfurling of a fantasy involving a double, undifferentiation counterbalancing the lived experience of separation. Furthermore, a ‘telepathic’ dream occurred as confirmation of this twin relationship which illustrates the analysand's refusal to renounce her narcissistic object. Projective identifications, agglutinated ego nuclei along with primitive cross‐identifications could, among other concepts, account for such phenomena which are projective in nature yet real all the same. Such mechanisms could have the power to relay thoughts the moment undifferentiated parts of the ego – if not unborn parts of the self – were activated in a potentially symbiotic zone. Marked by a feeling of dispossession, the analyst's countertransference not only seemed to underscore this hypothesis, it also gave a partial explanation for it. Until the analyst could recognize his own nostalgia for a symbiotic relationship, he had to encourage the occurrence of those unexpected meetings which stemmed from a convergence between the transference and the countertransference.     

Glutamate receptors in the medial geniculate nucleus are necessary for expression and extinction of conditioned fear in rats

Auditory fear conditioning requires anatomical projections from the medial geniculate nucleus (MGN) of the thalamus to the amygdala. Several lines of work indicate that the MGN is a critical sensory relay for auditory information during conditioning, but is not itself involved in the encoding of long-term fear memories. In the present experiments, we examined whether the MGN plays a similar role in the extinction of conditioned fear. Twenty-four hours after Pavlovian fear conditioning, rats received bilateral intra-thalamic infusions of either with NBQX (an AMPA receptor antagonist; Experiment 1) or MK-801 (an NMDA receptor antagonist; Experiment 1), anisomycin (a protein synthesis inhibitor; Experiment 2) or U0126 (a MEK inhibitor; Experiment 3) immediately prior to an extinction session in a novel context. The next day rats received a tone test in a drug-free state to assess their extinction memory; freezing served as an index of fear. Glutamate receptor antagonism prevented both the expression and extinction of conditioned fear. In contrast, neither anisomycin nor U0126 affected extinction. These results suggest that the MGN is a critical sensory relay for auditory information during extinction training, but is not itself a site of plasticity underlying the formation of the extinction memory.     

Methodological evolution and clinical application of C.G. Jung's Word Association Experiment: a follow-up study

We became interested in the clinical application of the Word Association Experiment (AE) when we decided to use Jung's theory of complexes in the psycho-diagnostic evaluation and treatment of patients applying to our Psychotherapy Out-patients Unit (Psychiatric Clinic, Milan University). In psychopathological situations, complexes with a particularly high emotional charge become autonomous and disturbing, inhibiting the ego's functions. The representations and affective states corresponding to these complexes become dominant, conditioning the expression of symptoms and the subject's relational modes. In this experimental study we started out from the basic theory that our psycho-therapeutic work should lead to a progressive change in the patient's initial complex set up. Jung's Word Association Experiment allows us to identify those words which indicate and stimulate a specific activation of the complexes for each subject via specific markers of complexes. We therefore decided to determine whether AE, administered during the first phase of clinical-diagnostic evaluation and after one year of treatment, revealed any changes occurring in the patients' set up of complexes.     

Neurochemical mechanisms underlying amygdaloid modulation of aggressive behavior in the cat

Studies designed to determine the respective roles of substance P, excitatory amino acids, and enkephalins in amygdaloid modulation of defensive rage behavior in the cat are presented. The basic design of these studies involved three stages. In stage I, cannula electrodes for stimulation and drug infusion were implanted into medial hypothalamic or midbrain periaqueductal gray (PAG) sites from which defensive rage behavior could be elicited. Then, a stimulating electrode was implanted into a site within the medial, basal, or central nuclear complex from which modulation of the defensive rage response could be obtained. Amygdaloid modulation of defensive rage was determined in the following manner: it employed the paradigm of dual stimulation in which comparisons were made of response latencies between alternate trials of dual (i. e., amygdala = medial hypothalamus [or PAG]) and single stimulation of the hypothalamus or PAG alone. Thus, stage I established the baseline level ofmodulation (i. e., facilitation or suppression of defensive rage) in the predrug stimulation period. In stage II, a selective or nonselective receptor antagonist for a given transmitter system was administered either peripherally or intracerebrally at the defensive rage site, after which time the same dual stimulation paradigm was then repeated over the ensuing 180 min postinjection period in order to determine the effects of drug delivery upon amygdaloid modulation of defensive rage. Stage III of the study took place at the completion of the pharmacological testing phase. The retrograde axonal tracer, Fluoro-Gold, was microinjected into the defensive rage site within the medial hypothalamus or PAG, and following a 6-14 day survival period, animals were sacrificed and brains were processed for histological and immunocytochemical analyses for the neurotransmitters noted above. This procedure thus permitted identification of cells within the amygdala which were labeled retrogradely and which were also immunostained positively for substance P, excitatory amino acids, or enkephalin. For studies involving substance P, defensive rage was elicited from the medial hypothalamus and for studies examining the roles of excitatory amino acids and enkephalin, defensive rage was elicited from the PAG. In the first study, facilitation of hypothalamically elicited defensive rage was obtained with dual stimulation of the medial nucleus of the amygdala. In separate experiments, the selective NK₁ non-peptide antagonist, CP 96,345, was administered both peripherally as well as intracerebrally into the hypothalamic defensive rage sites in doses of 0.5-4.0 mg/kg (i. p.) and 0.5-2.5 nmol (i. c.). Following drug delivery, the facilitatory effects of medial amygdaloid stimulation were blocked in a dose- and time-dependent manner in which the effects were noted as early as 5 min postinjection. The maximum drug dose (4.0 mg/kg) employed for peripheral administration resulted in a 42% reduction in the facilitatory effects of the medical amygdala (P < 0.002). This drug, when microinjected directly into medial hypothalamic defensive rage sites at the maximum dose level of 2.5 nmol, resulted in an 84% reduction of the suppressive effects of amygdaloid stimulation (P < 0.5) at 5 min postinjection. In the next study, an N-methyl-D-aspartate (NMDA) antagonist, DL-α-amino-7-phosphonoheptanoic acid (AP-7), was administered either peripherally (0.1-1.0 mg/kg) or intracerebrally (0.2 and 2.0 nmol) into PAG defensive rage sites. Facilitation of defensive rage behavior, which was observed following dual stimulation of the basal amygdala and PAG, was significantly reduced by either route of drug administration in a dose- and time-dependent manner. At the maximum dose level of peripheral administration, AP-7 reduced amygdaloid facilitation of defensive rage by 63% (P < 0.001) for 60 min, postinjection. A smaller (i. e., 19%) but still significant (P < 0.05) reduction in facilitation was obtained following intracerebral administration of the drug. In a third study, the non-selective opioid receptor antagonist, naloxone (27.5 nmol), infused directly into PAG defensive rage sites, totally blocked the suppressive effects of central amygdaloid stimulation for a period of 30 min (P < 0.05) in a dose- and time-dependent manner. The anatomical phase of this study revealed the following relationships: 1) that large numbers of neurons projecting to the medial hypothalamus from the medial amygdala immunoreact positively for substance P; 2) that neurons projecting to the PAG from the basal complex of amygdala immunoreact positively for glutamate and aspartate; and 3) that neurons located within the central nucleus of the amygdala which project to the PAG immunoreact positively for met-enkephalin. Collectively, these observations provide new evidence which characterizes the likely neurotransmitters linked with specific amygdaloid pathways subserving the modulation of defensive rage behavior in the cat.     

习得性无助是习得的吗？——对习得性无助理论及其反思的评述

Seligman和Maier（1967）在动物实验的基础上提出了著名的习得性无助理论,但在2016年,Maier和Seligman二人却联合发文对该理论进行了反思：从最新的神经生物学证据来看,习得性无助的经典理论概括存在基本错误,习得性无助并非习得而来！所谓“习得性”无助,实质上是动物对厌恶刺激长期作用的先天适应性反应,而非认知学习的结果。本文简要梳理习得性无助理论的起源与发展,深入分析这一反思的核心内容、依据及意义,对其中否定习得性无助理论概括的观点,从证据的充分性、研究范式的效度、规范概念等角度作了进行进一步的探讨,并结合新的实验范式对未来研究提出建议。     

Serotonin's influence on predatory behavior of highly aggressive cba and weakly aggressive DD strains of mice

The effects of serotonin were studied on locust-killing behavior of mice from low (DD) and high (CBA) predatory aggressive strains. 5-HTP injected intraperitoneally (50 and 100 mg/kg) or 5-HT administered into the lateral ventricle (10 μg) significantly reduced locust-killing behavior in highly aggressive CBA mice. Imipramine (20, 30, and 40 mg/kg) elicited a dose-dependent inhibitory effect on predatory behavior. Fluoxetine (10 and 20 mg/kg) alone had a slight influence on locust-killing behavior but potentiated the action of the subthreshold dose of 5-HTP (25 mg/kg). Pretreatment with the blocker of 5-HT₂ type receptors methysergide (2 mg/kg) abolished the inhibitory effect of 5-HTP. These finding indicate that serotonin of the brain exerts an inhibitory effect on predatory behavior in mice. In contrast, neither lesion of the dorsal raphe nucleus (although significantly depleting the brain serotonin) nor treatment with methysergide (2 mg/kg) induced locust-killing behavior in weakly aggressive DD mice. Low predatory aggressiveness in DD mice is suggested to be related to the low tonus of the mechanisms activating killing behavior rather than to excessive serotonergic inhibitory influences.     

Another language,another place: To hide or be found?

The author examines some specifi c features of the analytic encounter when both patient and analyst are émigrés from the same cultural and linguistic background. This can result in splitting processes that operate silently and are diffi cult to reach, but can also provide rich material, as they offer the couple the opportunity to work through the pain and the guilt over what is lost—ultimately the lost mother—murdered and betrayed. Working through the split faces the analyst with important technical considerations, bearing in mind that the shared cultural identity can conceal itself in the more undifferentiated features of the couple's psyche and be projected on to the setting. As such, it needs to be put to analytic scrutiny if the treatment is to avoid a stalemate. These are specifi c cultural defences deployed in the problematic existential encounter with the foreigner other within oneself. Using clinical material from two cases, the author shows how the couple's access to a dual linguistic signifying system can enrich the analytic dialogue, but can also result in enactment. Careful monitoring of the transference-countertransference relationship is essential to the progress of the analytic work.     

伏隔核和中脑腹侧被盖区内食欲素在吗啡奖赏中的作用

实验采用条件性位置偏爱（CPP）模型考察中脑腹侧被盖区（VTA）和伏隔核壳区（NAcSh）内食欲素（orexin）在吗啡奖赏中的作用。Wistar大鼠分为盐水训练组和吗啡训练组。3轮吗啡（或盐水）匹配训练前,双侧VTA或NAcSh内给予OXR1拮抗剂SB334867（VTA: 0, 1, 5μg;NAcSh: 0, 1, 3μg）;或2轮吗啡（或盐水）匹配训练前NAcSh内给予orexin A（0, 2, 4, 6μg）,观察其对吗啡CPP建立的影响。结果表明,VTA内给予SB334867抑制吗啡CPP建立,并存在剂量效应关系;NAcSh内给予SB334867或orexin A均未影响吗啡CPP建立,而orexin A可增加吗啡处理大鼠的运动性。以上结果表明,VTA和NAcSh内的orexin在吗啡奖赏中扮演的角色不同,可能调控成瘾行为的不同成分     

The effects of lesions in the central nucleus of the amygdala on appetitive classical conditioning in rats

Abstract: Lesions in the central nucleus of the amygdala (cAMY) have been known to interfere with the acquisition of fear classical conditioning when footshock is used as an unconditioned stimulus (US). The present study examined whether or not a similar interference would occur with an appetitive US. Five rats with lesions in the cAMY (the cAMY group), and eight unoperated control rats were trained in an appetitive classical conditioning paradigm, which did not include elements of operant learning, using a visual conditioned stimulus (CS) (5 W of light for 10 s duration) paired with a food pellet US (45 mg, cheese flavor). The behavioral index of appetitive conditioning was an increase in rearing approach behavior to the CS after CS and US pairings. During CS and US pairings, the movement of the rat was limited so that this approach behavior could not occur. As a result, all control rats showed an increase in rearing, but the cAMY group did not. These results suggest that the cAMY is critical for appetitive as well as fear classical conditioning.